We are more than delighted with the care that Stewart Halperin and his team provides.We travelled from Harrogate in North Yorkshire to see Stewart as our little dog suffers from Acute Renal Failure, only 20% of her kidneys are working. We tried several vets in our region, they were very negative and told us she would only survive a few months at best. We found Stewart through the Internet as he and an American vet were working on the new stem cell treatment. We travelled to London to see Stewart, we immediately saw the difference. Stewart had a positive attitude and cared about the dog and not my credit card, unlike most of the other vets we had seen.

After a very in-depth examination and tests, he found that she was anaemic and got that resolved. He continues to monitor her treatment through our local vet and is in contact with us regularly for updates. We feel that Stewart has become a friend to us and we can contact him with any concerns that we may have. Our dog is now over 2 years old and we hope that with Stewarts help she lives a lot longer.

See the rest here:
Treat Arthritis in Dogs and Cats in the UK | Stem Cell Vet UK

Cancer is a group of diseases involving abnormal cell growth with the potential to invade or spread to other parts of the body.[1][2] Not all tumors are cancerous; benign tumors do not spread to other parts of the body.[2] Possible signs and symptoms include a lump, abnormal bleeding, prolonged cough, unexplained weight loss and a change in bowel movements.[3] While these symptoms may indicate cancer, they may have other causes.[3] Over 100 cancers affect humans.[2]

Tobacco use is the cause of about 22% of cancer deaths.[1] Another 10% is due to obesity, poor diet, lack of physical activity and drinking alcohol.[1][4] Other factors include certain infections, exposure to ionizing radiation and environmental pollutants.[5] In the developing world nearly 20% of cancers are due to infections such as hepatitis B, hepatitis C and human papillomavirus (HPV).[1] These factors act, at least partly, by changing the genes of a cell.[6] Typically many genetic changes are required before cancer develops.[6] Approximately 510% of cancers are due to inherited genetic defects from a person's parents.[7] Cancer can be detected by certain signs and symptoms or screening tests.[1] It is then typically further investigated by medical imaging and confirmed by biopsy.[8]

Many cancers can be prevented by not smoking, maintaining a healthy weight, not drinking too much alcohol, eating plenty of vegetables, fruits and whole grains, vaccination against certain infectious diseases, not eating too much processed and red meat, and avoiding too much sunlight exposure.[9][10] Early detection through screening is useful for cervical and colorectal cancer.[11] The benefits of screening in breast cancer are controversial.[11][12] Cancer is often treated with some combination of radiation therapy, surgery, chemotherapy, and targeted therapy.[1][13] Pain and symptom management are an important part of care. Palliative care is particularly important in people with advanced disease.[1] The chance of survival depends on the type of cancer and extent of disease at the start of treatment.[6] In children under 15 at diagnosis the five-year survival rate in the developed world is on average 80%.[14] For cancer in the United States the average five-year survival rate is 66%.[15]

In 2012 about 14.1 million new cases of cancer occurred globally (not including skin cancer other than melanoma).[6] It caused about 8.2 million deaths or 14.6% of human deaths.[6][16] The most common types of cancer in males are lung cancer, prostate cancer, colorectal cancer and stomach cancer. In females, the most common types are breast cancer, colorectal cancer, lung cancer and cervical cancer.[6] If skin cancer other than melanoma were included in total new cancers each year it would account for around 40% of cases.[17][18] In children, acute lymphoblastic leukaemia and brain tumors are most common except in Africa where non-Hodgkin lymphoma occurs more often.[14] In 2012, about 165,000 children under 15 years of age were diagnosed with cancer. The risk of cancer increases significantly with age and many cancers occur more commonly in developed countries.[6] Rates are increasing as more people live to an old age and as lifestyle changes occur in the developing world.[19] The financial costs of cancer were estimated at $1.16 trillion US dollars per year as of 2010.[20]

Cancers are a large family of diseases that involve abnormal cell growth with the potential to invade or spread to other parts of the body.[1][2] They form a subset of neoplasms. A neoplasm or tumor is a group of cells that have undergone unregulated growth and will often form a mass or lump, but may be distributed diffusely.[21][22]

All tumor cells show the six hallmarks of cancer. These characteristics are required to produce a malignant tumor. They include:[23]

The progression from normal cells to cells that can form a detectable mass to outright cancer involves multiple steps known as malignant progression.[24][25]

When cancer begins, it produces no symptoms. Signs and symptoms appear as the mass grows or ulcerates. The findings that result depend on the cancer's type and location. Few symptoms are specific. Many frequently occur in individuals who have other conditions. Cancer is a "great imitator". Thus, it is common for people diagnosed with cancer to have been treated for other diseases, which were hypothesized to be causing their symptoms.[26]

Local symptoms may occur due to the mass of the tumor or its ulceration. For example, mass effects from lung cancer can block the bronchus resulting in cough or pneumonia; esophageal cancer can cause narrowing of the esophagus, making it difficult or painful to swallow; and colorectal cancer may lead to narrowing or blockages in the bowel, affecting bowel habits. Masses in breasts or testicles may produce observable lumps. Ulceration can cause bleeding that, if it occurs in the lung, will lead to coughing up blood, in the bowels to anemia or rectal bleeding, in the bladder to blood in the urine and in the uterus to vaginal bleeding. Although localized pain may occur in advanced cancer, the initial swelling is usually painless. Some cancers can cause a buildup of fluid within the chest or abdomen.[26]

General symptoms occur due to effects that are not related to direct or metastatic spread. These may include: unintentional weight loss, fever, excessive fatigue and changes to the skin.[27]Hodgkin disease, leukemias and cancers of the liver or kidney can cause a persistent fever.[26]

Some cancers may cause specific groups of systemic symptoms, termed paraneoplastic phenomena. Examples include the appearance of myasthenia gravis in thymoma and clubbing in lung cancer.[26]

Cancer can spread from its original site by local spread, lymphatic spread to regional lymph nodes or by haematogenous spread via the blood to distant sites, known as metastasis. When cancer spreads by a haematogenous route, it usually spreads all over the body. However, cancer 'seeds' grow in certain selected site only ('soil') as hypothesized in the soil and seed hypothesis of cancer metastasis. The symptoms of metastatic cancers depend on the tumor location and can include enlarged lymph nodes (which can be felt or sometimes seen under the skin and are typically hard), enlarged liver or enlarged spleen, which can be felt in the abdomen, pain or fracture of affected bones and neurological symptoms.[26]

The majority of cancers, some 9095% of cases, are due to environmental factors. The remaining 510% are due to inherited genetics.[5]Environmental, as used by cancer researchers, means any cause that is not inherited genetically, such as lifestyle, economic and behavioral factors and not merely pollution.[28] Common environmental factors that contribute to cancer death include tobacco (2530%), diet and obesity (3035%), infections (1520%), radiation (both ionizing and non-ionizing, up to 10%), stress, lack of physical activity and environmental pollutants.[5]

It is not generally possible to prove what caused a particular cancer, because the various causes do not have specific fingerprints. For example, if a person who uses tobacco heavily develops lung cancer, then it was probably caused by the tobacco use, but since everyone has a small chance of developing lung cancer as a result of air pollution or radiation, the cancer may have developed for one of those reasons. Excepting the rare transmissions that occur with pregnancies and occasional organ donors, cancer is generally not a transmissible disease.[29]

Exposure to particular substances have been linked to specific types of cancer. These substances are called carcinogens.

Tobacco smoke, for example, causes 90% of lung cancer.[30] It also causes cancer in the larynx, head, neck, stomach, bladder, kidney, esophagus and pancreas.[31] Tobacco smoke contains over fifty known carcinogens, including nitrosamines and polycyclic aromatic hydrocarbons.[32]

Tobacco is responsible about one in five cancer deaths worldwide[32] and about one in three in the developed world[33]Lung cancer death rates in the United States have mirrored smoking patterns, with increases in smoking followed by dramatic increases in lung cancer death rates and, more recently, decreases in smoking rates since the 1950s followed by decreases in lung cancer death rates in men since 1990.[34][35]

In Western Europe, 10% of cancers in males and 3% of cancers in females are attributed to alcohol exposure, especially liver and digestive tract cancers.[36] Cancer from work-related substance exposures may cause between 220% of cases,[37] causing at least 200,000 deaths.[38] Cancers such as lung cancer and mesothelioma can come from inhaling tobacco smoke or asbestos fibers, or leukemia from exposure to benzene.[38]

Diet, physical inactivity and obesity are related to up to 3035% of cancer deaths.[5][39] In the United States excess body weight is associated with the development of many types of cancer and is a factor in 1420% of cancer deaths.[39] A UK study including data on over 5 million people showed higher body mass index to be related to at least 10 types of cancer and responsible for around 12,000 cases each year in that country.[40] Physical inactivity is believed to contribute to cancer risk, not only through its effect on body weight but also through negative effects on the immune system and endocrine system.[39] More than half of the effect from diet is due to overnutrition (eating too much), rather than from eating too few vegetables or other healthful foods.

Some specific foods are linked to specific cancers. A high-salt diet is linked to gastric cancer.[41]Aflatoxin B1, a frequent food contaminant, causes liver cancer.[41]Betel nut chewing can cause oral cancer.[41] National differences in dietary practices may partly explain differences in cancer incidence. For example, gastric cancer is more common in Japan due to its high-salt diet[42] while colon cancer is more common in the United States. Immigrant cancer profiles develop mirror that of their new country, often within one generation.[43]

Worldwide approximately 18% of cancer deaths are related to infectious diseases.[5] This proportion ranges from a high of 25% in Africa to less than 10% in the developed world.[5]Viruses are the usual infectious agents that cause cancer but cancer bacteria and parasites may also play a role.

Oncoviruses (viruses that can cause cancer) include human papillomavirus (cervical cancer), EpsteinBarr virus (B-cell lymphoproliferative disease and nasopharyngeal carcinoma), Kaposi's sarcoma herpesvirus (Kaposi's sarcoma and primary effusion lymphomas), hepatitis B and hepatitis C viruses (hepatocellular carcinoma) and human T-cell leukemia virus-1 (T-cell leukemias). Bacterial infection may also increase the risk of cancer, as seen in Helicobacter pylori-induced gastric carcinoma.[44][45] Parasitic infections associated with cancer include Schistosoma haematobium (squamous cell carcinoma of the bladder) and the liver flukes, Opisthorchis viverrini and Clonorchis sinensis (cholangiocarcinoma).[46]

Up to 10% of invasive cancers are related to radiation exposure, including both ionizing radiation and non-ionizing ultraviolet radiation.[5] Additionally, the majority of non-invasive cancers are non-melanoma skin cancers caused by non-ionizing ultraviolet radiation, mostly from sunlight. Sources of ionizing radiation include medical imaging and radon gas.

Ionizing radiation is not a particularly strong mutagen.[47] Residential exposure to radon gas, for example, has similar cancer risks as passive smoking.[47] Radiation is a more potent source of cancer when combined with other cancer-causing agents, such as radon plus tobacco smoke.[47] Radiation can cause cancer in most parts of the body, in all animals and at any age. Children and adolescents are twice as likely to develop radiation-induced leukemia as adults; radiation exposure before birth has ten times the effect.[47]

Medical use of ionizing radiation is a small but growing source of radiation-induced cancers. Ionizing radiation may be used to treat other cancers, but this may, in some cases, induce a second form of cancer.[47] It is also used in some kinds of medical imaging.[48]

Prolonged exposure to ultraviolet radiation from the sun can lead to melanoma and other skin malignancies.[49] Clear evidence establishes ultraviolet radiation, especially the non-ionizing medium wave UVB, as the cause of most non-melanoma skin cancers, which are the most common forms of cancer in the world.[49]

Non-ionizing radio frequency radiation from mobile phones, electric power transmission and other similar sources have been described as a possible carcinogen by the World Health Organization's International Agency for Research on Cancer.[50] However, studies have not found a consistent link between mobile phone radiation and cancer risk.[51]

The vast majority of cancers are non-hereditary ("sporadic"). Hereditary cancers are primarily caused by an inherited genetic defect. Less than 0.3% of the population are carriers of a genetic mutation that has a large effect on cancer risk and these cause less than 310% of cancer.[52] Some of these syndromes include: certain inherited mutations in the genes BRCA1 and BRCA2 with a more than 75% risk of breast cancer and ovarian cancer,[52] and hereditary nonpolyposis colorectal cancer (HNPCC or Lynch syndrome), which is present in about 3% of people with colorectal cancer,[53] among others.

Some substances cause cancer primarily through their physical, rather than chemical, effects.[54] A prominent example of this is prolonged exposure to asbestos, naturally occurring mineral fibers that are a major cause of mesothelioma (cancer of the serous membrane) usually the serous membrane surrounding the lungs.[54] Other substances in this category, including both naturally occurring and synthetic asbestos-like fibers, such as wollastonite, attapulgite, glass wool and rock wool, are believed to have similar effects.[54] Non-fibrous particulate materials that cause cancer include powdered metallic cobalt and nickel and crystalline silica (quartz, cristobalite and tridymite).[54] Usually, physical carcinogens must get inside the body (such as through inhalation) and require years of exposure to produce cancer.[54]

Physical trauma resulting in cancer is relatively rare.[55] Claims that breaking bones resulted in bone cancer, for example, have not been proven.[55] Similarly, physical trauma is not accepted as a cause for cervical cancer, breast cancer or brain cancer.[55] One accepted source is frequent, long-term application of hot objects to the body. It is possible that repeated burns on the same part of the body, such as those produced by kanger and kairo heaters (charcoal hand warmers), may produce skin cancer, especially if carcinogenic chemicals are also present.[55] Frequent consumption of scalding hot tea may produce esophageal cancer.[55] Generally, it is believed that the cancer arises, or a pre-existing cancer is encouraged, during the process of healing, rather than directly by the trauma.[55] However, repeated injuries to the same tissues might promote excessive cell proliferation, which could then increase the odds of a cancerous mutation.

Chronic inflammation has been hypothesized to directly cause mutation.[55][56] Inflammation can contribute to proliferation, survival, angiogenesis and migration of cancer cells by influencing the tumor microenvironment.[57][58]Oncogenes build up an inflammatory pro-tumorigenic microenvironment.[59]

Some hormones play a role in the development of cancer by promoting cell proliferation.[60]Insulin-like growth factors and their binding proteins play a key role in cancer cell proliferation, differentiation and apoptosis, suggesting possible involvement in carcinogenesis.[61]

Hormones are important agents in sex-related cancers, such as cancer of the breast, endometrium, prostate, ovary and testis and also of thyroid cancer and bone cancer.[60] For example, the daughters of women who have breast cancer have significantly higher levels of estrogen and progesterone than the daughters of women without breast cancer. These higher hormone levels may explain their higher risk of breast cancer, even in the absence of a breast-cancer gene.[60] Similarly, men of African ancestry have significantly higher levels of testosterone than men of European ancestry and have a correspondingly higher level of prostate cancer.[60] Men of Asian ancestry, with the lowest levels of testosterone-activating androstanediol glucuronide, have the lowest levels of prostate cancer.[60]

Other factors are relevant: obese people have higher levels of some hormones associated with cancer and a higher rate of those cancers.[60] Women who take hormone replacement therapy have a higher risk of developing cancers associated with those hormones.[60] On the other hand, people who exercise far more than average have lower levels of these hormones and lower risk of cancer.[60]Osteosarcoma may be promoted by growth hormones.[60] Some treatments and prevention approaches leverage this cause by artificially reducing hormone levels and thus discouraging hormone-sensitive cancers.[60]

There is an association between celiac disease and an increased risk of all cancers. People with untreated celiac disease have a higher risk, but this risk decreases with time after diagnosis and strict treatment, probably due to the adoption of a gluten-free diet, which seems to have a protective role against development of malignancy in people with celiac disease. However, the delay in diagnosis and initiation of a gluten-free diet seems to increase the risk of malignancies.[62] Rates of gastrointestinal cancers are increased in people with Crohn's disease and ulcerative colitis, due to chronic inflammation. Also, immunomodulators and biologic agents used to treat these diseases may promote developing extra-intestinal malignancies.[63]

Cancer is fundamentally a disease of tissue growth regulation. In order for a normal cell to transform into a cancer cell, the genes that regulate cell growth and differentiation must be altered.[64]

The affected genes are divided into two broad categories. Oncogenes are genes that promote cell growth and reproduction. Tumor suppressor genes are genes that inhibit cell division and survival. Malignant transformation can occur through the formation of novel oncogenes, the inappropriate over-expression of normal oncogenes, or by the under-expression or disabling of tumor suppressor genes. Typically, changes in multiple genes are required to transform a normal cell into a cancer cell.[65]

Genetic changes can occur at different levels and by different mechanisms. The gain or loss of an entire chromosome can occur through errors in mitosis. More common are mutations, which are changes in the nucleotide sequence of genomic DNA.

Large-scale mutations involve the deletion or gain of a portion of a chromosome. Genomic amplification occurs when a cell gains copies (often 20 or more) of a small chromosomal locus, usually containing one or more oncogenes and adjacent genetic material. Translocation occurs when two separate chromosomal regions become abnormally fused, often at a characteristic location. A well-known example of this is the Philadelphia chromosome, or translocation of chromosomes 9 and 22, which occurs in chronic myelogenous leukemia and results in production of the BCR-abl fusion protein, an oncogenic tyrosine kinase.

Small-scale mutations include point mutations, deletions and insertions, which may occur in the promoter region of a gene and affect its expression, or may occur in the gene's coding sequence and alter the function or stability of its protein product. Disruption of a single gene may also result from integration of genomic material from a DNA virus or retrovirus, leading to the expression of viral oncogenes in the affected cell and its descendants.

Replication of the data contained within the DNA of living cells will probabilistically result in some errors (mutations). Complex error correction and prevention is built into the process and safeguards the cell against cancer. If significant error occurs, the damaged cell can self-destruct through programmed cell death, termed apoptosis. If the error control processes fail, then the mutations will survive and be passed along to daughter cells.

Some environments make errors more likely to arise and propagate. Such environments can include the presence of disruptive substances called carcinogens, repeated physical injury, heat, ionising radiation or hypoxia.[66]

The errors that cause cancer are self-amplifying and compounding, for example:

The transformation of a normal cell into cancer is akin to a chain reaction caused by initial errors, which compound into more severe errors, each progressively allowing the cell to escape more controls that limit normal tissue growth. This rebellion-like scenario is an undesirable survival of the fittest, where the driving forces of evolution work against the body's design and enforcement of order. Once cancer has begun to develop, this ongoing process, termed clonal evolution, drives progression towards more invasive stages.[67] Clonal evolution leads to intra-tumour heterogeneity (cancer cells with heterogeneous mutations) that complicates designing effective treatment strategies.

Characteristic abilities developed by cancers are divided into categories, specifically evasion of apoptosis, self-sufficiency in growth signals, insensitivity to anti-growth signals, sustained angiogenesis, limitless replicative potential, metastasis, reprogramming of energy metabolism and evasion of immune destruction.[24][25]

The classical view of cancer is a set of diseases that are driven by progressive genetic abnormalities that include mutations in tumor-suppressor genes and oncogenes and chromosomal abnormalities. Later epigenetic alterations' role was identified.[68]

Epigenetic alterations refer to functionally relevant modifications to the genome that do not change the nucleotide sequence. Examples of such modifications are changes in DNA methylation (hypermethylation and hypomethylation), histone modification[69] and changes in chromosomal architecture (caused by inappropriate expression of proteins such as HMGA2 or HMGA1).[70] Each of these alterations regulates gene expression without altering the underlying DNA sequence. These changes may remain through cell divisions, last for multiple generations and can be considered to be epimutations (equivalent to mutations).

Epigenetic alterations occur frequently in cancers. As an example, one study listed protein coding genes that were frequently altered in their methylation in association with colon cancer. These included 147 hypermethylated and 27 hypomethylated genes. Of the hypermethylated genes, 10 were hypermethylated in 100% of colon cancers and many others were hypermethylated in more than 50% of colon cancers.[71]

While epigenetic alterations are found in cancers, the epigenetic alterations in DNA repair genes, causing reduced expression of DNA repair proteins, may be of particular importance. Such alterations are thought to occur early in progression to cancer and to be a likely cause of the genetic instability characteristic of cancers.[72][73][74][75]

Reduced expression of DNA repair genes disrupts DNA repair. This is shown in the figure at the 4th level from the top. (In the figure, red wording indicates the central role of DNA damage and defects in DNA repair in progression to cancer.) When DNA repair is deficient DNA damage remains in cells at a higher than usual level (5th level) and cause increased frequencies of mutation and/or epimutation (6th level). Mutation rates increase substantially in cells defective in DNA mismatch repair[76][77] or in homologous recombinational repair (HRR).[78] Chromosomal rearrangements and aneuploidy also increase in HRR defective cells.[79]

Higher levels of DNA damage cause increased mutation (right side of figure) and increased epimutation. During repair of DNA double strand breaks, or repair of other DNA damage, incompletely cleared repair sites can cause epigenetic gene silencing.[80][81]

Deficient expression of DNA repair proteins due to an inherited mutation can increase cancer risks. Individuals with an inherited impairment in any of 34 DNA repair genes (see article DNA repair-deficiency disorder) have increased cancer risk, with some defects ensuring a 100% lifetime chance of cancer (e.g. p53 mutations).[82] Germ line DNA repair mutations are noted on the figure's left side. However, such germline mutations (which cause highly penetrant cancer syndromes) are the cause of only about 1 percent of cancers.[83]

In sporadic cancers, deficiencies in DNA repair are occasionally caused by a mutation in a DNA repair gene, but are much more frequently caused by epigenetic alterations that reduce or silence expression of DNA repair genes. This is indicated in the figure at the 3rd level. Many studies of heavy metal-induced carcinogenesis show that such heavy metals cause reduction in expression of DNA repair enzymes, some through epigenetic mechanisms. DNA repair inhibition is proposed to be a predominant mechanism in heavy metal-induced carcinogenicity. In addition, frequent epigenetic alterations of the DNA sequences code for small RNAs called microRNAs (or miRNAs). MiRNAs do not code for proteins, but can "target" protein-coding genes and reduce their expression.

Cancers usually arise from an assemblage of mutations and epimutations that confer a selective advantage leading to clonal expansion (see Field defects in progression to cancer). Mutations, however, may not be as frequent in cancers as epigenetic alterations. An average cancer of the breast or colon can have about 60 to 70 protein-altering mutations, of which about three or four may be "driver" mutations and the remaining ones may be "passenger" mutations.[84]

Metastasis is the spread of cancer to other locations in the body. The dispersed tumors are called metastatic tumors, while the original is called the primary tumor. Almost all cancers can metastasize.[85] Most cancer deaths are due to cancer that has metastasized.[86]

Metastasis is common in the late stages of cancer and it can occur via the blood or the lymphatic system or both. The typical steps in metastasis are local invasion, intravasation into the blood or lymph, circulation through the body, extravasation into the new tissue, proliferation and angiogenesis. Different types of cancers tend to metastasize to particular organs, but overall the most common places for metastases to occur are the lungs, liver, brain and the bones.[85]

Most cancers are initially recognized either because of the appearance of signs or symptoms or through screening. Neither of these lead to a definitive diagnosis, which requires the examination of a tissue sample by a pathologist. People with suspected cancer are investigated with medical tests. These commonly include blood tests, X-rays, CT scans and endoscopy.

People may become extremely anxious and depressed post-diagnosis. The risk of suicide in people with cancer is approximately double the normal risk.[87]

Cancers are classified by the type of cell that the tumor cells resemble and is therefore presumed to be the origin of the tumor. These types include:

Cancers are usually named using -carcinoma, -sarcoma or -blastoma as a suffix, with the Latin or Greek word for the organ or tissue of origin as the root. For example, cancers of the liver parenchyma arising from malignant epithelial cells is called hepatocarcinoma, while a malignancy arising from primitive liver precursor cells is called a hepatoblastoma and a cancer arising from fat cells is called a liposarcoma. For some common cancers, the English organ name is used. For example, the most common type of breast cancer is called ductal carcinoma of the breast. Here, the adjective ductal refers to the appearance of the cancer under the microscope, which suggests that it has originated in the milk ducts.

Benign tumors (which are not cancers) are named using -oma as a suffix with the organ name as the root. For example, a benign tumor of smooth muscle cells is called a leiomyoma (the common name of this frequently occurring benign tumor in the uterus is fibroid). Confusingly, some types of cancer use the -noma suffix, examples including melanoma and seminoma.

Some types of cancer are named for the size and shape of the cells under a microscope, such as giant cell carcinoma, spindle cell carcinoma and small-cell carcinoma.

The tissue diagnosis from the biopsy indicates the type of cell that is proliferating, its histological grade, genetic abnormalities and other features. Together, this information is useful to evaluate the prognosis of the patient and to choose the best treatment. Cytogenetics and immunohistochemistry are other types of tissue tests. These tests may provide information about molecular changes (such as mutations, fusion genes and numerical chromosome changes) and may thus also indicate the prognosis and best treatment.

Cancer prevention is defined as active measures to decrease cancer risk.[89] The vast majority of cancer cases are due to environmental risk factors. Many of these environmental factors are controllable lifestyle choices. Thus, cancer is generally preventable.[90] Between 70% and 90% of common cancers are due to environmental factors and therefore potentially preventable.[91]

Greater than 30% of cancer deaths could be prevented by avoiding risk factors including: tobacco, excess weight/obesity, insufficient diet, physical inactivity, alcohol, sexually transmitted infections and air pollution.[92] Not all environmental causes are controllable, such as naturally occurring background radiation and cancers caused through hereditary genetic disorders and thus are not preventable via personal behavior.

While many dietary recommendations have been proposed to reduce cancer risks, the evidence to support them is not definitive.[9][93] The primary dietary factors that increase risk are obesity and alcohol consumption. Diets low in fruits and vegetables and high in red meat have been implicated but reviews and meta-analyses do not come to a consistent conclusion.[94][95] A 2014 meta-analysis find no relationship between fruits and vegetables and cancer.[96]Coffee is associated with a reduced risk of liver cancer.[97] Studies have linked excess consumption of red or processed meat to an increased risk of breast cancer, colon cancer and pancreatic cancer, a phenomenon that could be due to the presence of carcinogens in meats cooked at high temperatures.[98][99] In 2015 the IARC reported that eating processed meat (e.g., bacon, ham, hot dogs, sausages) and, to a lesser degree, red meat was linked to some cancers.[100][101]

Dietary recommendations for cancer prevention typically include an emphasis on vegetables, fruit, whole grains and fish and an avoidance of processed and red meat (beef, pork, lamb), animal fats and refined carbohydrates.[9][93]

Medications can be used to prevent cancer in a few circumstances.[102] In the general population, NSAIDs reduce the risk of colorectal cancer; however, due to cardiovascular and gastrointestinal side effects, they cause overall harm when used for prevention.[103]Aspirin has been found to reduce the risk of death from cancer by about 7%.[104]COX-2 inhibitors may decrease the rate of polyp formation in people with familial adenomatous polyposis; however, it is associated with the same adverse effects as NSAIDs.[105] Daily use of tamoxifen or raloxifene reduce the risk of breast cancer in high-risk women.[106] The benefit versus harm for 5-alpha-reductase inhibitor such as finasteride is not clear.[107]

Vitamins are not effective at preventing cancer,[108] although low blood levels of vitamin D are correlated with increased cancer risk.[109][110] Whether this relationship is causal and vitamin D supplementation is protective is not determined.[111]Beta-carotene supplementation increases lung cancer rates in those who are high risk.[112]Folic acid supplementation is not effective in preventing colon cancer and may increase colon polyps.[113] It is unclear if selenium supplementation has an effect.[114]

Vaccines have been developed that prevent infection by some carcinogenic viruses.[115]Human papillomavirus vaccine (Gardasil and Cervarix) decrease the risk of developing cervical cancer.[115] The hepatitis B vaccine prevents infection with hepatitis B virus and thus decreases the risk of liver cancer.[115] The administration of human papillomavirus and hepatitis B vaccinations is recommended when resources allow.[116]

Unlike diagnostic efforts prompted by symptoms and medical signs, cancer screening involves efforts to detect cancer after it has formed, but before any noticeable symptoms appear.[117] This may involve physical examination, blood or urine tests or medical imaging.[117]

Cancer screening is not available for many types of cancers. Even when tests are available, they may not be recommended for everyone. Universal screening or mass screening involves screening everyone.[118]Selective screening identifies people who are at higher risk, such as people with a family history.[118] Several factors are considered to determine whether the benefits of screening outweigh the risks and the costs of screening.[117] These factors include:

The U.S. Preventive Services Task Force (USPSTF) issues recommendations for various cancers:

Screens for gastric cancer using photofluorography due to the high incidence there.[19]

Genetic testing for individuals at high-risk of certain cancers is recommended by unofficial groups.[116][132] Carriers of these mutations may then undergo enhanced surveillance, chemoprevention, or preventative surgery to reduce their subsequent risk.[132]

Many treatment options for cancer exist. The primary ones include surgery, chemotherapy, radiation therapy, hormonal therapy, targeted therapy and palliative care. Which treatments are used depends on the type, location and grade of the cancer as well as the patient's health and preferences. The treatment intent may or may not be curative.

Chemotherapy is the treatment of cancer with one or more cytotoxic anti-neoplastic drugs (chemotherapeutic agents) as part of a standardized regimen. The term encompasses a variety of drugs, which are divided into broad categories such as alkylating agents and antimetabolites.[133] Traditional chemotherapeutic agents act by killing cells that divide rapidly, a critical property of most cancer cells.

Targeted therapy is a form of chemotherapy that targets specific molecular differences between cancer and normal cells. The first targeted therapies blocked the estrogen receptor molecule, inhibiting the growth of breast cancer. Another common example is the class of Bcr-Abl inhibitors, which are used to treat chronic myelogenous leukemia (CML).[134] Currently, targeted therapies exist for breast cancer, multiple myeloma, lymphoma, prostate cancer, melanoma and other cancers.[135]

The efficacy of chemotherapy depends on the type of cancer and the stage. In combination with surgery, chemotherapy has proven useful in cancer types including breast cancer, colorectal cancer, pancreatic cancer, osteogenic sarcoma, testicular cancer, ovarian cancer and certain lung cancers.[136] Chemotherapy is curative for some cancers, such as some leukemias,[137][138] ineffective in some brain tumors,[139] and needless in others, such as most non-melanoma skin cancers.[140] The effectiveness of chemotherapy is often limited by its toxicity to other tissues in the body. Even when chemotherapy does not provide a permanent cure, it may be useful to reduce symptoms such as pain or to reduce the size of an inoperable tumor in the hope that surgery will become possible in the future.

Radiation therapy involves the use of ionizing radiation in an attempt to either cure or improve symptoms. It works by damaging the DNA of cancerous tissue, killing it. To spare normal tissues (such as skin or organs, which radiation must pass through to treat the tumor), shaped radiation beams are aimed from multiple exposure angles to intersect at the tumor, providing a much larger dose there than in the surrounding, healthy tissue. As with chemotherapy, cancers vary in their response to radiation therapy.[141][142][143]

Radiation therapy is used in about half of cases. The radiation can be either from internal sources (brachytherapy) or external sources. The radiation is most commonly low energy x-rays for treating skin cancers, while higher energy x-rays are used for cancers within the body.[144] Radiation is typically used in addition to surgery and or chemotherapy. For certain types of cancer, such as early head and neck cancer, it may be used alone.[145] For painful bone metastasis, it has been found to be effective in about 70% of patients.[145]

Surgery is the primary method of treatment for most isolated, solid cancers and may play a role in palliation and prolongation of survival. It is typically an important part of definitive diagnosis and staging of tumors, as biopsies are usually required. In localized cancer, surgery typically attempts to remove the entire mass along with, in certain cases, the lymph nodes in the area. For some types of cancer this is sufficient to eliminate the cancer.[136]

Palliative care refers to treatment that attempts to help the patient feel better and may be combined with an attempt to treat the cancer. Palliative care includes action to reduce physical, emotional, spiritual and psycho-social distress. Unlike treatment that is aimed at directly killing cancer cells, the primary goal of palliative care is to improve quality of life.

People at all stages of cancer treatment typically receive some kind of palliative care. In some cases, medical specialty professional organizations recommend that patients and physicians respond to cancer only with palliative care.[146] This applies to patients who:[147]

Palliative care may be confused with hospice and therefore only indicated when people approach end of life. Like hospice care, palliative care attempts to help the patient cope with their immediate needs and to increase comfort. Unlike hospice care, palliative care does not require people to stop treatment aimed.

Multiple national medical guidelines recommend early palliative care for patients whose cancer has produced distressing symptoms or who need help coping with their illness. In patients first diagnosed with metastatic disease, palliative care may be immediately indicated. Palliative care is indicated for patients with a prognosis of less than 12 months of life even given aggressive treatment.[148][149][150]

A variety of therapies using immunotherapy, stimulating or helping the immune system to fight cancer, have come into use since 1997. Approaches include antibodies, checkpoint therapy and adoptive cell transfer.[151]

Complementary and alternative cancer treatments are a diverse group of therapies, practices and products that are not part of conventional medicine.[152] "Complementary medicine" refers to methods and substances used along with conventional medicine, while "alternative medicine" refers to compounds used instead of conventional medicine.[153] Most complementary and alternative medicines for cancer have not been studied or tested using conventional techniques such as clinical trials. Some alternative treatments have been investigated and shown to be ineffective but still continue to be marketed and promoted. Cancer researcher Andrew J. Vickers stated, "The label 'unproven' is inappropriate for such therapies; it is time to assert that many alternative cancer therapies have been 'disproven'."[154]

Survival rates vary by cancer type and by the stage at which it is diagnosed, ranging from majority survival to complete mortality five years after diagnosis. Once a cancer has metastasized, prognosis normally becomes much worse. About half of patients receiving treatment for invasive cancer (excluding carcinoma in situ and non-melanoma skin cancers) die from that cancer or its treatment.[19]

Survival is worse in the developing world,[19] partly because the types of cancer that are most common there are harder to treat than those associated with developed countries.[155]

Those who survive cancer develop a second primary cancer at about twice the rate of those never diagnosed.[156] The increased risk is believed to be primarily due to the same risk factors that produced the first cancer, partly due to treatment of the first cancer and to better compliance with screening.[156]

Predicting short- or long-term survival depends on many factors. The most important are the cancer type and the patient's age and overall health. Those who are frail with other health problems have lower survival rates than otherwise healthy people. Centenarians are unlikely to survive for five years even if treatment is successful. People who report a higher quality of life tend to survive longer.[157] People with lower quality of life may be affected by depression and other complications and/or disease progression that both impairs quality and quantity of life. Additionally, patients with worse prognoses may be depressed or report poorer quality of life because they perceive that their condition is likely to be fatal.

Cancer patients have an increased risk of blood clots in veins. The use of heparin appears to improve survival and decrease the risk of blood clots.[158]

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Cancer - Wikipedia, the free encyclopedia

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Supercourse: Epidemiology, the Internet, and Global Health

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Is there a regimen missing from this list? Would you like to share a different dosage/schedule or an additional reference for a regimen? Have you noticed an error? Do you have an idea that will help the site grow to better meet your needs and the needs of many others? You are invited to contribute to the site. Are you looking for a regimen but can't find it here? It is possible that we've moved it to the obsolete regimens page. If you still can't find it, please let us know so we can add it!

76 regimens on this page

106 variants on this page

Recommended in NHL-B1 and NHL-B2 "to improve the performance status of patients and to ameliorate side-effects of the first chemotherapy cycle." Mandated in RICOVER-60 and SMARTE-R-CHOP-14. Note: NHL-B1 gave the option of a 5 to 7 day course of prednisone.

7-day course

Treatment in NHL-B1 and NHL-B2 followed by randomization to CHOP versus CHOP-14 versus CHOEP versus CHOEP-14. Treatment in RICOVER-60 followed by randomization to CHOP-14 versus R-CHOP-14. Treatment in SMARTE-R-CHOP-14 followed by R-CHOP-14.

ACVBP-R: Adriamycin (Doxorubicin), Cyclophosphamide, Vindesine, Bleomycin, Prednisone, Rituximab

Synonyms: R-ACVBP

Structured Concept: none

14-day cycle for 4 cycles

Treatment followed in 4 weeks by methotrexate consolidation.

CHOP: Cyclophosphamide, Hydroxydaunorubicin (Doxorubicin), Oncovin (Vincristine), Prednisone

Synonyms: CHOP-21, ACOP, CAVP, COPA, VACP, VCAP

Structured Concept: C9549 (NCI-T), C0055598 (NCI-MT/UMLS)

21-day cycle for 8 cycles

Treatment in NHL-B1 and NHL-B2 preceded by pre-phase vincristine & prednisone.

21-day cycle for 6 cycles

"Initial bulky disease": patients with "lymphoma masses or conglomerates with a diameter 7.5 cm) or extranodal involvement"

21-day cycle for 3 cycles, followed in 3 weeks by:

21-day cycle for 8 cycles

21-day cycle for 6 to 8 cycles

Patients with CR/PR proceeded to receive maintenance rituximab versus observation.

CHOP-DI: Cyclophosphamide, Hydroxydaunorubicin (Doxorubicin), Oncovin (Vincristine), Prednisone, Dose Intense I-CHOP: Intensified Cyclophosphamide, Hydroxydaunorubicin (Doxorubicin), Oncovin (Vincristine), Prednisone

Synonyms: CHOP-14, CHOP-DI, I-CHOP

Structured Concept: none

14-day cycle for up to 6 cycles

14-day cycle for 6 cycles

Treatment preceded by pre-phase vincristine & prednisone (recommended in NHL-B1 and mandatory in RICOVER-60).

Supportive medications (per Pfreundschuh et al. 2004):

14-day cycle for 6 cycles; some patients in Pfreundschuh et al. 2008 received 14-day cycle for 8 cycles

"Initial bulky disease": patients with "lymphoma masses or conglomerates with a diameter =7.5 cm) or extranodal involvement"

CHOP: Cyclophosphamide, Hydroxydaunorubicin (Doxorubicin), Oncovin (Vincristine), Prednisone

This regimen is designed for elderly patients and is of lower intensity than standard CHOP.

21-day cycle for 6 cycles

CNOP: Cyclophosphamide, Novantrone (Mitoxantrone), Oncovin (Vincristine), Prednisone MCOP: Mitoxantrone, Cyclophosphamide, Oncovin (Vincristine), Prednisone

21-day cycle for 6 cycles

R-CHOEP-14: Rituximab, Cyclophosphamide, Hydroxydaunorubicin (Doxorubicin), Oncovin (Vincristine), Etoposide, Prednisone, 14-day cycles

14-day cycle for 8 cycles

14-day cycle for 8 cycles, followed by:

Note that IT treatment was not part of prophylaxis, except that Methotrexate (MTX) 15 mg IT was allowed at time of diagnostic LP.

Followed 3 weeks later by:

One course

R-CHOP: Rituximab, Cyclophosphamide, Hydroxydaunorubicin (Doxorubicin), Oncovin (Vincristine), Prednisone

Synonyms: R-CHOP-21, CHOP-R

Structured Concept: C9760 (NCI-T), C0393023 (NCI-MT/UMLS)

Note: most of the variation between these regimen variants is in the dose or type of steroid.

Note: Cunningham et al. 2013 states that the regimen is based on Coiffier et al. 2002, but notably it uses prednisolone instead of prednisone. AGMT NHL-14 states that R-CHOP was "given in standard doses" per LNH-98.5, but this regimen uses prednisone, whereas the title and text of Fridrik et al. 2016 implies that prednisolone was used. The authors have confirmed that prednisolone was used, due to prednisone not being available in Austria.

Per investigator discretion, but Cunningham et al. 2013 recommended that patients who had involvement of the "bone marrow, peripheral blood, nasal or paranasal sinuses, orbit, and testis" (they probably intended to say "or testis") receive:

21-day cycle for 8 cycles

This regimen was used for non-germinal center B-cell (non-GCB) DLBCL.

21-day cycle for 6 cycles

As described in Delarue et al. 2013 (LNH03-6B):

21-day cycle for 8 cycles

21-day cycle for 6 cycles

21-day cycle for 6 to 8 cycles

This trial also included a randomization to maintenance rituximab versus observation for responders; however an advantage was only seen in the group receiving CHOP upfront, which is no longer standard of care.

21-day cycle for 6 cycles

"At the end of chemotherapy, radiotherapy (RT) was scheduled for sites of previous bulky disease or partially responding sites."

21-day cycle for 3 cycles, followed by:

Involved-field radiation therapy to begin 3 weeks after last cycle of R-CHOP, see paper for details.

This regimen is for primary testicular lymphoma. All patients had a diagnostic orchiectomy prior to starting chemotherapy.

21-day cycle for 6 cycles (up to 8 cycles for stage II patients), followed by:

25 to 30 Gy to the contralateral testis. For patients with stage II disease, involved-field radiation therapy was added, see paper for details.

R-CHOP: Rituximab, Cyclophosphamide, Hydroxydaunorubicin (Doxorubicin), Oncovin (Vincristine), Prednisone

Synonyms: R-CHOP-14, Dose-dense rituximab-CHOP

Structured Concept: none

Two arms were assessed; results are pending from this comparison. These higher doses were for males, only.

OR

14-day cycle for 6 cycles (8 doses of rituximab regardless of total number of CHOP-14 cycles)

14-day cycle for 8 cycles

Per investigator discretion, but Cunningham et al. 2013 recommended that patients who had involvement of the "bone marrow, peripheral blood, nasal or paranasal sinuses, orbit, and testis" (they probably intended to say "or testis") receive:

14-day cycle for 6 cycles; then give additional doses of rituximab as described below

14-day cycle for 2 cycles

Treatment preceded by pre-phase vincristine & prednisone.

14-day cycle for 6 to 8 cycles (8 doses of rituximab regardless of total number of cycles)

Patients with initial bulky disease received:

"Initial bulky disease": patients with "lymphoma masses or conglomerates with a diameter >=7.5 cm) or extranodal involvement"

Treatment preceded by pre-phase vincristine & prednisone.

14-day cycle for 6 cycles

Patients with initial bulky disease received:

"Initial bulky disease": patients with "lymphoma masses or conglomerates with a diameter =7.5 cm) or extranodal involvement"

R-CVP: Rituximab, Cyclophosphamide, Vincristine, Prednisone

Structured Concept: C63473 (NCI-T), C1882520 (NCI-MT/UMLS)

21-day cycle for up to 8 cycles

See references for CVP

R-HCVAD: Rituximab, Hyperfractionated Cyclophosphamide, Vincristine, Adriamycin (Doxorubicin), Dexamethasone R-MA: Rituximab, Methotrexate, Ara-C (Cytarabine)

Intended for high-risk DLBCL (IPI 3). The authors report "excellent outcome" in patients 45 years old, however patients >45 years old had "unacceptable mortality."

Next cycle to start once ANC count is 1 x 10^9/L and platelet count is 100 x 10^9/L.

Although the protocol does not specify, it is assumed that if these thresholds are not met by day 21, the next cycle will start with the dose reductions as specified.

21-day cycles

"Recommended in patients with paraspinal disease, paranasal sinus disease, testicular disease, bone marrow disease, diffuse osseous disease or 2 sites of extranodal disease. Actual administration of prophylactic intrathecal chemotherapy was at the treating physician's discretion."

R-miniCEOP: Rituximab, mini, Cyclophosphamide, Epirubicin, O?? (vinblastine), Prednisone

21-day cycle for 6 cycles

Patients with initial bulky disease and/or partially responding sites received:

"At the end of chemotherapy, radiotherapy (RT) was scheduled for sites of previous bulky disease or partially responding sites."

CHOP: Cyclophosphamide, Hydroxydaunorubicin (Doxorubicin), Oncovin (Vincristine), Prednisone

This regimen is intended for limited-stage aggressive B-cell NHL; the majority of patients studied had DLBCL.

21-day cycle for 3 cycles, followed 3 weeks later by:

Involved-field radiation therapy, see paper for details.

Continued here:
Diffuse large B-cell lymphoma | HemOnc.org - A Hematology ...

Track-1 Cell Therapy:

Cell therapyas performed by alternativemedicinepractitioners is very different from the controlled research done by conventionalstem cellmedical researchers. Alternative practitioners refer to their form of cell therapy by several other different names includingxenotransplanttherapy,glandular therapy, and fresh cell therapy. Proponents ofcell therapyclaim that it has been used successfully to rebuild damaged cartilage in joints, repair spinal cord injuries,strengthen a weakenedimmune system, treat autoimmune diseases such as AIDS, and help patients withneurological disorderssuch as Alzheimers disease,Parkinson's diseaseand epilepsy.

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6th International Conference onTissue Engineering & Regenerative Medicine, Baltimore, USA, Aug 20-22, 2017; 8th World Congress and Expo onCell & Stem Cell Research,Orlando, USA, March 20-22, 2017; 15thWorld Congress on Biotechnology and Biotech Industries Meet,Rome, Italy,March 20-21,2017; 2nd International Conference onGenetic Counselling and Genomic Medicine ,Beijing, China,July 10-12, 2017; International Conference onClinical and Molecular Genetics, Las Vegas, USA, April 24-26, 2017.

Track-2 Gene therapy:

Gene therapyand cell therapy are overlapping fields of biomedical research with the goals of repairing the direct cause of genetic diseases in the DNA orcellularpopulation, respectively. The development of suitablegene therapytreatments for manygenetic diseasesand some acquired diseases has encountered many challenges and uncovered new insights into gene interactions and regulation. Further development often involves uncovering basic scientific knowledge of the affected tissues, cells, and genes, as well as redesigning vectors, formulations, and regulatory cassettes for the genes.Cell therapyis expanding its repertoire of cell types for administration.Cell therapytreatment strategies include isolation and transfer of specific stem cell populations, administration of effector cells, and induction of mature cells to becomepluripotent cells, and reprogramming of mature cells.

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2nd International Conference onMolecular Biology , London, UK ,June 22-24, 2017; 3rd World Bio Summit & Expo, Abu Dhabi, UAE, June 19-21, 2017; 5th International Conference onIntegrative Biology, London, UK, June 19-21, 2017; 2nd World Congress on Human Genetics, Chicago, USA, July 24-26, 2017; 9th International Conference onGenomics and Pharmacogenomics, Chicago, USA, July 13-14, 2017.

Track-3 Cell and gene therapy products:

Articles containing or consisting ofhuman cellsor tissues that are intended for implantation,transplantation, infusion, or transfer to a human recipient.Gene therapiesare novel and complex products that can offer unique challenges in product development. Hence, ongoing communication between the FDA and stakeholders is essential to meet these challenges.Gene therapy productsare being developed around the world, the FDA is engaged in a number of international harmonization activities in this area.

Examples:Musculoskeletal tissue, skin, ocular tissue, human heart valves;vascular graft, dura mater, reproductive tissue/cells, Stem/progenitor cells,somatic cells, Cells transduced withgene therapyvectors , Combination products (e.g., cells or tissue + device)

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Track-4 Cellular therapy:

Cellular therapy, also calledlive cell therapy, cellular suspensions, glandular therapy, fresh cell therapy, sick cell therapy,embryonic cell therapy, andorgan therapy- refers to various procedures in which processed tissue from animal embryos, foetuses or organs, is injected or taken orally. Products are obtained from specific organs or tissues said to correspond with the unhealthy organs or tissues of the recipient. Proponents claim that the recipient's body automatically transports the injected cells to thetarget organs, where they supposedly strengthen them and regenerate their structure. The organs and glands used in cell treatment include brain, pituitary,thyroid, adrenals, thymus, liver,kidney, pancreas, spleen, heart,ovary, testis, and parotid. Several different types of cell or cell extract can be given simultaneously - some practitioners routinely give up to 20 or more at once.

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Track-5 Cancer gene therapy:

Cancer therapiesare drugs or other substances that block the growth and spread ofcancerby interfering with specific molecules ("molecular targets") that are involved in the growth, progression, and spread ofcancer. Many cancer therapies have been approved by the Food and Drug Administration (FDA) to treat specific types of cancer. The development of targetedtherapiesrequires the identification of good targets that is, targets that play a key role in cancer cell growth and survival. One approach to identify potential targets is to compare the amounts of individualproteinsin cancer cells with those in normal cells.Proteinsthat are present in cancer cells but not normal cells or that are more abundant incancercells would be potential targets, especially if they are known to be involved incell growthor survival.

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2nd Biotechnology World Convention,London, UK,May 25-27, 2017; International Conference on Animal and Human Cell Culture, Jackson Ville, USA, Sep 25-27, 2017; 9th International Conference onCancer Genomics, Chicago, USA, May 29-31, 2017; 6th International Conference onTissue Engineering & Regenerative Medicine, Baltimore, USA, Aug 20-22, 2017; 8th World Congress and Expo onCell & Stem Cell Research, Orlando, USA, March 20-22, 2017.

Track-6 Nano therapy:

Nano Therapymay be defined as the monitoring, repair, construction and control of human biological systems at themolecular level, using engineerednanodevicesand nanostructures. Basic nanostructured materials, engineeredenzymes, and the many products of biotechnology will be enormously useful in near-term medical applications. However, the full promise ofnanomedicineis unlikely to arrive until after the development of precisely controlled or programmable medical Nano machines andnanorobots.

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Track-7 Skin cell therapy:

Stem cellshave newly become a huge catchphrase in theskincarebiosphere. Skincare specialists are not usingembryonic stem cells; it is impossible to integrate live materials into a skincare product. Instead, scientists are creating products with specialized peptides andenzymesor plantstem cellswhich, when applied topically on the surface, help to protect the human skinstem cellsfrom damage and deterioration or stimulate the skins own stem cells. Currently, the technique is mainly used to save the lives of patients who have third degree burns over very large areas of their bodies.

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5th International Conference and Exhibition onCell and Gene Therapy,Madrid,Spain,Mar 2-3, 2017;International Conference onCell Signalling and Cancer Therapy,Paris, France,Aug 20-22, 2017;2nd Biotechnology World Convention,London, UK,May 25-27, 2017; International Conference on Animal and Human Cell Culture, Jackson Ville, USA, Sep 25-27, 2017; 9th International Conference onCancer Genomics, Chicago, USA, May 29-31, 2017.

Track-8 HIV gene therapy:

Highly activeantiretroviral therapydramatically improves survival inHIV-infected patients. However, persistence of HIV in reservoirs has necessitated lifelong treatment that can be complicated bycumulative toxicities, incomplete immune restoration, and the emergence of drug-resistant escapemutants. Cell and gene therapies offer the promise of preventing progressiveHIV infectionby interfering with HIV replication in the absence of chronicantiviral therapy.

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Track-9 Diabetes for gene therapy:

Cell therapyapproaches for this disease are focused on developing the most efficient methods for the isolation ofpancreasbeta cells or appropriatestem cells, appropriate location forcell transplant, and improvement of their survival upon infusion. Alternatively, gene andcell therapyscientists are developing methods to reprogram some of the other cells of the pancreas to secreteinsulin. Currently ongoingclinical trialsusing these gene andcell therapystrategies hold promise for improved treatments of type I diabetes in the future. The firstgene therapyapproach to diabetes was put forward shortly after the cloning of theinsulingene. It was proposed that non-insulin producing cells could be made into insulin-producingcells using a suitable promoter and insulin gene construct, and that these substitute cells could restore insulin production in type 1 and some type 2 diabetics.

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Track-10 Viral gene therapy:

Converting avirusinto a vector Theviral life cyclecan be divided into two temporally distinct phases: infection and replication. Forgene therapyto be successful, an appropriate amount of a therapeutic gene must be delivered into the target tissue without substantial toxicity. Eachviral vectorsystem is characterized by an inherent set of properties that affect its suitability for specific gene therapy applications. For some disorders, long-term expression from a relatively small proportion of cells would be sufficient (for example, genetic disorders), whereas otherpathologiesmight require high, but transient,gene expression. For example, gene therapies designed to interfere with a viral infectious process or inhibit the growth ofcancer cellsby reconstitution of inactivated tumour suppressor genes may require gene transfer into a large fraction of theabnormal cells.

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3rd International Conference onSynthetic Biology, Munich, Germany, July 20-21, 2017;5th International Conference and Exhibition onCell and Gene Therapy,Madrid, Spain,Mar 2-3, 2017; International Conference on Animal and Human Cell Culture, Jackson Ville, USA, Sep 25-27, 2017; 9th International Conference onCancer Genomics, Chicago, USA, May 29-31, 2017; 14th Asia-Pacific Biotech Congress,Beijing, China,April 10-12, 2017.

Track-11 Stem cell therapies:

Stem cells have tremendous promise to help us understand and treat a range of diseases, injuries and other health-related conditions. Their potential is evident in the use ofblood stem cellsto treat diseases of the blood, a therapy that has saved the lives of thousands of children withleukaemia; and can be seen in the use ofstem cellsfor tissue grafts to treat diseases or injury to the bone, skin and surface of the eye. Some bone, skin andcorneal(eye) injuries and diseases can be treated bygraftingor implanting tissues, and the healing process relies on stem cells within thisimplanted tissue.

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2nd World Congress on Human Genetics, Chicago, USA, July 24-26, 2017; 2nd International Conference onGenetic Counselling and Genomic Medicine ,Beijing, China,July 10-12, 2017; International Conference onClinical and Molecular Genetics, Las Vegas, USA, April 24-26, 2017; 2nd International Conference onMolecular Biology,London, UK,June 22-24, 2017; 15th Biotechnology Congress, Baltimore, USA, June 22-23, 2017.

Track-12 Stem cell preservation:

The ability to preserve the cells is critical to theirclinicalapplication. It improves patient access to therapies by increasing the genetic diversity of cells available. In addition, the ability to preserve cells improves the "manufacturability" of acell therapyproduct by permitting the cells to be stored until the patient is ready for administration of the therapy, permitting inventory control of products, and improving management of staffing atcell therapyfacilities. Finally, the ability to preservecell therapiesimproves the safety of cell therapy products by extending the shelf life of a product and permitting completion of safety and quality control testing before release of the product for use. preservation permits coordination between the manufacture of the therapy and patient care regimes.

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Track-13 Stem cell products:

The globalstemcell,Stem cell productsmarket will grow from about $5.6 billion in 2013 to nearly $10.6 billion in 2018, registering a compound annual growth rate (CAGR) of 13.6% from 2013 through 2018.This trackdiscusses the implications ofstemcellresearchand commercial trends in the context of the current size and growth of thepharmaceutical market, both in global terms and analysed by the most important national markets.

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Track-14 Genetically inherited diseases:

Agenetic diseaseis any disease that is caused by an abnormality in an individual'sgenome, the person's entiregeneticmakeup. The abnormality can range from minuscule to major -- from a discrete mutation in a single base in the DNA of a single gene to a grosschromosome abnormalityinvolving the addition or subtraction of an entirechromosomeor set of chromosomes.Most genetic diseases are the direct result of a mutation in one gene. However, one of the most difficult problems ahead is to find out how genes contribute to diseases that have a complex pattern ofinheritance, such as in the cases of diabetes,asthma,cancerandmental illness. In all these cases, no one gene has the yes/no power to say whether a person has a disease or not. It is likely that more than one mutation is required before the disease is manifest, and a number of genes may each make a subtle contribution to a person's susceptibility to a disease; genes may also affect how a person reacts toenvironmental factors.

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Track-15 Plant stem cells:

Plantshave emerged as powerful production platforms for the expression of fully functional recombinantmammalian proteins. These expression systems have demonstrated the ability to produce complexglycoproteinsin a cost-efficient manner at large scale. The full realization of thetherapeuticpotential of stem cells has only recently come into the forefront ofregenerative medicine. Stem cells are unprogrammed cells that can differentiate into cells with specific functions.Regenerative therapiesare used to stimulate healing and might be used in the future to treat various kinds of diseases.Regenerative medicinewill result in an extended healthy life span. A fresh apple is a symbol for beautiful skin. Hair greying for example could be shown to result from the fact that themelanocyte stem cellsin the hair follicle have died off.

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Track-16 Plant stem cell rejuvenation:

Asplantscannot escape from danger by running or taking flight, they need a special mechanism to withstandenvironmental stress. What empowers them to withstand harsh attacks and preserve life is the stem cell. According to Wikipedia, plantstem cellsnever undergo theagingprocess but constantly create new specialized and unspecialized cells, and they have the potential to grow into any organ, tissue, or cell in the body. The everlasting life is due to the hormones auxin andgibberellin. British scientists found that plant stem cells were much more sensitive toDNAdamage than other cells. And once they sense damage, they trigger death of these cells.

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Track-17 Clinical trials in cell and gene therapy:

Aclinical trialis a research study that seeks to determine if a treatment is safe and effective. Advancing new cell andgene therapies(CGTs) from the laboratory into early-phaseclinical trialshas proven to be a complex task even for experienced investigators. Due to the wide variety ofCGTproducts and their potential applications, a case-by-case assessment is warranted for the design of each clinical trial.

Objectives:Determine thepharmacokineticsof this regimen by the persistence of modified T cells in the blood of these patients, Evaluate theimmunogenicityof murine sequences in chimeric anti-CEA Ig TCR, Assess immunologic parameters which correlate with the efficacy of this regimen in these patients, Evaluate, in a preliminary manner, the efficacy of this regimen in patients with CEA bearingtumours.

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Track-18 Molecular epigenetics:

Epigeneticsis the study of heritable changes in thephenotypeof a cell or organism that are not caused by its genotype. The molecular basis of anepigeneticprofile arises from covalent modifications of protein andDNAcomponents ofchromatin. The epigenetic profile of a cell often dictates cell fate, as well as mammalian development,agingand disease. Epigenetics has evolved to become the science that explains how the differences in the patterns ofgene expressionin diverse cells or tissues are executed and inherited.

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Track-19 Bioengineering therapeutics:

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Please note: An erratum has been published for this article. To view the erratum, please click here.

Clare A. Dykewicz, M.D., M.P.H. Harold W. Jaffe, M.D., Director Division of AIDS, STD, and TB Laboratory Research National Center for Infectious Diseases

Jonathan E. Kaplan, M.D. Division of AIDS, STD, and TB Laboratory Research National Center for Infectious Diseases Division of HIV/AIDS Prevention --- Surveillance and Epidemiology National Center for HIV, STD, and TB Prevention

Clare A. Dykewicz, M.D., M.P.H., Chair Harold W. Jaffe, M.D. Thomas J. Spira, M.D. Division of AIDS, STD, and TB Laboratory Research

William R. Jarvis, M.D. Hospital Infections Program National Center for Infectious Diseases, CDC

Jonathan E. Kaplan, M.D. Division of AIDS, STD, and TB Laboratory Research National Center for Infectious Diseases Division of HIV/AIDS Prevention --- Surveillance and Epidemiology National Center for HIV, STD, and TB Prevention, CDC

Brian R. Edlin, M.D. Division of HIV/AIDS Prevention---Surveillance and Epidemiology National Center for HIV, STD, and TB Prevention, CDC

Robert T. Chen, M.D., M.A. Beth Hibbs, R.N., M.P.H. Epidemiology and Surveillance Division National Immunization Program, CDC

Raleigh A. Bowden, M.D. Keith Sullivan, M.D. Fred Hutchinson Cancer Research Center Seattle, Washington

David Emanuel, M.B.Ch.B. Indiana University Indianapolis, Indiana

David L. Longworth, M.D. Cleveland Clinic Foundation Cleveland, Ohio

Philip A. Rowlings, M.B.B.S., M.S. International Bone Marrow Transplant Registry/Autologous Blood and Marrow Transplant Registry Milwaukee, Wisconsin

Robert H. Rubin, M.D. Massachusetts General Hospital Boston, Massachusetts and Massachusetts Institute of Technology Cambridge, Massachusetts

Kent A. Sepkowitz, M.D. Memorial-Sloan Kettering Cancer Center New York, New York

John R. Wingard, M.D. University of Florida Gainesville, Florida

John F. Modlin, M.D. Dartmouth Medical School Hanover, New Hampshire

Donna M. Ambrosino, M.D. Dana-Farber Cancer Institute Boston, Massachusetts

Norman W. Baylor, Ph.D. Food and Drug Administration Rockville, Maryland

Albert D. Donnenberg, Ph.D. University of Pittsburgh Pittsburgh, Pennsylvania

Pierce Gardner, M.D. State University of New York at Stony Brook Stony Brook, New York

Roger H. Giller, M.D. University of Colorado Denver, Colorado

Neal A. Halsey, M.D. Johns Hopkins University Baltimore, Maryland

Chinh T. Le, M.D. Kaiser-Permanente Medical Center Santa Rosa, California

Deborah C. Molrine, M.D. Dana-Farber Cancer Institute Boston, Massachusetts

Keith M. Sullivan, M.D. Fred Hutchinson Cancer Research Center Seattle, Washington

CDC, the Infectious Disease Society of America, and the American Society of Blood and Marrow Transplantation have cosponsored these guidelines for preventing opportunistic infections (OIs) among hematopoietic stem cell transplant (HSCT) recipients. The guidelines were drafted with the assistance of a working group of experts in infectious diseases, transplantation, and public health. For the purposes of this report, HSCT is defined as any transplantation of blood- or marrow-derived hematopoietic stem cells, regardless of transplant type (i.e., allogeneic or autologous) or cell source (i.e., bone marrow, peripheral blood, or placental or umbilical cord blood). Such OIs as bacterial, viral, fungal, protozoal, and helminth infections occur with increased frequency or severity among HSCT recipients. These evidence-based guidelines contain information regarding preventing OIs, hospital infection control, strategies for safe living after transplantation, vaccinations, and hematopoietic stem cell safety. The disease-specific sections address preventing exposure and disease for pediatric and adult and autologous and allogeneic HSCT recipients. The goal of these guidelines is twofold: to summarize current data and provide evidence-based recommendations regarding preventing OIs among HSCT patients. The guidelines were developed for use by HSCT recipients, their household and close contacts, transplant and infectious diseases physicians, HSCT center personnel, and public health professionals. For all recommendations, prevention strategies are rated by the strength of the recommendation and the quality of the evidence supporting the recommendation. Adhering to these guidelines should reduce the number and severity of OIs among HSCT recipients.

In 1992, the Institute of Medicine (1) recommended that CDC lead a global effort to detect and control emerging infectious agents. In response, CDC published a plan (2) that outlined national disease prevention priorities, including the development of guidelines for preventing opportunistic infections (OIs) among immunosuppressed persons. During 1995, CDC published guidelines for preventing OIs among persons infected with human immunodeficiency virus (HIV) and revised those guidelines during 1997 and 1999 (3--5). Because of the success of those guidelines, CDC sought to determine the need for expanding OI prevention activities to other immunosuppressed populations. An informal survey of hematology, oncology, and infectious disease specialists at transplant centers and a working group formed by CDC determined that guidelines were needed to help prevent OIs among hematopoietic stem cell transplant (HSCT)* recipients.

The working group defined OIs as infections that occur with increased frequency or severity among HSCT recipients, and they drafted evidence-based recommendations for preventing exposure to and disease caused by bacterial, fungal, viral, protozoal, or helminthic pathogens. During March 1997, the working group presented the first draft of these guidelines at a meeting of representatives from public and private health organizations. After review by that group and other experts, these guidelines were revised and made available during September 1999 for a 45-day public comment period after notification in the Federal Register. Public comments were added when feasible, and the report was approved by CDC, the Infectious Disease Society of America, and the American Society of Blood and Marrow Transplantation. The pediatric content of these guidelines has been endorsed also by the American Academy of Pediatrics. The hematopoietic stem cell safety section was endorsed by the International Society of Hematotherapy and Graft Engineering.

The first recommendations presented in this report are followed by recommendations for hospital infection control, strategies for safe living, vaccinations, and hematopoietic stem cell safety. Unless otherwise noted, these recommendations address allogeneic and autologous and pediatric and adult HSCT recipients. Additionally, these recommendations are intended for use by the recipients, their household and other close contacts, transplant and infectious diseases specialists, HSCT center personnel, and public health professionals.

For all recommendations, prevention strategies are rated by the strength of the recommendation (Table 1) and the quality of the evidence (Table 2) supporting the recommendation. The principles of this rating system were developed by the Infectious Disease Society of America and the U.S. Public Health Service for use in the guidelines for preventing OIs among HIV-infected persons (3--6). This rating system allows assessments of recommendations to which adherence is critical.

HSCT is the infusion of hematopoietic stem cells from a donor into a patient who has received chemotherapy, which is usually marrow-ablative. Increasingly, HSCT has been used to treat neoplastic diseases, hematologic disorders, immunodeficiency syndromes, congenital enzyme deficiencies, and autoimmune disorders (e.g., systemic lupus erythematosus or multiple sclerosis) (7--10). Moreover, HSCT has become standard treatment for selected conditions (7,11,12). Data from the International Bone Marrow Transplant Registry and the Autologous Blood and Marrow Transplant Registry indicate that approximately 20,000 HSCTs were performed in North America during 1998 (Statistical Center of the International Bone Marrow Transplant Registry and Autologous Blood and Marrow Transplant Registry, unpublished data, 1998).

HSCTs are classified as either allogeneic or autologous on the basis of the source of the transplanted hematopoietic progenitor cells. Cells used in allogeneic HSCTs are harvested from a donor other than the transplant recipient. Such transplants are the most effective treatment for persons with severe aplastic anemia (13) and offer the only curative therapy for persons with chronic myelogenous leukemia (12). Allogeneic donors might be a blood relative or an unrelated donor. Allogeneic transplants are usually most successful when the donor is a human lymphocyte antigen (HLA)-identical twin or matched sibling. However, for allogeneic candidates who lack such a donor, registry organizations (e.g., the National Marrow Donor Program) maintain computerized databases that store information regarding HLA type from millions of volunteer donors (14--16). Another source of stem cells for allogeneic candidates without an HLA-matched sibling is a mismatched family member (17,18). However, persons who receive allogeneic grafts from donors who are not HLA-matched siblings are at a substantially greater risk for graft-versus-host disease (GVHD) (19). These persons are also at increased risk for suboptimal graft function and delayed immune system recovery (19). To reduce GVHD among allogeneic HSCTs, techniques have been developed to remove T-lymphocytes, the principal effectors of GVHD, from the donor graft. Although the recipients of T-lymphocyte--depleted marrow grafts generally have lower rates of GVHD, they also have greater rates of graft rejection, cytomegalovirus (CMV) infection, invasive fungal infection, and Epstein-Barr virus (EBV)-associated posttransplant lymphoproliferative disease (20).

The patient's own cells are used in an autologous HSCT. Similar to autologous transplants are syngeneic transplants, among whom the HLA-identical twin serves as the donor. Autologous HSCTs are preferred for patients who require high-level or marrow-ablative chemotherapy to eradicate an underlying malignancy but have healthy, undiseased bone marrows. Autologous HSCTs are also preferred when the immunologic antitumor effect of an allograft is not beneficial. Autologous HSCTs are used most frequently to treat breast cancer, non-Hodgkin's lymphoma, and Hodgkin's disease (21). Neither autologous nor syngeneic HSCTs confer a risk for chronic GVHD.

Recently, medical centers have begun to harvest hematopoietic stem cells from placental or umbilical cord blood (UCB) immediately after birth. These harvested cells are used primarily for allogeneic transplants among children. Early results demonstrate that greater degrees of histoincompatibility between donor and recipient might be tolerated without graft rejection or GVHD when UCB hematopoietic cells are used (22--24). However, immune system function after UCB transplants has not been well-studied.

HSCT is also evolving rapidly in other areas. For example, hematopoietic stem cells harvested from the patient's peripheral blood after treatment with hematopoietic colony-stimulating factors (e.g., granulocyte colony-stimulating factor [G-CSF or filgastrim] or granulocyte-macrophage colony-stimulating factor [GM-CSF or sargramostim]) are being used increasingly among autologous recipients (25) and are under investigation for use among allogeneic HSCT. Peripheral blood has largely replaced bone marrow as a source of stem cells for autologous recipients. A benefit of harvesting such cells from the donor's peripheral blood instead of bone marrow is that it eliminates the need for general anesthesia associated with bone marrow aspiration.

GVHD is a condition in which the donated cells recognize the recipient's cells as nonself and attack them. Although the use of intravenous immunoglobulin (IVIG) in the routine management of allogeneic patients was common in the past as a means of producing immune modulation among patients with GVHD, this practice has declined because of cost factors (26) and because of the development of other strategies for GVHD prophylaxis (27). For example, use of cyclosporine GVHD prophylaxis has become commonplace since its introduction during the early 1980s. Most frequently, cyclosporine or tacrolimus (FK506) is administered in combination with other immunosuppressive agents (e.g., methotrexate or corticosteroids) (27). Although cyclosporine is effective in preventing GVHD, its use entails greater hazards for infectious complications and relapse of the underlying neoplastic disease for which the transplant was performed.

Although survival rates for certain autologous recipients have improved (28,29), infection remains a leading cause of death among allogeneic transplants and is a major cause of morbidity among autologous HSCTs (29). Researchers from the National Marrow Donor Program reported that, of 462 persons receiving unrelated allogeneic HSCTs during December 1987--November 1990, a total of 66% had died by 1991 (15). Among primary and secondary causes of death, the most common cause was infection, which occurred among 37% of 307 patients (15).**

Despite high morbidity and mortality after HSCT, recipients who survive long-term are likely to enjoy good health. A survey of 798 persons who had received an HSCT before 1985 and who had survived for >5 years after HSCT, determined that 93% were in good health and that 89% had returned to work or school full time (30). In another survey of 125 adults who had survived a mean of 10 years after HSCT, 88% responded that the benefits of transplantation outweighed the side effects (31).

During the first year after an HSCT, recipients typically follow a predictable pattern of immune system deficiency and recovery, which begins with the chemotherapy or radiation therapy (i.e., the conditioning regimen) administered just before the HSCT to treat the underlying disease. Unfortunately, this conditioning regimen also destroys normal hematopoiesis for neutrophils, monocytes, and macrophages and damages mucosal progenitor cells, causing a temporary loss of mucosal barrier integrity. The gastrointestinal tract, which normally contains bacteria, commensal fungi, and other bacteria-carrying sources (e.g., skin or mucosa) becomes a reservoir of potential pathogens. Virtually all HSCT recipients rapidly lose all T- and B-lymphocytes after conditioning, losing immune memory accumulated through a lifetime of exposure to infectious agents, environmental antigens, and vaccines. Because transfer of donor immunity to HSCT recipients is variable and influenced by the timing of antigen exposure among donor and recipient, passively acquired donor immunity cannot be relied upon to provide long-term immunity against infectious diseases among HSCT recipients.

During the first month after HSCT, the major host-defense deficits include impaired phagocytosis and damaged mucocutaneous barriers. Additionally, indwelling intravenous catheters are frequently placed and left in situ for weeks to administer parenteral medications, blood products, and nutritional supplements. These catheters serve as another portal of entry for opportunistic pathogens from organisms colonizing the skin (e.g., . coagulase-negative Staphylococci, Staphylococcus aureus, Candida species, and Enterococci) (32,33).

Engraftment for adults and children is defined as the point at which a patient can maintain a sustained absolute neutrophil count (ANC) of >500/mm3 and sustained platelet count of >20,000, lasting >3 consecutive days without transfusions. Among unrelated allogeneic recipients, engraftment occurs at a median of 22 days after HSCT (range: 6--84 days) (15). In the absence of corticosteroid use, engraftment is associated with the restoration of effective phagocytic function, which results in a decreased risk for bacterial and fungal infections. However, all HSCT recipients and particularly allogeneic recipients, experience an immune system dysfunction for months after engraftment. For example, although allogeneic recipients might have normal total lymphocyte counts within >2 months after HSCT, they have abnormal CD4/CD8 T-cell ratios, reflecting their decreased CD4 and increased CD8 T-cell counts (27). They might also have immunoglobulin G (IgG)2, IgG4, and immunoglobulin A (IgA) deficiencies for months after HSCT and have difficulty switching from immunoglobulin M (IgM) to IgG production after antigen exposure (32). Immune system recovery might be delayed further by CMV infection (34).

During the first >2 months after HSCT, recipients might experience acute GVHD that manifests as skin, gastrointestinal, and liver injury, and is graded on a scale of I--IV (32,35,36). Although autologous or syngeneic recipients might occasionally experience a mild, self-limited illness that is acute GVHD-like (19,37), GVHD occurs primarily among allogeneic recipients, particularly those receiving matched, unrelated donor transplants. GVHD is a substantial risk factor for infection among HSCT recipients because it is associated with a delayed immunologic recovery and prolonged immunodeficiency (19). Additionally, the immunosuppressive agents used for GVHD prophylaxis and treatment might make the HSCT recipient more vulnerable to opportunistic viral and fungal pathogens (38).

Certain patients, particularly adult allogeneic recipients, might also experience chronic GVHD, which is graded as either limited or extensive chronic GVHD (19,39). Chronic GVHD appears similar to autoimmune, connective-tissue disorders (e.g., scleroderma or systemic lupus erythematosus) (40) and is associated with cellular and humoral immunodeficiencies, including macrophage deficiency, impaired neutrophil chemotaxis (41), poor response to vaccination (42--44), and severe mucositis (19). Risk factors for chronic GVHD include increasing age, allogeneic HSCT (particularly those among whom the donor is unrelated or a non-HLA identical family member) (40), and a history of acute GVHD (24,45). Chronic GVHD was first described as occurring >100 days after HSCT but can occur 40 days after HSCT (19). Although allogeneic recipients with chronic GVHD have normal or high total serum immunoglobulin levels (41), they experience long-lasting IgA, IgG, and IgG subclass deficiencies (41,46,47) and poor opsonization and impaired reticuloendothelial function. Consequently, they are at even greater risk for infections (32,39), particularly life-threatening bacterial infections from encapsulated organisms (e.g., Stre. pneumoniae, Ha. influenzae, or Ne. meningitidis). After chronic GVHD resolves, which might take years, cell-mediated and humoral immunity function are gradually restored.

HSCT recipients experience certain infections at different times posttransplant, reflecting the predominant host-defense defect(s) (Figure). Immune system recovery for HSCT recipients takes place in three phases beginning at day 0, the day of transplant. Phase I is the preengraftment phase (<30 days after HSCT); phase II, the postengraftment phase (30--100 days after HSCT); and phase III, the late phase (>100 days after HSCT). Prevention strategies should be based on these three phases and the following information:

Preventing infections among HSCT recipients is preferable to treating infections. How ever, despite recent technologic advances, more research is needed to optimize health outcomes for HSCT recipients. Efforts to improve immune system reconstitution, particularly among allogeneic transplant recipients, and to prevent or resolve the immune dysregulation resulting from donor-recipient histoincompatibility and GVHD remain substantial challenges for preventing recurrent, persistent, or progressive infections among HSCT patients.

Preventing Exposure

Because bacteria are carried on the hands, health-care workers (HCWs) and others in contact with HSCT recipients should routinely follow appropriate hand-washing practices to avoid exposing recipients to bacterial pathogens (AIII).

Preventing Disease

Preventing Early Disease (0--100 Days After HSCT). Routine gut decontamination is not recommended for HSCT candidates (51--53) (DIII). Because of limited data, no recommendations can be made regarding the routine use of antibiotics for bacterial prophylaxis among afebrile, asymptomatic neutropenic recipients. Although studies have reported that using prophylactic antibiotics might reduce bacteremia rates after HSCT (51), infection-related fatality rates are not reduced (52). If physicians choose to use prophylactic antibiotics among asymptomatic, afebrile, neutropenic recipients, they should routinely review hospital and HSCT center antibiotic-susceptibility profiles, particularly when using a single antibiotic for antibacterial prophylaxis (BIII). The emergence of fluoquinolone-resistant coagulase-negative Staphylococci and Es. coli (51,52), vancomycin-intermediate Sta. aureus and vancomycin-resistant Enterococcus (VRE) are increasing concerns (54). Vancomycin should not be used as an agent for routine bacterial prophylaxis (DIII). Growth factors (e.g., GM-CSF and G-CSF) shorten the duration of neutropenia after HSCT (55); however, no data were found that indicate whether growth factors effectively reduce the attack rate of invasive bacterial disease.

Physicians should not routinely administer IVIG products to HSCT recipients for bacterial infection prophylaxis (DII), although IVIG has been recommended for use in producing immune system modulation for GVHD prevention. Researchers have recommended routine IVIG*** use to prevent bacterial infections among the approximately 20%--25% of HSCT recipients with unrelated marrow grafts who experience severe hypogamma-globulinemia (e.g., IgG < 400 mg/dl) within the first 100 days after transplant (CIII). For example, recipients who are hypogammaglobulinemic might receive prophylactic IVIG to prevent bacterial sinopulmonary infections (e.g., from Stre. pneumoniae) (8) (CIII). For hypogammaglobulinemic allogeneic recipients, physicians can use a higher and more frequent dose of IVIG than is standard for non-HSCT recipients because the IVIG half-life among HSCT recipients (generally 1--10 days) is much shorter than the half-life among healthy adults (generally 18--23 days) (56--58). Additionally, infections might accelerate IgG catabolism; therefore, the IVIG dose for a hypogammaglobulinemic recipient should be individualized to maintain trough serum IgG concentrations >400--500 mg/dl (58) (BII). Consequently, physicians should monitor trough serum IgG concentrations among these patients approximately every 2 weeks and adjust IVIG doses as needed (BIII) (Appendix).

Preventing Late Disease (>100 Days After HSCT). Antibiotic prophylaxis is recommended for preventing infection with encapsulated organisms (e.g., Stre. pneumoniae, Ha. influenzae, or Ne. meningitidis) among allogeneic recipients with chronic GVHD for as long as active chronic GVHD treatment is administered (59) (BIII). Antibiotic selection should be guided by local antibiotic resistance patterns. In the absence of severe demonstrable hypogammaglobulinemia (e.g., IgG levels < 400 mg/dl, which might be associated with recurrent sinopulmonary infections), routine monthly IVIG administration to HSCT recipients >90 days after HSCT is not recommended (60) (DI) as a means of preventing bacterial infections.

Other Disease Prevention Recommendations. Routine use of IVIG among autologous recipients is not recommended (61) (DII). Recommendations for preventing bacterial infections are the same among pediatric or adult HSCT recipients.

Preventing Exposure

Appropriate care precautions should be taken with hospitalized patients infected with Stre. pneumoniae (62,63) (BIII) to prevent exposure among HSCT recipients.

Preventing Disease

Information regarding the currently available 23-valent pneumococcal polysaccharide vaccine indicates limited immunogenicity among HSCT recipients. However, because of its potential benefit to certain patients, it should be administered to HSCT recipients at 12 and 24 months after HSCT (64--66) (BIII). No data were found regarding safety and immunogenicity of the 7-valent conjugate pneumococcal vaccine among HSCT recipients; therefore, no recommendation regarding use of this vaccine can be made.

Antibiotic prophylaxis is recommended for preventing infection with encapsulated organisms (e.g., Stre. pneumoniae, Ha. influenzae, and Ne. meningitidis) among allogeneic recipients with chronic GVHD for as long as active chronic GVHD treatment is administered (59) (BIII). Trimethoprim-sulfamethasaxole (TMP-SMZ) administered for Pneumocystis carinii pneumonia (PCP) prophylaxis will also provide protection against pneumococcal infections. However, no data were found to support using TMP-SMZ prophylaxis among HSCT recipients solely for the purpose of preventing Stre. pneumoniae disease. Certain strains of Stre. pneumoniae are resistant to TMP-SMZ and penicillin. Recommendations for preventing pneumococcal infections are the same for allogeneic or autologous recipients.

As with adults, pediatric HSCT recipients aged >2 years should be administered the current 23-valent pneumococcal polysaccharide vaccine because the vaccine can be effective (BIII). However, this vaccine should not be administered to children aged <2 years because it is not effective among that age population (DI). No data were found regarding safety and immunogenicity of the 7-valent conjugate pneumococcal vaccine among pediatric HSCT recipients; therefore, no recommendation regarding use of this vaccine can be made.

Preventing Exposure

Because Streptococci viridans colonize the oropharynx and gut, no effective method of preventing exposure is known.

Preventing Disease

Chemotherapy-induced oral mucositis is a potential source of Streptococci viridans bacteremia. Consequently, before conditioning starts, dental consults should be obtained for all HSCT candidates to assess their state of oral health and to perform any needed dental procedures to decrease the risk for oral infections after transplant (67) (AIII).

Generally, HSCT physicians should not use prophylactic antibiotics to prevent Streptococci viridans infections (DIII). No data were found that demonstrate efficacy of prophylactic antibiotics for this infection. Furthermore, such use might select antibiotic-resistant bacteria, and in fact, penicillin- and vancomycin-resistant strains of Streptococci viridans have been reported (68). However, when Streptococci viridans infections among HSCT recipients are virulent and associated with overwhelming sepsis and shock in an institution, prophylaxis might be evaluated (CIII). Decisions regarding the use of Streptococci viridans prophylaxis should be made only after consultation with the hospital epidemiologists or infection-control practitioners who monitor rates of nosocomial bacteremia and bacterial susceptibility (BIII).

HSCT physicians should be familiar with current antibiotic susceptibilities for patient isolates from their HSCT centers, including Streptococci viridans (BIII). Physicians should maintain a high index of suspicion for this infection among HSCT recipients with symptomatic mucositis because early diagnosis and aggressive therapy are currently the only potential means of preventing shock when severely neutropenic HSCT recipients experience Streptococci viridans bacteremia (69).

Preventing Exposure

Adults with Ha. influenzae type b (Hib) pneumonia require standard precautions (62) to prevent exposing the HSCT recipient to Hib. Adults and children who are in contact with the HSCT recipient and who have known or suspected invasive Hib disease, including meningitis, bacteremia, or epiglottitis, should be placed in droplet precautions until 24 hours after they begin appropriate antibiotic therapy, after which they can be switched to standard precautions. Household contacts exposed to persons with Hib disease and who also have contact with HSCT recipients should be administered rifampin prophylaxis according to published recommendations (70,71); prophylaxis for household contacts of a patient with Hib disease are necessary if all contacts aged <4 years are not fully vaccinated (BIII) (Appendix). This recommendation is critical because the risk for invasive Hib disease among unvaccinated household contacts aged <4 years is increased, and rifampin can be effective in eliminating Hib carriage and preventing invasive Hib disease (72--74). Pediatric household contacts should be up-to-date with Hib vaccinations to prevent possible Hib exposure to the HSCT recipient (AII).

Preventing Disease

Although no data regarding vaccine efficacy among HSCT recipients were found, Hib conjugate vaccine should be administered to HSCT recipients at 12, 14, and 24 months after HSCT (BII). This vaccine is recommended because the majority of HSCT recipients have low levels of Hib capsular polysaccharide antibodies >4 months after HSCT (75), and allogeneic recipients with chronic GVHD are at increased risk for infection from encapsulated organisms (e.g., Hib) (76,77). HSCT recipients who are exposed to persons with Hib disease should be offered rifampin prophylaxis according to published recommendations (70) (BIII) (Appendix).

Antibiotic prophylaxis is recommended for preventing infection with encapsulated organisms (e.g., Stre. pneumoniae, Ha. influenzae, or Ne. meningitidis) among allogeneic recipients with chronic GVHD for as long as active chronic GVHD treatment is administered (59) (BIII). Antibiotic selection should be guided by local antibiotic-resistance patterns. Recommendations for preventing Hib infections are the same for allogeneic or autologous recipients. Recommendations for preventing Hib disease are the same for pediatric or adult HSCT recipients, except that any child infected with Hib pneumonia requires standard precautions with droplet precautions added for the first 24 hours after beginning appropriate antibiotic therapy (62,70) (BIII). Appropriate pediatric doses should be administered for Hib conjugate vaccine and for rifampin prophylaxis (71) (Appendix).

Preventing Exposure

HSCT candidates should be tested for the presence of serum anti-CMV IgG antibodies before transplantation to determine their risk for primary CMV infection and reactivation after HSCT (AIII). Only Food and Drug Administration (FDA) licensed or approved tests should be used. HSCT recipients and candidates should avoid sharing cups, glasses, and eating utensils with others, including family members, to decrease the risk for CMV exposure (BIII).

Sexually active patients who are not in long-term monogamous relationships should always use latex condoms during sexual contact to reduce their risk for exposure to CMV and other sexually transmitted pathogens (AII). However, even long-time monogamous pairs can be discordant for CMV infections. Therefore, during periods of immuno-compromise, sexually active HSCT recipients in monogamous relationships should ask partners to be tested for serum CMV IgG antibody, and discordant couples should use latex condoms during sexual contact to reduce the risk for exposure to this sexually transmitted OI (CIII).

After handling or changing diapers or after wiping oral and nasal secretions, HSCT candidates and recipients should practice regular hand washing to reduce the risk for CMV exposure (AII). CMV-seronegative recipients of allogeneic stem cell transplants from CMV-seronegative donors (i.e., R-negative or D-negative) should receive only leukocyte-reduced or CMV-seronegative red cells or leukocyte-reduced platelets (<1 x 106 leukocytes/unit) to prevent transfusion-associated CMV infection (78) (AI). However, insufficient data were found to recommend use of leukocyte-reduced or CMV-seronega tive red cells and platelets among CMV-seronegative recipients who have CMV-seropositive donors (i.e., R-negative or D-positive).

All HCWs should wear gloves when handling blood products or other potentially contaminated biologic materials (AII) to prevent transmission of CMV to HSCT recipients. HSCT patients who are known to excrete CMV should be placed under standard precautions (62) for the duration of CMV excretion to avoid possible transmission to CMV-seronegative HSCT recipients and candidates (AIII). Physicians are cautioned that CMV excretion can be episodic or prolonged.

Preventing Disease and Disease Recurrence

HSCT recipients at risk for CMV disease after HSCT (i.e., all CMV-seropositive HSCT recipients, and all CMV-seronegative recipients with a CMV-seropositive donor) should be placed on a CMV disease prevention program from the time of engraftment until 100 days after HSCT (i.e., phase II) (AI). Physicians should use either prophylaxis or preemptive treatment with ganciclovir for allogeneic recipients (AI). In selecting a CMV disease prevention strategy, physicians should assess the risks and benefits of each strategy, the needs and condition of the patient, and the hospital's virology laboratory support capability.

Prophylaxis strategy against early CMV (i.e., <100 days after HSCT) for allogeneic recipients involves administering ganciclovir prophylaxis to all allogeneic recipients at risk throughout phase II (i.e., from engraftment to 100 days after HSCT). The induction course is usually started at engraftment (AI), although physicians can add a brief prophylactic course during HSCT preconditioning (CIII) (Appendix).

Preemptive strategy against early CMV (i.e., <100 days after HSCT) for allogeneic recipients is preferred over prophylaxis for CMV-seronegative HSCT recipients of seropositive donor cells (i.e., D-positive or R-negative) because of the low attack rate of active CMV infection if screened or filtered blood product support is used (BII). Preemptive strategy restricts ganciclovir use for those patients who have evidence of CMV infection after HSCT. It requires the use of sensitive and specific laboratory tests to rapidly diagnose CMV infection after HSCT and to enable immediate administration of ganciclovir after CMV infection has been detected. Allogeneic recipients at risk should be screened >1 times/week from 10 days to 100 days after HSCT (i.e., phase II) for the presence of CMV viremia or antigenemia (AIII).

HSCT physicians should select one of two diagnostic tests to determine the need for preemptive treatment. Currently, the detection of CMV pp65 antigen in leukocytes (antigenemia) (79,80) is preferred for screening for preemptive treatment because it is more rapid and sensitive than culture and has good positive predictive value (79--81). Direct detection of CMV-DNA (deoxyribonucleic acid) by polymerase chain reaction (PCR) (82) is very sensitive but has a low positive predictive value (79). Although CMV-DNA PCR is less sensitive than whole blood or leukocyte PCR, plasma CMV-DNA PCR is useful during neutropenia, when the number of leukocytes/slide is too low to allow CMV pp65 antigenemia testing.

Virus culture of urine, saliva, blood, or bronchoalveolar washings by rapid shell-vial culture (83) or routine culture (84,85) can be used; however, viral culture techniques are less sensitive than CMV-DNA PCR or CMV pp65 antigenemia tests. Also, rapid shell-viral cultures require >48 hours and routine viral cultures can require weeks to obtain final results. Thus, viral culture techniques are less satisfactory than PCR or antigenemia tests. HSCT centers without access to PCR or antigenemia tests should use prophylaxis rather than preemptive therapy for CMV disease prevention (86) (BII). Physicians do use other diagnostic tests (e.g., hybrid capture CMV-DNA assay, Version 2.0 [87] or CMV pp67 viral RNA [ribonucleic acid] detection) (88); however, limited data were found regarding use among HSCT recipients, and therefore, no recommendation for use can be made.

Allogeneic recipients <100 days after HSCT (i.e., during phase II) should begin preemptive treatment with ganciclovir if CMV viremia or any antigenemia is detected or if the recipient has >2 consecutively positive CMV-DNA PCR tests (BIII). After preemptive treatment has been started, maintenance ganciclovir is usually continued until 100 days after HSCT or for a minimum of 3 weeks, whichever is longer (AI) (Appendix). Antigen or PCR tests should be negative when ganciclovir is stopped. Studies report that a shorter course of ganciclovir (e.g., for 3 weeks or until negative PCR or antigenemia occurs) (89--91) might provide adequate CMV prevention with less toxicity, but routine weekly screening by pp65 antigen or PCR test is necessary after stopping ganciclovir because CMV reactivation can occur (BIII).

Presently, only the intravenous formulation of ganciclovir has been approved for use in CMV prophylactic or preemptive strategies (BIII). No recommendation for oral ganciclovir use among HSCT recipients can be made because clinical trials evaluating its efficacy are still in progress. One group has used ganciclovir and foscarnet on alternate days for CMV prevention (92), but no recommendation can be made regarding this strategy because of limited data. Patients who are ganciclovir-intolerant should be administered foscarnet instead (93) (BII) (Appendix). HSCT recipients receiving ganciclovir should have ANCs checked >2 times/week (BIII). Researchers report managing ganciclovir-associated neutropenia by adding G-CSF (94) or temporarily stopping ganciclovir for >2 days if the patient's ANC is <1,000 (CIII). Ganciclovir can be restarted when the patient's ANC is >1,000 for 2 consecutive days. Alternatively, researchers report substituting foscarnet for ganciclovir if a) the HSCT recipient is still CMV viremic or antigenemic or b) the ANC remains <1,000 for >5 days after ganciclovir has been stopped (CIII) (Appendix). Because neutropenia accompanying ganciclovir administration is usually brief, such patients do not require antifungal or antibacterial prophylaxis (DIII).

Currently, no benefit has been reported from routinely administering ganciclovir prophylaxis to all HSCT recipients at >100 days after HSCT (i.e., during phase III). However, persons with high risk for late CMV disease should be routinely screened biweekly for evidence of CMV reactivation as long as substantial immunocompromise persists (BIII). Risk factors for late CMV disease include allogeneic HSCT accompanied by chronic GVHD, steroid use, low CD4 counts, delay in high avidity anti-CMV antibody, and recipients of matched unrelated or T-cell--depleted HSCTs who are at high risk (95--99). If CMV is still detectable by routine screening >100 days after HSCT, ganciclovir should be continued until CMV is no longer detectable (AI). If low-grade CMV antigenemia (<5 positive cells/slide) is detected on routine screening, the antigenemia test should be repeated in 3 days (BIII). If CMV antigenemia indicates >5 cells/slide, PCR is positive, or the shell-vial culture detects CMV viremia, a 3-week course of preemptive ganciclovir treatment should be administered (BIII) (Appendix). Ganciclovir should also be started if the patient has had >2 consecutively positive viremia or PCR tests (e.g., in a person receiving steroids for GVHD or who received ganciclovir or foscarnet at <100 days after HSCT). Current investigational strategies for preventing late CMV disease include the use of targeted prophylaxis with antiviral drugs and cellular immunotherapy for those with deficient or absent CMV-specific immune system function.

If viremia persists after 4 weeks of ganciclovir preemptive therapy or if the level of antigenemia continues to rise after 3 weeks of therapy, ganciclovir-resistant CMV should be suspected. If CMV viremia recurs during continuous treatment with ganciclovir, researchers report restarting ganciclovir induction (100) or stopping ganciclovir and starting foscarnet (CIII). Limited data were found regarding the use of foscarnet among HSCT recipients for either CMV prophylaxis or preemptive therapy (92,93).

Infusion of donor-derived CMV-specific clones of CD8+ T-cells into the transplant recipient is being evaluated under FDA Investigational New Drug authorization; therefore, no recommendation can be made. Although, in a substantial cooperative study, high-dose acyclovir has had certain efficacy for preventing CMV disease (101), its utility is limited in a setting where more potent anti-CMV agents (e.g., ganciclovir) are used (102). Acyclovir is not effective in preventing CMV disease after autologous HSCT (103) and is, therefore, not recommended for CMV preemptive therapy (DII). Consequently, valacyclovir, although under study for use among HSCT recipients, is presumed to be less effective than ganciclovir against CMV and is currently not recommended for CMV disease prevention (DII).

Although HSCT physicians continue to use IVIG for immune system modulation, IVIG is not recommended for CMV disease prophylaxis among HSCT recipients (DI). Cidofovir, a nucleoside analog, is approved by FDA for the treatment of AIDS-associated CMV retinitis. The drug's major disadvantage is nephrotoxicity. Cidofovir is currently in FDA phase 1 trial for use among HSCT recipients; therefore, recommendations for its use cannot be made.

Use of CMV-negative or leukocyte-reduced blood products is not routinely required for all autologous recipients because most have a substantially lower risk for CMV disease. However, CMV-negative or leukocyte-reduced blood products can be used for CMV-seronegative autologous recipients (CIII). Researchers report that CMV-seropositive autologous recipients be evaluated for preemptive therapy if they have underlying hematologic malignancies (e.g., lymphoma or leukemia), are receiving intense conditioning regimens or graft manipulation, or have recently received fludarabine or 2-chlorodeoxyadenosine (CDA) (CIII). This subpopulation of autologous recipients should be monitored weekly from time of engraftment until 60 days after HSCT for CMV reactivation, preferably with quantitative CMV pp65 antigen (80) or quantitative PCR (BII).

Autologous recipients at high risk who experience CMV antigenemia (i.e., blood levels of >5 positive cells/slide) should receive 3 weeks of preemptive treatment with ganciclovir or foscarnet (80), but CD34+-selected patients should be treated at any level of antigenemia (BII) (Appendix). Prophylactic approach to CMV disease prevention is not appropriate for CMV-seropositive autologous recipients. Indications for the use of CMV prophylaxis or preemptive treatment are the same for children or adults.

Preventing Exposure

All transplant candidates, particularly those who are EBV-seronegative, should be advised of behaviors that could decrease the likelihood of EBV exposure (AII). For example, HSCT recipients and candidates should follow safe hygiene practices (e.g., frequent hand washing [AIII] and avoiding the sharing of cups, glasses, and eating utensils with others) (104) (BIII), and they should avoid contact with potentially infected respiratory secretions and saliva (104) (AII).

Preventing Disease

Infusion of donor-derived, EBV-specific cytotoxic T-lymphocytes has demonstrated promise in the prophylaxis of EBV-lymphoma among recipients of T-cell--depleted unrelated or mismatched allogeneic recipients (105,106). However, insufficient data were found to recommend its use. Prophylaxis or preemptive therapy with acyclovir is not recommended because of lack of efficacy (107,108) (DII).

Preventing Exposure

HSCT candidates should be tested for serum anti-HSV IgG before transplant (AIII); however, type-specific anti-HSV IgG serology testing is not necessary. Only FDA-licensed or -approved tests should be used. All HSCT candidates, particularly those who are HSV-seronegative, should be informed of the importance of avoiding HSV infection while immunocompromised and should be advised of behaviors that will decrease the likelihood of HSV exposure (AII). HSCT recipients and candidates should avoid sharing cups, glasses, and eating utensils with others (BIII). Sexually active patients who are not in a long-term monogamous relationship should always use latex condoms during sexual contact to reduce the risk for exposure to HSV as well as other sexually transmitted pathogens (AII). However, even long-time monogamous pairs can be discordant for HSV infections. Therefore, during periods of immunocompromise, sexually active HSCT recipients in such relationships should ask partners to be tested for serum HSV IgG antibody. If the partners are discordant, they should consider using latex condoms during sexual contact to reduce the risk for exposure to this sexually transmitted OI (CIII). Any person with disseminated, primary, or severe mucocutaneous HSV disease should be placed under contact precautions for the duration of the illness (62) (AI) to prevent transmission of HSV to HSCT recipients.

Preventing Disease and Disease Recurrence

Acyclovir. Acyclovir prophylaxis should be offered to all HSV-seropositive allogeneic recipients to prevent HSV reactivation during the early posttransplant period (109--113) (AI). Standard approach is to begin acyclovir prophylaxis at the start of the conditioning therapy and continue until engraftment occurs or until mucositis resolves, whichever is longer, or approximately 30 days after HSCT (BIII) (Appendix). Without supportive data from controlled studies, routine use of antiviral prophylaxis for >30 days after HSCT to prevent HSV is not recommended (DIII). Routine acyclovir prophylaxis is not indicated for HSV-seronegative HSCT recipients, even if the donors are HSV-seropositive (DIII). Researchers have proposed administration of ganciclovir prophylaxis alone (86) to HSCT recipients who required simultaneous prophylaxis for CMV and HSV after HSCT (CIII) because ganciclovir has in vitro activity against CMV and HSV 1 and 2 (114), although ganciclovir has not been approved for use against HSV.

Valacyclovir. Researchers have reported valacyclovir use for preventing HSV among HSCT recipients (CIII); however, preliminary data demonstrate that very high doses of valacyclovir (8 g/day) were associated with thrombotic thrombocytopenic purpura/hemolytic uremic syndrome among HSCT recipients (115). Controlled trial data among HSCT recipients are limited (115), and the FDA has not approved valacyclovir for use among recipients. Physicians wishing to use valacyclovir among recipients with renal impairment should exercise caution and decrease doses as needed (BIII) (Appendix).

Foscarnet. Because of its substantial renal and infusion-related toxicity, foscarnet is not recommended for routine HSV prophylaxis among HSCT recipients (DIII).

Famciclovir. Presently, data regarding safety and efficacy of famciclovir among HSCT recipients are limited; therefore, no recommendations for HSV prophylaxis with famciclovir can be made.

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Guidelines for Preventing Opportunistic Infections Among ...

Accreditation Statement

This activity (World Immunology Summit 2016) has been planned and implemented in accordance with the accreditation requirements and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint providership of PeerPoint Medical Education Institute and Conference Series, LLC. PeerPoint Medical Education Institute is accredited by the ACCME to provide continuing medical education for physicians.

Designation Statement

PeerPoint Medical Education Institute designates the live format for this educational activity for AMA PRA Category 1 Credits. Physicians should only claim credit commensurate with the extent of their participation in the activity.

Conference series invites participants from all over the world to attend "6th International Conference and Exhibition on Immunology" October 24-26, 2016 Chicago, USA includes prompt keynote presentations, Oral talks, Poster presentations and Exhibitions.

Presenters can availupto 20 CME credits..

The annual International Conference on Immunology offer a unique platform for academia, Societies and Industries interested in immunology and Biomedical sciences to share the latest trends and important issues in the field. Immunology Summit-2016 brings together the Global leaders in Immunology and relevant fields to present their research at this exclusive scientific program. The Immunology Conference hosting presentations from editors of prominent refereed journals, renowned and active investigators and decision makers in the field of Immunology. Immunology Summit 2016 Organizing Committee also intended to encourage Young investigators at every career stage to submit abstracts reporting their latest scientific findings in oral and poster sessions.

Track 1:ClinicalImmunology: Current & Future Research

Immunology is the study of the immune system. The immune system is how all animals, including humans, protect themselves against diseases. The study of diseases caused by disorders of the immune system is clinical immunology. The disorders of the immune system fall into two broad categories:

Immunodeficiency, in this immune system fails to provide an adequate response.

Autoimmunity, in this immune system attacks its own host's body.

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Track 2:Cancer and Tumor Immunobiology

The immune system is the bodys first line of defence against most diseases and unnatural invaders.Cancer Immunobiologyis a branch ofimmunologyand it studies interactions between theimmune systemandcancer cells. These cancer cells, through subtle alterations, become immortal malignant cells but are often not changed enough to elicit an immune reaction.Understanding how the immune system worksor does not workagainst cancer is a primary focus of Cancer Immunology investigators. Certain cells of the immune system, including natural killer cells, dendritic cells (DCs) and effector T cells, are capable of driving potent anti-tumour responses.

Tumor Immunobiology

The immune system can promote the elimination of tumours, but often immune responses are modulated or suppressed by the tumour microenvironment. The Tumour microenvironment is an important aspect of cancer biology that contributes to tumour initiation, tumour progression and responses to therapy. Cells and molecules of the immune system are a fundamental component of the tumour microenvironment. Importantly, therapeutic strategies can harness the immune system to specifically target tumour cells and this is particularly appealing owing to the possibility of inducing tumour-specific immunological memory, which might cause long-lasting regression and prevent relapse in cancer patients. The composition and characteristics of the tumour micro environment vary widely and are important in determining the anti-tumour immune response. Tumour cells often induce an immunosuppressive microenvironment, which favours the development of immuno suppressive populations of immune cells, such as myeloid-derived suppressor cells and regulatory T cells.

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Track 3:Inflammation and Therapies

Inflammation is the body's attempt at self-protection; the aim being to remove harmful stimuli, including damaged cells, irritants, or pathogens - and begin the healing process. In Inflammation the body's whiteblood cellsand substances they produce protect us from infection with foreign organisms, such as bacteria and viruses. However, in some diseases, likearthritis, the body's defense system, the immune system triggers an inflammatory response when there are no foreign invaders to fight off. In these diseases, called autoimmune diseases, the body's normally protective immune system causes damage to its own tissues. The body responds as if normal tissues are infected or somehow abnormal. Inflammation involves immune cells, blood vessels, and molecular mediators. The purpose of inflammation is to eliminate the initial cause of cell injury, clear out necrotic cells and tissues damaged from the original insult and the inflammatory process, and to initiate tissue repair. signs of acute inflammation are pain, heat, redness, swelling, and loss of function

Therapies

Inflammation Therapy is a treatment for chronic disease involving a combination of lifestyle factors and medications designed to enable the immune system to fight the disease. Techniques used include heat therapy, cold therapy, electrical stimulation, traction, massage, and acupuncture. Heat increases blood flow and makes connective tissue more flexible. It temporarily decreases joint stiffness, pain, and muscle spasms. Heat also helps reduce inflammation and the buildup of fluid in tissues (edema). Heat therapy is used to treat inflammation (including various forms of arthritis), muscle spasm, and injuries such as sprains and strains. Cold therapy Applying cold may help numb tissues and relieve muscle spasms, pain due to injuries, and low back pain or inflammation that has recently developed. Cold may be applied using an ice bag, a cold pack, or fluids (such as ethyl chloride) that cool by evaporation. The therapist limits the time and amount of cold exposure to avoid damaging tissues and reducing body temperature (causing hypothermia). Cold is not applied to tissues with a reduced blood supply (for example, when the arteries are narrowed by peripheral arterial disease).

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Track 4:Molecular and Structural Immunology

Molecular Immunology

Molecular immunology deals with immune responses at cellular and molecular level. Molecular immunology has been evolved for better understanding of the sub-cellular immune responses for prevention and treatment of immune related disorders and immune deficient diseases. Journal of molecular immunology focuses on the invitro and invivo immunological responses of the host. Molecular Immunology focuses on the areas such as immunological disorders, invitro and invivo immunological host responses, humoral responses, immunotherapies for treatment of cancer, treatment of autoimmune diseases such as Hashimotos disease, myasthenia gravis, rheumatoid arthritis and systemic lupus erythematosus. Treatment of Immune deficiencies such as hypersensitivities, chronic granulomatous disease, diagnostic immunology research aspects, allografts, etc..

Structural Immunology

Host immune system is an important and sophisticated system, maintaining the balance of host response to "foreign" antigens and ignorance to the normal-self. To fulfill this achievement the system manipulates a cell-cell interaction through appropriate interactions between cell-surface receptors and cell-surface ligands, or cell-secreted soluble effector molecules to their ligands/receptors/counter-receptors on the cell surface, triggering further downstream signaling for response effects. T cells and NK cells are important components of the immune system for defending the infections and malignancies and maintaining the proper response against over-reaction to the host. Receptors on the surface of T cells and NK cells include a number of important protein molecules, for example, T cell receptor (TCR), co-receptor CD8 or CD4, co-stimulator CD28, CTLA4, KIR, CD94/NKG2, LILR (ILT/LIR/CD85), Ly49, and so forth.

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Track 5:Transplantation Immunology

Transplantation is an act of transferring cells, tissues, or organ from one site to other. Graft is implanted cell, tissue or organ. Development of the field of organ and tissue transplantation has accelerated remarkably since the human major histocompatibility complex (mhc) was discovered in 1967. Matching of donor and recipient for mhc antigens has been shown to have a significant positive effect on graft acceptance. The roles of the different components of the immune system involved in the tolerance or rejection of grafts and in graft-versus-host disease have been clarified. These components include: antibodies, antigen presenting cells, helper and cytotoxic t cell subsets, immune cell surface molecules, signaling mechanisms and cytokines that they release. The development of pharmacologic and biological agents that interfere with the alloimmune response and graft rejection has had a crucial role in the success of organ transplantation. Combinations of these agents work synergistically, leading to lower doses of immunosuppressive drugs and reduced toxicity. Significant numbers of successful solid organ transplants include those of the kidneys, liver, heart and lung.

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Track 6:Infectious Diseases, Emerging and Reemerging diseases: Confronting Future Outbreaks

Infectious diseasesare disorders caused by organisms such as bacteria, viruses,fungior parasites. Many organisms live in and on our bodies. They're normally harmless or even helpful, but under certain conditions, some organisms may causedisease.Someinfectious diseasescan be passed from person to person. Many infectious diseases, such asmeaslesand chickenpox, can be prevented by vaccines. Frequent and thorough hand-washing also helps protect you from infectious diseases.

There are four main kinds of germs:

Bacteria - one-celled germs that multiply quickly and may release chemicals which can make you sick

Viruses- capsules that contain genetic material, and use your own cells to multiply

Fungi - primitive plants, like mushrooms or mildew

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Track 7:Autoimmune Diseases

An autoimmune disease develops when your immune system, which defends your body against disease, decides your healthy cells are foreign. As a result, your immune system attacks healthy cells. An autoimmune disorder may result in the destruction of body tissue, abnormal growth of an organ, Changes in organ function. Depending on the type, an autoimmune disease can affect one or many different types of body tissue. Areas often affected by autoimmune disorders include Blood vessels, Connective tissues, Endocrineglands such as the thyroid or pancreas, Joints Muscles, Red blood cells, Skin It can also cause abnormal organ growth and changes in organ function. There are as many as 80 types of autoimmune diseases. Many of them have similar symptoms, which makes them very difficult to diagnose. Its also possible to have more than one at the same time. Common autoimmune disorders include Addison's disease, Dermatomyositis, Graves' disease, Hashimoto's thyroiditis, Multiple sclerosis, Myasthenia gravis, Pernicious anemia, Reactive arthritis. Autoimmune diseases usually fluctuate between periods of remission (little or no symptoms) and flare-ups (worsening symptoms). Currently, treatment for autoimmune diseases focuses on relieving symptoms because there is no curative therapy.

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Track 8:Viral Immunology: Emerging and Re-emerging Diseases

Immunology is the study of all aspects of the immune system in all organisms. It deals with the physiological functioning of the immune system in states of both health and disease; malfunctions of the immune system in immunological disorders (autoimmune diseases, hypersensitivities, immune deficiency, transplant rejection); the physical, chemical and physiological characteristics of the components of the immune system in vitro, in situ, and in vivo.

Viruses are strongly immunogenic and induces 2 types of immune responses; humoral and cellular. The repertoire of specificities of T and B cells are formed by rearrangements and somatic mutations. T and B cells do not generally recognize the same epitopes present on the same virus. B cells see the free unaltered proteins in their native 3-D conformation whereas T cells usually see the Ag in a denatured form in conjunction with MHC molecules. The characteristics of the immune reaction to the same virus may differ in different individuals depending on their genetic constitutions.

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Track 9:Pediatric Immunology

A child suffering from allergies or other problems with his immune system is referred as pediatric immunology. Childs immune system fights against infections. If the child has allergies, their immune system wrongly reacts to things that are usually harmless. Pet dander, pollen, dust, mold spores, insect stings, food, and medications are examples of such things. This reaction may cause their body to respond with health problems such as asthma, hay fever, hives, eczema (a rash), or a very severe and unusual reaction calledanaphylaxis. Sometimes, if your childs immune system is not working right, he may suffer from frequent, severe, and/or uncommon infections. Examples of such infections are sinusitis (inflammation of one or more of the sinuses), pneumonia (infection of the lung), thrush (a fungus infection in the mouth), and abscesses (collections of pus surrounded by inflamed tissue) that keep coming back.

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Track 10:Immunotherapy & Cancer Immunotherapy: From Basic Biology to Translational Research

Immunotherapy is treatment that uses certain parts of a persons immune system to fight diseases such as cancer. This can be done in a couple of ways:

Stimulating your own immune system to work harder or smarter to attack cancer cells Giving you immune system components, such as man-made immune system proteins

Some types of immunotherapy are also sometimes called biologic therapy or biotherapy. In the last few decades immunotherapy has become an important part of treating some types of cancer. Newer types of immune treatments are now being studied, and theyll impact how we treat cancer in the future. Immunotherapy includes treatments that work in different ways. Some boost the bodys immune system in a very general way. Others help train the immune system to attack cancer cells specifically.

Cancer immunotherapy is the use of the immune system to treat cancer. The main types of immunotherapy now being used to treat cancer include:

Monoclonal antibodies: these are man-made versions of immune system proteins. Antibodies can be very useful in treating cancer because they can be designed to attack a very specific part of a cancer cell.

Immune checkpoint inhibitors: these drugs basically take the brakes off the immune system, which helps it recognize and attack cancer cells.

Cancer vaccines: vaccines are substances put into the body to start an immune response against certain diseases. We usually think of them as being given to healthy people to help prevent infections. But some vaccines can help prevent or treat cancer.

Other, non-specific immunotherapies: these treatments boost the immune system in a general way, but this can still help the immune system attack cancer cells.

Immunotherapy drugs are now used to treat many different types of cancer. For more information about immunotherapy as a treatment for a specific cancer, please see our information on that type of cancer.

Related: Immunology Conferences|Immunologists Meetings|Conference Series LLC

2nd International Conference and Exhibition on Antibodies and Therapeutics, July 11-12, 2016 Philadelphia, Pennsylvania, USA; InternationalConference on Tumor Immunologyand Immunotherapy, July 28-30, 2016 Melbourne, Australia; InternationalConference on Cancer Immunologyand Immunotherapy, July 28-30, 2016 Melbourne, Australia, 2nd internationalCongress on Neuroimmunology& therapeutics, Dec 01-03, 2016, USA;International Congress of Immunology;2nd international conference on innate immunity, July 21-22, 2016, Germany;5th European Immunology Conferences, July 21-23, 2016 Berlin, Germany; 9th European Mucosal Immunology meetings, October 9 - 12 October, Scotland; international congress on immunology, august 21-26, 2016, Australia; 4th European Immunology events September 6-9, 2015, Austria

Track 11:Immunology and Diabetes

Immunologyis the study of the immune system, which is responsible for protecting the body from foreign cells such as viruses, bacteria and parasites. Immune system cells called T and B lymphocytes identify and destroy these invaders. Thelymphocytesusually recognize and ignore the bodys own tissue (a condition called immunological self-tolerance), but certain autoimmune disorders trigger a malfunction in the immune response causing an attack on the bodys own cells due to a loss ofimmune tolerance.

Type 1 diabetes is anautoimmune diseasethat occurs when the immune system mistakenly attacks insulin-producing islet cells in the pancreas. This attack begins years before type 1 diabetes becomes evident, so by the time someone is diagnosed, extensive damage has already been done and the ability to produceinsulinis lost.

Related: Immunology Conferences|Immunologists Meetings|Conference Series LLC

InternationalConference onMucosalImmunology, July 28-29, 2016, Australia; International Conference onAllergy, March 29-30, 2016, Spain; 2ndInternationalCongress onNeuroimmunology&Therapeutics, Dec 01-03, 2016, USA;7th InternationalConference on Allergy, Asthma and Clinical Immunology, September 14-15, 2016 Amsterdam, Netherlands; Asthma EventsSeptember 14-15, 2016 Amsterdam, Netherlands;2nd InternationalConference on Antibodiesand Therapeutics, July 11-12, 2016 Philadelphia, Pennsylvania, USA; InternationalConference on Tumor Immunologyand Immunotherapy, July 28-30, 2016 Melbourne, Australia; InternationalConference on Cancer Immunologyand Immunotherapy, July 28-30, 2016 Melbourne, Australia; Immunology events InternationalcongressonImmunology, August 21-26, 2016, Australia; British society for Immunology Annual Immunology Congress, 6-9 Dec, 2016, Liverpool, UK

Track 12:Immune Tolerance

Immunological toleranceis the failure to mount animmuneresponse to an antigen. It can be: Natural or "self"tolerance. This is the failure (a good thing) to attack the body's own proteins and other antigens. If the immunesystem should respond to "self",an autoimmune diseasemay result. Natural or "self" tolerance: Induced tolerance: This is tolerance to externalantigens that has been created by deliberately manipulating theimmune system.

Related: Immunology Conferences|Immunologists Meetings|Conference Series LLC

InternationalConference onMucosalImmunology, July 28-29, 2016, Australia; International Conference onAllergy, March 29-30, 2016, Spain; 2ndInternationalCongress onNeuroimmunology&Therapeutics, Dec 01-03, 2016, USA;7th InternationalConference on Allergy, Asthma and Clinical Immunology, September 14-15, 2016 Amsterdam, Netherlands; Asthma EventsSeptember 14-15, 2016 Amsterdam, Netherlands;2nd InternationalExhibition on Antibodiesand Therapeutics, July 11-12, 2016 Philadelphia, Pennsylvania, USA; InternationalConference on Tumor Immunologyand Immunotherapy, July 28-30, 2016 Melbourne, Australia; InternationalConference on Cancer Immunologyand Immunotherapy, July 28-30, 2016 Melbourne, Australia; Immunology events InternationalcongressonImmunology, August 21-26, 2016, Australia; British society for Immunology Annual Immunology Congress, 6-9 Dec, 2016, Liverpool, UK

Track 13:Vaccines and Immunotherapy

Vaccine is a biological preparation that improves immunity to particular disease. It contains certain agent that not only resembles a disease causing microorganism but it also stimulates bodys immune system to recognise the foreign agents. Vaccines are dead or inactivated organisms or purified products derived from them. whole organism vaccines purified macromolecules as vaccines,recombinant vaccines, DNA vaccines. The immune system recognizes vaccine agents as foreign, destroys them, and "remembers" them. The administration of vaccines is called vaccination. In order to provide best protection, children are recommended to receive vaccinations as soon as their immune systems are sufficiently developed to respond to particular vaccines with additional "booster" shots often required to achieve "full immunity".

Immunotherapy is treatment that uses certain parts of a persons immune system to fight diseases such as cancer. This can be done in a couple of ways:

Stimulating your own immune system to work harder or smarter to attack cancer cells

Giving you immune system components, such as man-made immune system proteins

Some types of immunotherapy are also sometimes called biologic therapy or biotherapy. In the last few decades immunotherapy has become an important part of treating some types of cancer. Newer types of immune treatments are now being studied, and theyll impact how we treat cancer in the future. Immunotherapy includes treatments that work in different ways. Some boost the bodys immune system in a very general way. Others help train the immune system to attack cancer cells specifically. Immunotherapy works better for some types of cancer than for others. Its used by itself for some of these cancers, but for others it seems to work better when used with other types of treatment.

Related: Immunology Conferences|Immunologists Meetings|Conference Series LLC

10th Euro Global Summit andExpo on Vaccines & VaccinationJune 16-18, 2016 Rome, Italy; 11th Global Summit andExpo on Vaccines, Vaccination and TherapeuticsSeptember 12-14, 2016 Phoenix, Arizona, USA; 12th Asia Pacific Global Summit andExpo on Vaccines & VaccinationNovember 24-26, 2016 Melbourne, Australia;International Congress of Immunology;7th InternationalConference on Allergy, Asthma and Clinical Immunology, September 14-15, 2016 Amsterdam, Netherlands; International Conference on Autoimmunity, October 13-14, 2016 Manchester, UK;World Vaccine CongressApril 10-12, 2017 Washington; 10thVaccine Congress4-7 September 2016, Amsterdam, The Netherlands 10thVaccine Congress, 4-7 September 2016, Amsterdam British society for Immunology Annual Immunology Congress, 6-9 Dec, 2016, Liverpool, UK; 5th European Immunology Conferences, July 21-23, 2016 Berlin, Germany;USA Immunology Conferences

Track 14:Immunologic Techniques, Microbial Control and Therapeutics

Immunological techniques include both experimental methods to study the immune system and methods to generate or use immunological reagents as experimental tools. The most common immunological methods relate to the production and use of antibodies to detect specific proteins in biological samples. Various laboratory techniques exist that rely on the use of antibodies to visualize components of microorganisms or other cell types and to distinguish one cell or organism type from another. Immunologic techniques are used for: Quantitating and detectingantibodiesand/orantigens, Purifying immunoglobulins, lymphokines and other molecules of the immune system, Isolating antigens and other substances important in immunological processes, Labelling antigens and antibodies, Localizing antigens and/or antibodies in tissues and cells, Detecting, and fractionatingimmunocompetent cells, Assaying forcellular immunity, Documenting cell-cell interactions, Initiating immunity and unresponsiveness, Transplantingtissues, Studying items closely related to immunity such as complement,reticuloendothelial systemand others, Molecular techniques for studying immune cells and theirreceptors, Imaging of the immune system, Methods for production or their fragments ineukaryoticandprokaryotic cells.

Microbial control:

Control of microbial growth, as used here, means to inhibit or prevent growth of microorganisms. This control is achieved in two basic ways: (1) by killing microorganisms or (2) by inhibiting the growth of microorganisms. Control of growth usually involves the use of physical or chemical agents which either kill or prevent the growth of microorganisms. Agents which kill cells are called cidal agents; agents which inhibit the growth of cells (without killing them) are referred to as static agents. Thus, the term bactericidal refers to killing bacteria, and bacteriostatic refers to inhibiting the growth of bacterial cells. A bactericide kills bacteria, a fungicide kills fungi, and so on. In microbiology, sterilization refers to the complete destruction or elimination of all viable organisms in or on a substance being sterilized. There are no degrees of sterilization: an object or substance is either sterile or not. Sterilization procedures involve the use of heat, radiation or chemicals, or physical removal of cells.

Related: Immunology Conferences|Immunologists Meetings|Conference Series LLC

2nd international conference on innate immunity, July 21-22, 2016, Germany; 2nd International Conference and Exhibition on Antibodies and Therapeutics, July 11-12, 2016 Philadelphia, Pennsylvania, USA;7th InternationalConference on Allergy, Asthma and Clinical Immunology, September 14-15, 2016 Amsterdam, Netherlands, September 14-15, 2016 Amsterdam, Netherlands;International Conference on Autoimmunity, October 13-14, 2016 Manchester, UK; Immunology 2016, American Association of Immunologists, Annual MeetingMay 13-17, Los Angeles, USA;9th EuropeanMucosal Immunology meetings, October 9 - 12 October, Scotland;

Track 15:Immunodeficiency

Immunodeficiency is a state in which theimmune system's ability to fightinfectious diseaseis compromised or entirely absent. Immunodeficiency disorders prevent your body from adequately fighting infections and diseases. An immunodeficiency disorder also makes it easier for you to catch viruses and bacterial infections in the first place. Immunodeficiency disorders are often categorized as either congenital or acquired. A congenital, or primary, disorder is one you were born with. Acquired, or secondary, disorders are disorders you get later in life. Acquired disorders are more common thancongenital disorders. Immune system includes the following organs: spleen, tonsils, bone marrow, lymph nodes. These organs make and release lymphocytes. Lymphocytes are white blood cells classified as B cells and T cells. B and T cells fight invaders called antigens. B cells release antibodies specific to the disease your body detects. T cells kill off cells that are under attack by disease. An immunodeficiency disorder disrupts your bodys ability to defend itself against these antigens. Types of immunodeficiency disorder are Primary immunodeficiency disorders & Secondary immunodeficiency disorders.

Primary immunodeficiency disorders are immune disorders you are born with. Primary disorders include:

X-linked agammaglobulinemia (XLA)

Common variable immunodeficiency (CVID)

Severe combined immunodeficiency(SCID)

Secondary disorders happen when an outside source, such as a toxic chemical or infection, attacks your body. Severe burns and radiation also can cause secondary disorders.

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Worlds Leading Immunology Congress | Conferenceseries

What are stem cells?

Stem cells are powerful healing cells in the body that can become other types of cells. There are many adult stem cells in fat tissue, however they lie dormant. Stem cell therapy allows us to isolate stem cells from an animals own fat tissue, activate them, and re-inject them directly into damaged areas. For example, in the case of arthritis, stem cells become new cartilage cells, reducing pain and increasing mobility.

Stem cells treat the source of the problem by becoming new tissue to replace damaged tissue. Other treatments, such as drugs, though very useful, merely attempt to reduce symptoms. The treatment is very low risk, because it uses the animals own stem cells. With our technology, over 95% of animals treated show improvement.

Stem cell therapy for animals has been commercially available since 2004, and thousands of animals have been treated around the world. The technology has only recently come to the UK.

This procedure is very safe. The biggest risk is using a general anesthetic, to remove the fat tissue from which we isolate the stem cells. We always carry out a full pre anesthetic blood test and use the safest available anesthetics. Typically, the fat is collected in about 30 minutes. Processing the sample in our lab takes 4 hours, during which the stem cells are isolated, concentrated and activated. In the thousands of animals treated across the world, Vets have not noted side-effects from this stem cell therapy.

An initial consultation is carried out where we discuss all your concerns and carry out a full clinical examination. We will assess the current treatment protocol you have in place and make adjustments or recommendations so that we are happy that you have the benefit of all the most up to date therapies. This assessment will look at the suitability of any or all of the following conventional treatments:

In many cases, the patients we see are being treated with some or all of these but are still struggling with their condition.

In these cases we look at stem cell therapy as an additional benefit.

The procedure is carried out in one day as an outpatient, and patients do not need an overnight stay with us.

We need some blood tests and a urine test for anesthetic safety. Once we are happy with these, we administer a short general anesthetic. Typically this lasts 30 to 90 minutes.

We need to have x-rays of the affected joints and also a chest x-ray. Where recent x-rays are available from your own Vet, we will not need to repeat these.

We then harvest approximately 40 grams of fat from a site behind the shoulder or just inside the tummy and your pet is woken from the anesthetic. There will be a few stitches that need to come out in 10 days.

A small blood sample is taken and prepared into a platelet rich plasma solution.The fat is processed to isolate, concentrate and activate stem cells in our lab, and this takes around 4 hours. The stem cells are mixed with the platelet rich plasma in preparation for injection.Once we have the stem cells, we administer a light sedative to allow us to inject the cells directly into the affected joints. A portion of the cells are given intravenously.

We recommend that the patient be kept quiet for the first 10 days.

We typically see improvement starting after 3 weeks, and then continuing up to around 2 months.

We typically see 1-3 years of relief after the initial treatment. We will bank additional stem cells, so repeat treatment is easy. We have a UK cell banking facility in Hampshire. If symptoms return, we request a dose of cells from the bank, and inject them. No repeat surgery is necessary.

Yes. Because we dont know exactly what happens when cancer patients are treated with stem cells based on human studies, we do not treat those patients, and it is for this reason that we take a chest x-ray on the day of the procedure.

The cost of stem cell therapy for arthritis at our clinic is 2500 plus VAT. This fee includes the initial consultation, blood tests, urine test, x-rays and the stem cell treatment, as well as a follow up consultation. There is an additional fee for banking stem cells of 300 per year which can be paid directly to the storage laboratory.

Some insurance companies will now cover the cost of the treatment, but not the cost of cell banking. You will need to check with your insurance company to see what costs they may cover.

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What Is Stem Cell Therapy - Stem Cell Vet UK

It is always a pleasure to feature the perspective of other pet writers on Patricks Blog. This guest blog from Dawg Business Jana Rade is especially current as she shares her personal perspective on stem cell therapy. As a pet parent to Jasmine, Jana has seen the ups and downs of this cutting edge treatment.

Thank you Lorie Huston, my fellow vet, for initially hosting this post on her excellent Pet Health Care Gazette site.

Jasmine, the stem cell child

Jasmine was five years old when she started limping on her hind leg in the summer of 2008. We didnt think much of it at first, because it has happened before and resolved eventually without a diagnosis or treatment from any of her vets.

Something about it was different though. Unlike in the past, Jasmine started to be reluctant to exercise and play. That wasnt like her, quite the opposite. We always had a hard time keeping her subdued while we wanted her injury to heal.

Even though we didnt expect much from the vet visit this time either, I felt that we should at least give it a try. This time, however, the vet said he was suspecting a torn ACL and suggested an exam by an orthopedic specialist.

When I looked up what a torn ACL was, I wasnt happy at all! Surgery? On my little girl? Six months recovery?

While we were waiting for our appointment with the specialist and hoping that maybe it could be something else, I started researching possible treatment options.

The most common and recommended treatment, a TPLO surgery, we didnt like the least bit. I liked the TTA a bit better, but turned out that it was not available up here at that time. The extracapsular repair looked the least invasive, but all the articles and resources I found were frowning on using it in large breed dog.

We considered a brace, but felt that Jasmine was too young and too active for that.

Meanwhile, the verdict from the orthopedic specialist was in and it was even gloomier that we thought it could be. Not only her left ACL was torn, but her right one was in a bad shape too. Recommendation? TPLO surgery for the left knee right away and another one for her right knee as soon as possible.

Two highly invasive surgeries back-to-back and taking away a year of her life? There has to be another option!?

I put my work and my life on hold and devoted all my time to researching. The more I researched, the more our hopes shrunk.

Searching high and low, one vet from Australia suggested that for a partial tear would could try prolotherapy. I researched it, sounded kind of promising. Finding a vet doing this treatment in Ontario was another story. Eventually I found one. I discussed Jasmines case with her and she said that it could work, pending her evaluation.

Not to do anything behind his back, I brought this up to Jasmines vet. He quickly looked it up and told us it was a horrible idea with high risk of bone infection that could result in amputation. Wow, not every day youre told that youre trying to maim your dog!

Both the Australian vet and the holistic vet I found in Ontario insisted that the risk is minimal when its done properly, but I was already freaked out too much.

(Interestingly, Jasmines new vet does this procedure sometimes for select cases)

When I was sharing my desperation with the holistic vet, she said there might be another way. And that was the first time I heard the words stem cells. She said it was a new treatment that was really a shortcut to what prolotherapy is designed to achieve.

Back on the computer I started researching this. When I learned what stem cells are and what they do, I got quite excited. Sounded right. Made sense.

Other than theoretical information there wasnt much to be found back then. But I found a story of Allie, the Boxer and her stem cell treatment. That was pretty much the only real-life story available at that time. But we were sold on the idea.

I called Jasmines vet again and told him about my find. He talked about rejection. These would be her own stem cells, I said. From bone marrow? he asked? No, from her fat tissue, I replied. Sounds like a scam. he concluded. This time he didnt even bother looking anything up!

Dont you just love being treated like an idiot? I wasnt something I accidentally stumbled upon on the internet, I spend days researching and talked to many people, including vets.

Well, at least he wasnt talking about amputation this time

Regardless of the lack of support on his part, we still really liked the idea and wanted to find out whether or not it could be an option for Jasmine.

I went on Vet-Stems website where they had a directory of vets certified to do the procedure. There were some in Ontario and some even within driving distance.

I took the list and started calling. One of the vets seemed interested in the discussion and in Jasmines case. He spent a great deal of time talking to me on the phone. While he felt that surgery is probably the best solution for her, he was willing to discuss the stem cell option. He said that he wanted to try this treatment on their resident dog who had bad arthritis.

While I was really taken by him, what I really wanted was somebody who had experience with this treatment. I told him that and he was cool with it. However, when I called all the other certified vets, nobody has actually done it yet.

We were even willing to drive down to the states, but nobody within reasonable distance has done it either.

Ok, this was clearly something new, huh?

Yet, we still liked this idea better than the invasive surgery.

Since finding a vet who already had some experience with the treatment turned out impossible, we decided to go with the one who took all that time to talk with me on the phone. He sounded that he cared about animals, and he sounded like a no-nonsense but open to different things guy.

We booked a consultation with him.

He asked to see the x-rays from the orthopedic specialist. He wasnt happy that we had only x-rays of her knees. He wanted to see her shoulders and hips also. So we agreed that hed take his own set.

When we came in, he examined Jasmine head-to-toe, took his own x-rays and found arthritis not only in her knees, but shoulders, jaws and neck also.

I will skip here the whole ordeal about him finding an abdominal mass and the cancer scare, I wrote about that earlier.

The part of that which is relevant to this story is that a resulting exploratory surgery resulted in delay in dealing with her knees.

And to make things more interesting, by the time we were able to schedule Jasmines treatment, her left ACL suddenly tore completely.

That was another blow. Do we have to go with the TPLO after all? The new vet also mentioned the option of extracapsular repair. I told him about what I found on this surgery for large breed dogs, but he said hes done it many times in large dogs successfully. It was certainly less invasive.

He already had a great deal of our trust by then. It would be less invasive. And the worst that could happen would be that we end up where we started. We decided that was what we were going to do.

What about the stem cells though? The treatment clearly wasnt going to help her left knee. But maybe it could save her right one, fix her arthritis and help with recovery from the surgery.

Normally, when using stem cells for ACL tear, a thorough evaluation of the damage by MRI or arthroscopy. In Jasmines case though, already using the treatment in combination with the surgery and for her arthritis, we eventually decided just do it and hope for the best.

On the day of the knee surgery her vet also took a bit of fat tissue from Jasmines shoulder and sent it off the VetStem to be processed. Two days later he injected the stem cells into both knees, her shoulders and gave her one IV dose for the areas that couldnt be injected, such as her neck.

There was nothing left do to than work on her post-op rehab and hope for the best. The first month after the treatment, Jasmines vet looked disappointed, as he couldnt see any difference in her recovery compare to dogs who got the knee surgery only.

Two months later though, Jasmine was getting a bounce back in her step and her vet started to look excited. She was doing remarkably well! We had nothing to compare it with, but it was clear that she was feeling well.

As we got accustomed to in the past two years, just when we were all happy and everything looked good, something was bound to go wrong.

Three months after her surgery her right knee just went. She didnt do anything crazy, just boom. That was really disappointing, but not really surprising. When using stem cell treatment for an ACL injury, the knee should be protected and ideally stabilized using a brace. Not only we couldnt do all that, but the leg had to carry double the load.

But at the end we were happy that her right leg got her through the post-op on the left one, which was now strong enough to take over.

So there we were, back on the operating table. Given what the stem cells did the first time around, this time it was no question for us whether we should combine the second surgery with the treatment also.

Her recovery the second time around was just as remarkable.

Today, over two years after the surgery and the treatments, her knees and shoulders are looking great. Before, her shoulders were very wide, as they were compensating for the bad rear. Now her body has the right proportion. There a little bit of loose skin on both shoulders as a reminder of how broad they used to be.

Jasmine is seven and a half years old now, but she has her life back! Even her jaws are feeling better, as she is showing interest in chewing on bones again, which she hasnt done before.

We thank Vet-Stem not only for the awesome treatment, but also for finding our amazing vet.

Of course Jasmines odyssey doesnt end there, and neither does her stem cell treatment experience. But more on that next time.

Jana

Jana Rade is a graphic designer by profession and never aspired to learning about dog health issues until she met Jasmine. Unfortunately, she received a crash course in the subject due to Jasmines many health issues and has since become an advocate for other pet owners and their four-legged friends. In her blog, Dawg Business, Jana shares her experiences and the lessons she has learned with others. She shares this message with all dog owners: At the end, your dogs health is up to you!

Tagged as: ACL, Australia, Boxer, Canada, canine, Dawg Business, Jana Rade, Jasmine, Ontario, pet, pet owner, pet writer, Rottweiler, stem cell, surgery, TPLO, Vet Stem, VetStem

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Pet Owner Perspective On Stem Cell Therapy Dr. Patrick ...

JoVE Immunology and Infection

Dimitrios N. Vatakis1,2,3, Gregory C. Bristol1,2, Sohn G. Kim1,2, Bernard Levin1,2, Wei Liu4, Caius G. Radu4, Scott G. Kitchen1,2,3, Jerome A. Zack1,2,5

1Department of Medicine, Division of Hematology-Oncology, David Geffen School of Medicine at UCLA, 2UCLA AIDS Institute, 3Eli & Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA, 4Department of Medical and Molecular Pharmacology, David Geffen School of Medicine at UCLA, 5Department of Microbiology, Immunology and Molecular Genetics, David Geffen School of Medicine at UCLA

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The generation and characterization of tumor specific T cells using humanized mice is described here. Human thymic tissue and genetically modified human hematopoietic stem cells are transplanted into immunocompromised mice. This results in the reconstitution of an engineered human immune system allowing for in vivo examination of anti-tumor immune responses.

Date Published: 12/18/2012, Issue 70; doi: 10.3791/4181

Keywords: Cancer Biology, Issue 70, Stem Cell Biology, Immunology, Biomedical Engineering, Medicine, Bioengineering, Genetics, Oncology, Humanized mice, stem cell transplantation, stem cells, in vivo animal imaging, T cells, cancer, animal model

Vatakis, D. N., Bristol, G. C., Kim, S. G., Levin, B., Liu, W., Radu, C. G., et al. Using the BLT Humanized Mouse as a Stem Cell based Gene Therapy Tumor Model. J. Vis. Exp. (70), e4181, doi:10.3791/4181 (2012).

Small animal models such as mice have been extensively used to study human disease and to develop new therapeutic interventions. Despite the wealth of information gained from these studies, the unique characteristics of mouse immunity as well as the species specificity of viral diseases such as human immunodeficiency virus (HIV) infection led to the development of humanized mouse models. The earlier models involved the use of C. B 17 scid/scid mice and the transplantation of human fetal thymus and fetal liver termed thy/liv (SCID-hu) 1, 2 or the adoptive transfer of human peripheral blood leukocytes (SCID-huPBL) 3. Both models were mainly utilized for the study of HIV infection.

One of the main limitations of both of these models was the lack of stable reconstitution of human immune cells in the periphery to make them a more physiologically relevant model to study HIV disease. To this end, the BLT humanized mouse model was developed. BLT stands for bone marrow/liver/thymus. In this model, 6 to 8 week old NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ (NSG) immunocompromised mice receive the thy/liv implant as in the SCID-hu mouse model only to be followed by a second human hematopoietic stem cell transplant 4. The advantage of this system is the full reconstitution of the human immune system in the periphery. This model has been used to study HIV infection and latency 5-8.

We have generated a modified version of this model in which we use genetically modified human hematopoietic stem cells (hHSC) to construct the thy/liv implant followed by injection of transduced autologous hHSC 7, 9. This approach results in the generation of genetically modified lineages. More importantly, we adapted this system to examine the potential of generating functional cytotoxic T cells (CTL) expressing a melanoma specific T cell receptor. Using this model we were able to assess the functionality of our transgenic CTL utilizing live positron emission tomography (PET) imaging to determine tumor regression (9).

The goal of this protocol is to describe the process of generating these transgenic mice and assessing in vivo efficacy using live PET imaging. As a note, since we use human tissues and lentiviral vectors, our facilities conform to CDC NIH guidelines for Biosafety Level 2 (BSL2) with special precautions (BSL2+). In addition, the NSG mice are severely immunocompromised thus, their housing and maintenance must conform to the highest health standards (http://jaxmice.jax.org/research/immunology/005557-housing.html).

A. Generation of BLT mice

The generation of BLT mice is divided into three (3) parts: (1) processing of fetal tissue and preparation of CD34 human hematopoietic stem cells, (2) transplantation of human tissue, and (3) secondary transplant. For all the protocols, we have provided Table 1 with reagent information.

1. Tissue Processing and Isolation of CD34 Human Hematopoietic Stem Cells

Fresh fetal tissue or tissue shipped overnight on ice from various organ procurement agencies can be used. Often fetal tissue is not sterile, as evidenced by the production of 1,000 bacterial colonies on blood agar per milliliter of surrounding medium. We routinely wash the tissue twice in 40 ml of sterile PBS. While this does not remove all bacteria, it can make a difference between a successful transplant series and an outcome in which most of the recipient mice succumb to bacterial infection. As an added step, to further disinfect the tissue, we culture the cell suspension in the presence of antibiotics.

1.1 Processing of Fetal Thymic Tissue

1.2 Processing of Fetal Liver Tissue

1.3 Sorting and Transduction of CD34 Hematopoietic Stem Cells

2. Tissue Transplantation

The goal of this step is to transplant a human fetal thymus/liver organoid under the NSG mouse kidney capsule. This organoid better mimics the process of human T cell selection and maturation processes as the human hematopoietic stem cells will use the human thymus and not the mouse as the site for their differentiation to different T cell and other lymphoid lineages. The use of CD34- cells in the transplantation process is to re-generate the fetal liver stroma and allowing for better transplantation and growth of the implant. The age of NSG mice used is 6-8 weeks old.

3. Secondary Transplantation

The goal of this step in the generation of BLT mice is to populate the moue bone marrow with human hematopoietic stem cells. The transplanted implant from procedure (2) is not sufficient to support full reconstitution of the human immune system in these mice. During the secondary transplant, we sub-lethally irradiate the mice to deplete murine bone marrow cells thus generating "space" for the implantation of the human CD34+ cells.

B. In vivo Positron Emission Tomography (PET)

For our studies we examine glucose uptake ([18F]-fluorodeoxyglucose ([18F]FDG) thus mice are fasted 4-6 hr prior to imaging. MicroPET/CT scans are done using the microPET Inveon scanner (Siemens Preclinical Solutions) and MicroCATII CT scanner (Siemens PreclinicalSolutions). Image analysis is done using OsiriX (Pixmeo, Switzerland) software. The goal is to measure the metabolic activity of the tumor and ultimately to use PET imaging as an alternative to physically measuring tumor regression. As seen in Figure 2, we have encountered tumors that based on physical appearance and size are not targeted but live PET imaging revealed extensive tissue necrosis. This methodology can serve as a more sensitive and accurate indicator of tumor regression.

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A flow chart of the transplantation process is shown in Figure 1A. A picture of the thy/liv implant is shown in Figure 1B. The thymic tissue develops normally and has a physiological distribution of human CD4 and CD8 T cells. Following reconstitution, the animals carry a human immune system with normal distribution of CD4, CD8 T cells and other immune cell lineages.

The discrepancy between tumor size and live tissue is shown in Figure 2. While the CT scan (grey area) indicated a large tumor growth, in vivo PET imaging showed that it was mostly necrotic and scar tissue (Figure 2). This underscores the utility of PET imaging as a more sensitive and accurate way to assess tumor regression and clearance.

Figure 1. (A) A schematic diagram on the modified BLT model used in these studies for the generation of chimeric mice carrying MART-1 specific T cells. The Thy/Liv implant was reconstructed from transduced and non-transduced CD34 cells isolated from an autologous fetal liver. A fraction of the transduced cells is frozen and injected into the irradiated mice 4-6 weeks later. (B) A representative image of the thy/liv implant in humanized mice. The implants have a physiological tissue distribution and CD4/CD8 ratios as shown by the IHC and flow cytometry figures. Click here to view larger figure.

Figure 2. A PET and CT image of a mouse carrying a melanoma tumor. The grey area indicates the physical size of the tumor while the red color indicates the tumor's metabolic activity, which is very limited.

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The modified BLT humanized mouse model coupled with in vivo PET imaging are powerful tools to study chronic human diseases. This system takes the BLT mouse model and advances it beyond the limited scope for HIV research. In addition, it is a great system in which we can examine various gene therapy protocols as well as diagnostic techniques before they can reach the clinical setting. The latter coupled with the low cost of using mice versus primates makes this a very useful model.

The PET imaging technology allowed us to assess the efficacy of our approach. If we relied exclusively on physical measurements of the tumor, we would have underestimated the potency of the antitumor response generated by our transgenic T cells. The extensive scarring and necrotic tissue gave the appearance of a large tumor, which in reality was dead tissue.

In conclusion, the utility of the modified BLT mouse model can be extended to other disease models. While some disadvantages still persist such as the shorter lifespan of mice, this can be a very strong tool to in vivo assess many aspects of human immunity, test and develop novel therapeutic interventions.

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No conflicts of interest declared.

We would like to thank Alvin Welch and Larry Pang for their technical assistance. This work was funded in part by the National Institutes of Health (NIH) award P50 CA086306, the California Institute for Regenerative Medicine (CIRM) grants RC1-00149-1 and RS1-00203-1; CIRM New Faculty Award RN2-00902-1, the Caltech-UCLA Joint Center for Translational Medicine, UCLA Center for AIDS Research (CFAR) NIH/NIAID AI028697, the UCLA AIDS Institute, the CIRM Tools and Technology Award RT1-01126, and the UC Multicampus Research Program and Initiatives from the California Center for Antiviral Drug Discovery (number MRPI-143226).

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Using the BLT Humanized Mouse as a Stem Cell based Gene ...