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Gracell Biotechnologies to Present Clinical Data on BCMA/CD19 Dual-targeting CAR-T GC012F in RRMM and B-NHL and CD19/CD7 Dual-directed Allogeneic…

SAN DIEGO, Calif., SUZHOU and SHANGHAI, China , May 12, 2022 /PRNewswire/ -- Gracell Biotechnologies Inc. ("Gracell" or the "Company",NASDAQ: GRCL), a global clinical-stage biopharmaceutical company dedicated to developing highly efficacious and affordable cell therapies for the treatment of cancer, today announced the details of three abstracts that it will present at the European Hematology Association 2022 Hybrid Congress (EHA2022 Congress), being held from June 9 June 12 in Vienna, Austria. The abstracts highlight the clinical data from ongoing investigator-initiated trials (IITs) of BCMA/CD19 dual-targeting FasTCAR candidate GC012F in two indications of B-cell non-hodgkin's lymphoma (B-NHL) and relapsed/refractory multiple myeloma (RRMM), and allogeneic TruUCAR candidate GC502 in B-cell acute lymphoblastic leukemia (B-ALL).

"We are very excited to share our data for both our FasTCAR candidate GC012F in two indications of RRMM and B-NHL, and allogeneic TruUCAR candidate GC502 in B-ALL at the EHA2022 Congress," said Dr. Martina Sersch, Chief Medical Officer of Gracell. "The new data, including the expanded indication of GC012F into B-NHL, demonstrates the potential of our platforms and provides further validation. The clinical data of BCMA/CD19 dual-targeting GC012F in the treatment of B-NHL shows promising early results, along with benefits of the next-day manufacturing enabled by the FasTCAR platform. The CD19/CD7 dual-directed CAR-T therapy GC502 is our second allogeneic candidate on our TruUCAR platform, demonstrating the potential wide applicability of the TruUCAR design."

BCMA/CD19 Dual-Targeting FasTCAR-T GC012F for the Treatment of B-NHL

GC012F is an autologous CAR-T therapeutic candidate dual-targeting B cell maturation antigen (BCMA) and CD19. It is developed using Gracell's proprietary FasTCAR platform which enables next-day manufacturing, and is currently being evaluated in IITs in China including in RRMM and B-NHL. GC012F is the first BCMA/CD19 dual-targeting CAR-T in human trials for B-NHL.

Gracell will present the early results of the first-in-human phase 1 IIT in China evaluating the safety and tolerability of GC012F in B-NHL patients. Three patients who had received a median of two prior lines of therapy were enrolled, all of which presented with bulky disease. As of the February 22, 2022 data cutoff date, the enrolled patients had received one single infusion of GC012F at three different doses of 3.7x104 cells/kg and 2-3x105 cells/kg.

All three patients had achieved a complete response (CR) confirmed by PET- CT at day 28 after GC012F infusion. At 3-month follow-up, both of the two assessable patients had ongoing response. No dose-limiting toxicities were observed and no immune effector cell-associated neurotoxicity syndrome (ICANS) were observed. CRS presented as Grade 1 in two patients and Grade 3 in one patient (duration of two days) with no Grade 4 or 5 events.

Details of the presentation are as follows:

BCMA/CD19 Dual-Targeting FasTCAR-T GC012F for the Treatment of RRMM

Gracell will also present as an oral abstract presentation the updated results from the first-in-human IIT evaluating GC012F for the treatment of RRMM patients. This data is currently under embargo and will be published on the EHA2022 Hybrid Congress website on Thursday, May 26 concurrently with ASCO.

Details of the presentation are as follows:

CD19/CD7 Dual-directed Allogeneic TruUCAR-T GC502 for the Treatment of B-ALL

GC502 leverages the novel dual-directed CAR design of Gracell's proprietary TruUCAR platform, designed to generate high-quality allogeneic CAR-T cell therapies that can be administered "off-the-shelf" at lower cost and with faster patient's access. TruUCAR-enabled GC502 utilizes the dual-directed CAR design with one CAR targeting CD19 on malignant cells and a second CAR targeting CD7 to suppress host-versus-graft rejection. An enhancer molecule is embedded in the basic construct of TruUCAR to enhance proliferation of TruUCAR T cells.

Between September 2021 and January 2022, four r/r B-ALL patients were enrolled and treated in an open-label, non-randomized, prospective IIT in China in two different dose levels and with two different formulations. Patients were heavily pretreated, and all had previously received either autologous or donor derived CD19 or CD19/CD22 targeted CAR-T therapy. As of the January 28, 2022 data cutoff date, all four patients had received a single dose of GC502, including one patient at dose level 1 (DL1) 1.0x107 cells/kg and three patients at dose level 2 (DL2) 1.5x107 cells/kg. Patients received a Flu/Cy based lymphodepletion regimen prior to treatment with GC502.

Three of four patients achieved minimal residual disease negative complete response or complete response with incomplete count recovery (MRD- CR/CRi), and one patient achieved a partial response at month one and subsequently received allogeneic hematopoietic stem-cell transplantation (allo-HSCT) on day 39.

Cytokine release syndrome (CRS) presented as Grade 2 and Grade 3 with no Grade 4 or 5 events. No immune effector cell-associated neurotoxicity syndrome (ICANS) or acute graft-versus-host disease (aGvHD) were observed.

Details of the presentation are as follows:

For more information about the EHA2022 Hybrid Congress, visit http://www.ehaweb.org.

About GC012F

GC012F is a FasTCAR-enabled dual-targeting CAR-T product candidate that is currently being evaluated in IIT studies in China for the treatment of multiple myeloma and B-cell non-Hodgkin's lymphoma. GC012F simultaneously targets CD19 and BCMA to drive fast, deep and durable responses, which can potentially improve efficacy and reduce relapse in multiple myeloma and B-NHL patients.

About B-NHL

Non-Hodgkin's lymphoma (NHL) is a group of blood cancers that developed from lymphocytes, most commonly derived from B cells (B-NHL). Globally, approximately 510,000 patients are diagnosed with NHL every year with about 80,470 patients expected to be diagnosed with NHL in the United States in 2022[1]. B-NHL accounts for approximately 85% of NHL diagnoses.

[1] Data source: American Cancer Society

About GC502

GC502 is a TruUCAR-enabled CD19/CD7 dual-directed, off-the-shelf allogeneic CAR-T product candidate that is being studied in an ongoing Phase 1 IIT in China for the treatment of B-cell malignancies. GC502 is manufactured using T cells from non-human leukocyte antigen (HLA) matched healthy donors. An enhancer molecule is embedded in the basic construct of TruUCAR to enhance proliferation of TruUCAR T cells. Optimized for CD19/CD7 dual-CAR functionality and in vivo durability, GC502 has demonstrated robust anti-tumor effects with potential to suppress host versus graft (HvG) rejection in preclinical models.

About B-ALL

Acute lymphoblastic leukemia (ALL) is a type of blood cancer characterized by proliferation of immature lymphocytes in the bone marrow, which can involve either T lymphocytes (T-ALL), or B lymphocytes (B-ALL). Globally, approximately 64,000 patients are diagnosed with ALL every year with an estimated 6,660 new cases to be diagnosed in the United States in 2022[2]. B-ALL accounts for 75% of ALL diagnoses in adults.

[2] Data source: American Cancer Society

About FasTCAR

CAR-T cells manufactured on Gracell's proprietary FasTCAR platform appear younger, less exhausted and show enhanced proliferation, persistence, bone marrow migration and tumor cell clearance activities as demonstrated in preclinical studies. With next day manufacturing, FasTCAR is able to significantly improve cell production efficiency which may result in meaningful cost savings, and, together with fast turnaround time, enables enhanced accessibility of cell therapies for cancer patients.

About TruUCAR

TruUCAR is Gracell's proprietary technology platform and is designed to generate CAR-T cell therapies from high quality allogeneic T cells that can be administered "off-the-shelf" at lower cost and with improved accessibility of cell therapies for cancer patients. With differentiated design enabled by gene editing, TruUCAR is designed to control HvG as well as GvHD without the need for being co-administered with additional strong immunosuppressant after conventional lymphodepletion. The novel dual-CAR design allows tumor antigen-CAR moiety to target malignant cells, while the CD7 CAR moiety is designed to suppress rejection (HvG response) of allogeneic CAR-T cells by host T and NK cells (HvG).

About Gracell

Gracell Biotechnologies Inc.("Gracell") is a global clinical-stage biopharmaceutical company dedicated to discovering and developing breakthrough cell therapies. Leveraging its pioneering FasTCAR and TruUCAR technology platforms and SMART CARTMtechnology module, Gracell is developing a rich clinical-stage pipeline of multiple autologous and allogeneic product candidates with the potential to overcome major industry challenges that persist with conventional CAR-T therapies, including lengthy manufacturing time, suboptimal cell quality, high therapy cost, and lack of effective CAR-T therapies for solid tumors. For more information on Gracell, please visit http://www.gracellbio.com.Follow @GracellBio on LinkedIn.

Cautionary Noted Regarding Forward-Looking Statements

Statements in this press release about future expectations, plans and prospects, as well as any other statements regarding matters that are not historical facts, may constitute "forward-looking statements" within the meaning of The Private Securities Litigation Reform Act of 1995. These statements include, but are not limited to, statements relating to the expected trading commencement and closing date of the offering. The words "anticipate," "believe," "continue," "could," "estimate," "expect," "intend," "may," "plan," "potential," "predict," "project," "should," "target," "will," "would" and similar expressions are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words. Actual results may differ materially from those indicated by such forward-looking statements as a result of various important factors, including factors discussed in the section entitled "Risk Factors" in Gracell's most recent annual report on Form 20-F as well as discussions of potential risks, uncertainties, and other important factors in Gracell's subsequent filings with the Securities and Exchange Commission. Any forward-looking statements contained in this press release speak only as of the date hereof, and Gracell specifically disclaims any obligation to update any forward-looking statement, whether as a result of new information, future events or otherwise. Readers should not rely upon the information on this page as current or accurate after its publication date.

Media contacts

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Investor contacts

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SOURCE Gracell Biotechnologies Inc.

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Gracell Biotechnologies to Present Clinical Data on BCMA/CD19 Dual-targeting CAR-T GC012F in RRMM and B-NHL and CD19/CD7 Dual-directed Allogeneic...

Principles of Treatment in Germany – 100 Mile Free Press

German medicine is associated with high quality and reliability, and this explains the desire of foreign patients to undergo examination and therapy in German hospitals, especially when it comes to the complex pathologies and receiving qualified medical help. As a consequence, one of the most sought-after areas of medical tourism is treatment in Germany.

Why go to Germany for treatment?

For people whose lives depend on the quality of medical services, Germany is an excellent option. The countrys health care and medical education systems receive huge investments. High-quality medical care is available in more than 2,500 German hospitals and approximately 1,400 rehabilitation centers. More than 145,000 doctors treat patients in Germany.

All university hospitals in the country participate in international scientific research. At the same time, German legislation clearly regulates all prices and treatment protocols. The cost of treatment, even at the highest level, is within limits defined by the government policy.

The treatment of any disease in Germany begins with an examination. Modern medicine can cure many diseases, but only if they are detected timely. Therefore, check-up programs are top-rated in German hospitals. People often come to Germany to undergo examination for suspected oncology, autoimmune conditions, neurological disorders, etc.

Feel free to visit the Booking Health website to know more about treatment in Germany.

Cancer treatment in Germany

Like no other field of medicine, oncology is developing at a rapid pace. Cancer is no longer an incurable disease and imminent death. Treatment methods are becoming more and more complex and require highly qualified doctors. Only with an accurate examination and selection of the appropriate therapy cancer can be successfully treated and, in some cases, even cured. Cancer treatment and general medical care in Germany are undeniably at the highest level and have gained worldwide recognition.

Cancer treatment in Germany is carried out by interdisciplinary tumor boards. Doctors of several specialties work together to help the patient.

First of all, comprehensive examination is performed to confirm the diagnosis, including MRI/CT/PET-CT scans, scintigraphy, blood tests for tumor markers, and biopsy.

Results are ready pretty quickly, and a further treatment scheme is developed. It may consist of the following components:

One of the essential features of surgical interventions in Germany is wide usage of minimally invasive methods. Endoscopic and robot-assisted surgeries are connected with minimal trauma of healthy tissues and short hospital stay. They arent accompanied by pain or other side effects, and are well-tolerated by patients.

Going to Germany for treatment during a lockdown

Undoubtedly, medical tourism in Germany has changed due to the COVID-19 pandemic. However, its successfully adjusted to the current requirements offering foreign patients the opportunity to undergo medical treatment in Germany during a lockdown.

The medical tourism provider Booking Health will readily assist you with examinations, consultations, and treatment by leading specialists in any medical field. Booking Health will organize treatment during a lockdown, taking upon paperwork, negotiations with hospitals, issuing a medical visa, translating your documents, providing insurance from complications and cost of treatment guarantee, etc. The company cooperates with the leading university and academic hospitals in Germany.

On the Booking Health website you will find reliable information about German medicine and the treatment of various diseases. If you want to start treatment in German hospitals, go ahead and leave a request with basic medical information so that a specialist can contact you and answer your questions.

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Principles of Treatment in Germany - 100 Mile Free Press

Molecular Imaging (PET and SPECT) for Children with Hypoxic-ischemic-encephalopathy and Cerebral Palsy before and after cell therapy – Newswise

Abstract: Glucose metabolism has been the focus of research in order to understand pathological conditions associated with diseases such as neonatal hypoxic-ischemic-encephalopathy (HIE), cerebral palsy (CP) and cerebral infarction.

Objective:To evaluate the use of molecular imaging (SPECT and PET) for children with HIE and CP before and after cell therapy, and to propose future perspectives on the use of those modalities for assessment of brain function in children with these conditions.

Methods:PubMed search for studies using PET or SPECT scans for HIE and CP in children.

Results:We identified 18 PET and 17 SPECT studies that have been performed in cases under age of 19 over the past three decades (19912021). Six papers on PET use consisted of one with human umbilical cord derived mesenchymal stromal cells, one mobilized peripheral blood mononuclear cells, three autologous bone marrow mononuclear cells and one allogeneic umbilical cord blood. 4/6 papers reported that PET-CT scan revealed increased glucose metabolism and 1/6 showed no significant change in glucose metabolism after cell therapy. One article on SPECT reported that 2/5 cases had improvement of cerebral perfusion in the thalamus after treatment.

Discussion:SPECT in the first few weeks of life is useful and more sensitive than MRI in predicting major neurological disability. SPECT is not appropriate for neonates because of the risk of radiation, improvement of other clinical test equipment. PET studies reported high glucose metabolism in the early neonatal periods in children with mild to moderate HIE, but not in the most severe cases, including those neonates that died.We suggested that PET could be more useful tool to estimate effectiveness of stem cell therapy than SPECT.

Conclusion:PET might be a good clinical modalities to clarify mechanism of stem cell therapy for CP. We need further clinical studies to clarify more precisely.

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Molecular Imaging (PET and SPECT) for Children with Hypoxic-ischemic-encephalopathy and Cerebral Palsy before and after cell therapy - Newswise

Minnesota’s Eaglets Are "Putting On The Pounds" – KROC-AM

St Paul (KROC AM News) -Theyre only about a week old but the two eaglets in Minnesota's most famous bald eagle nest are keeping their parents busy with their non-stop demand for food.

The eggs were laid Feb 12 and 16 in the nest that is watched by thousands of Minnesotans and others through the Minnesota DNRs EagleCam.

(CLICKS PICTURES TO ENLARGE)

The male parent has been bringing fish and other food to the nest on a daily basis while the female feeds them and keeps them warm.

Check out the big chunk of food the eaglet is trying to swallow. The mother tried feeding it to both eaglets but it was too large and kept falling out of their beaks. She finally ate it.

The male parent just delivered a new meal, a half-devoured fish.

The eaglets will grow rapidly over the next several weeks and if they survive, will likely fledge in about three months.

Here is detailed info on eaglets from JourneyNorth.com

To prepare yourself for a potential incident, always keep your vet's phone number handy, along with an after-hours clinic you can call in an emergency. The ASPCA Animal Poison Control Center also has a hotline you can call at (888) 426-4435 for advice.

Even with all of these resources, however, the best cure for food poisoning is preventing it in the first place. To give you an idea of what human foods can be dangerous, Stacker has put together a slideshow of 30 common foods to avoid. Take a look to see if there are any that surprise you.

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Minnesota's Eaglets Are "Putting On The Pounds" - KROC-AM

Three Penn Vet Faculty Appointed to Endowed Professorships – university, Penn

Three Penn Vet Faculty Appointed to Endowed Professorships

Andrew M. Hoffman, the Gilbert S. Kahn Dean of the School of Veterinary Medicine at the University of Pennsylvania, announced professorship appointments for three faculty members. Thomas D. Parsons has been appointed the Marie A. Moore Professor of Animal Welfare and Ethics, Christopher J. Lengner has been appointed the Harriet Ellison Woodward Associate Professor of Biomedical Sciences, and Amy L. Johnson has been appointed the Marilyn M. Simpson Associate Professor of Equine Medicine. Each of the appointments will go into effect on July 1, 2022.

Thomas D. Parsons, who is currently a professor of swine medicine in the department of clinical studies at New Bolton Center; professor of otorhinolaryngology at the Perelman School of Medicine (PSOM); and director of the Swine Teaching and Research Center, is a graduate of Amherst College. He received his VMD and PhD (neuroscience) from the University of Pennsylvania. While at Penn, Dr. Parsons studied in the veterinary medical scientist training program and then was supported by the von Humboldt Society to train at the Max Planck Institute for Biomedical Research in Heidelberg, Germany. He joined Penns faculty in 1995 as assistant professor of swine medicine; he was promoted to associate professor of swine production medicine in 2005 and became a full professor in 2019. Dr. Parsons is a charter member of the American College of Animal Welfare, and serves as the faculty coordinator for Penns masters program in animal welfare and behavior, as well as head of mammalian field investigations for the Pennsylvania Diagnostic Laboratories at New Bolton Center (PADLS). His research focuses on the advancement of sustainable models of agriculture through the study of animal behavior, health, welfare, and applications of technology. Parsons is recognized globally by scholars and industry leaders for re-envisioning swine housing and feeding systems to improve welfare.

Christopher J. Lengner, who is currently an associate professor in the department of biomedical sciences at Penn Vet; associate professor in the department of cell and developmental biology at the Perelman School of Medicine (PSOM); co-director of the Center for Animal Transgenesis, and associate director of the Institute for Regenerative Medicine; is a graduate of the Worcester Polytechnic Institute. He received his PhD from the University of Massachusetts Medical School, then went on to become a Ruth Kirschstein Postdoctoral Fellow at the Whitehead Institute and at MIT in the lab of Rudolf Jaenisch. As a postdoc, he made seminal contributions to the field of epigenetic reprogramming in the generation of induced pluripotent stem cellsknowledge which is now broadly applied in disease modeling and development of cell-based therapies. Dr. Lengner joined Penns faculty in 2011 as an assistant professor. In 2017 he was named associate professor, and he was appointed a Penn Fellow in 2019. He is a member of the PSOMs NIH P30 Center for Molecular Studies in Digestive and Liver Diseases and the Tumor Biology Program of the Abramson Cancer Center. Currently, the Lengner lab employs genetic and genomic tools in organoid models to understand the molecular mechanisms that govern stem cell self-renewal, and how those mechanisms become dysregulated in disease states, particularly cancer. Dr. Lengners research has appeared in nearly 100 peer-reviewed publications including in field-leading journals such as Cell, Stem Cell, Cancer Cell, and Gastroenterology.

Amy L. Johnson, who is currently an associate professor of large animal medicine and neurology, in the department of clinical studies at New Bolton Center, is a graduate of the University of Pennsylvania. She received her DVM with distinction from Cornell University College of Veterinary Medicine. Dr. Johnson completed a residency in large animal internal medicine at Cornell, followed by a residency in neurology at Penn. She was the first American veterinarian, and the second veterinarian in the world, granted dual certification in neurology and large animal internal medicine through the American College of Veterinary Internal Medicine (ACVIM). Dr. Johnson joined Penn Vet as a lecturer at New Bolton Center in 2007; became an assistant professor in 2011; and in 2019, was promoted to associate professor and assumed the role of section chief of Internal Medicine and Ophthalmology. Dr. Johnsons primary research focus is on improving antemortem diagnosis of neurologic disease in horses; with a secondary interest in infectious diseases including equine protozoal myeloencephalitis (EPM) and Lyme neuroborreliosis.

Doctors Parsons, Lengner, and Johnson are excellent role models; the consummate blend of scientist, teacher, and mentor that our endowed professors should embody, said Dean Hoffman. All three of them reflect the values and dedication that are vital to the mission of Penn Vet and to our community. I am delighted to have them on our faculty; their collective research and academic leadership are undeniably fitting for these signature professorships.

The awarding of named endowed professorships are the highest honor bestowed upon faculty at the University of Pennsylvania. Endowed professorships reflect excellence in scholarly achievement and embody a commitment to scientific discovery, clinical excellence, mentorship, and service.

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Three Penn Vet Faculty Appointed to Endowed Professorships - university, Penn

Role of Stem-Cell Transplantation in Leukemia Treatment

Stem Cells Cloning. 2020; 13: 6777.

1Department of Biochemistry, School of Medicine, College of Medicine and Health Sciences, University of Gondar, Gondar, Ethiopia

1Department of Biochemistry, School of Medicine, College of Medicine and Health Sciences, University of Gondar, Gondar, Ethiopia

1Department of Biochemistry, School of Medicine, College of Medicine and Health Sciences, University of Gondar, Gondar, Ethiopia

2Department of Immunology and Molecular Biology, School of Biomedical and Laboratory, College of Medicine and Health Sciences, University of Gondar, Gondar, Ethiopia

1Department of Biochemistry, School of Medicine, College of Medicine and Health Sciences, University of Gondar, Gondar, Ethiopia

2Department of Immunology and Molecular Biology, School of Biomedical and Laboratory, College of Medicine and Health Sciences, University of Gondar, Gondar, Ethiopia

Correspondence: Gashaw Dessie Department of Biochemistry, School of Medicine, College of Medicine and Health Sciences, University of Gondar, Gondar, Ethiopia, Phone: Tel +251-97-515-2796, Email dessiegashaw@yahoo.com

Received 2020 May 15; Accepted 2020 Jul 25.

Stem cells (SCs) play a major role in advanced fields of regenerative medicine and other research areas. They are involved in the regeneration of damaged tissue or cells, due to their self-renewal characteristics. Tissue or cells can be damaged through a variety of diseases, including hematologic and nonhematologic malignancies. In regard to this, stem-cell transplantation is a cellular therapeutic approach to restore those impaired cells, tissue, or organs. SCs have a therapeutic potential in the application of stem-cell transplantation. Research has been focused mainly on the application of hematopoietic SCs for transplantation. Cord blood cells and human leukocyte antigenhaploidentical donors are considered optional sources of hematopoietic stemcell transplantation. On the other hand, pluripotent embryonic SCs and induced pluripotent SCs hold promise for advancement of stem-cell transplantation. In addition, nonhematopoietic mesenchymal SCs play their own significant role as a functional bone-marrow niche and in the management of graft-vs-host disease effects during the posttransplantation process. In this review, the role of different types of SCs is presented with regard to their application in SC transplantation. In addition to this, the therapeutic value of autologous and allogeneic hematopoietic stemcell transplantation is assessed with respect to different types of leukemia. Highly advanced and progressive scientific research has focused on the application of stem-cell transplantation on specific leukemia types. We evaluated and compared the therapeutic potential of SC transplantation with various forms of leukemia. This review aimed to focus on the application of SCs in the treatment of leukemia.

Keywords: stem cell, leukemia, transplantation

Stem cells (SCs) are undifferentiated cells that can be differentiated into other types of cell andalso have the potential to proliferate and self-renew to producenew SCs. In mammals, there are two broad type of SC. Embryonic SCs (ESCs) are present in the early life of the embryo and isolated from the inner cell massor morula of the blastocyst (future germ layer, such as endoderm, ectoderm, or mesoderm of the embryo).14 The surrounding section of the morula is known as the trophoblast, which can develop to the future placenta. Adult SCs (ASCs) are found in various tissue types of developed mammals.5 ASCs are useful for tissue regeneration and repair after severe injuries.1,6

SC populations may behave abnormally or be altered by genetic or environmental factor, resulting in the development of cancer. Leukemia comprises a group of hematologic disorders that usually begin in the bone marrow and resultin a high number of abnormal blood cells. It is the result of deregulation of normal hematopoietic SC (HSC) development by genetic mutation that produces a cell population known as leukemic SCs (LSCs). The generation of blood cells depends on the regulation of differentiation and proliferation characteristics of HSCs.7 Deregulated differentiation and proliferation activity of HSCs, including chromosomal translocation and somatic mutation, leads to different hematologic disorders. There are four major abnormalities identified under LSCs: such as acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL),8 chronic LL (CLL) and chronic ML (CML).4 Leukemia and lymphoma (Hodgkins lymphoma [HL] and non-HL [NHL]) are the two major types of blood cancers that result from uncontrolled proliferation of white blood cells, and were the first to be treated clinically using HSC transplantation (HSCT).1,9-11 In addition, HSCT is used as a therapeutic option for many nonhematopoietic malignancies, aplastic anemia, and certain inherited disorders like severe thalassemia, sickle-cell disease, and other inherited metabolic disorders. Historically, HSCs were obtained only from bone marrow, but are now mostly harvested from peripheral blood after mobilization through administration of hemaTtopoietic growth factor and from the umbilical cord blood (UCB) of newborns.4,9

SC-based therapies become the major concern of researchers after the first effective bone-marrow transplant in 1968.12 Globally, food and drug administrations design regulations on the application of SC therapies. An increase in scientific knowledge of cell-differentiation pathways has promoted the application of SC therapy.12 Since the application of SC therapy emerged as a new insight into cellular therapeutic potential, food and drug administrations have continuously driven awareness and designed regulation with regard to SC therapies. SCs serve as a novel cellular therapeutic approach in the field of regenerative medicine to treat various disorders.13 In addition to renewing and proliferating themselves, they are capable of differentiation to specialized functional cells.14 This enables them to substitute various injured cells, such as cardiomyocytes, fibroblasts, and endothelial cells.15 In addition, regenerative medicine has significant therapeutic potential through the application of SCT to restore impaired blood cells.16

HSCT has broad application in treating different malignant and nonmalignant hematologic disorders. Researchers have noted that >40,000 HSCTs are performed every year to treat these disorders.17 In this context, autologous SCT (auto-SCT) and allogeneic SCT (allo-SCT) are the best known and most applicable.18 There are SC types that have the capability of being the source for SCTs. Bone-marrow SCs are the major sources for treating hematologic and nonhematologic disorders.19 Similarly, peripheral blood CD34+ cell have hematopoiesis potential for HSCT.20 With respect to recent scientific advancement,HSCs are generated from pluripotent ESCs that require the transition state from endothelial to hematopoietic progenitor cells to resolve HLA-mismatched problem.21 The recent investigation done by Serap et al (2019) and his colleagues hypothesized that achievement of effective HSCT may also associate with non-hematopoietic progenitor cells, very small embryonic-like SCs (VSELSCs).22 They differentiate into HSCs in vitro.23 With specific forward reprogramming protocols, induced pluripotent SCs (iPSCs) have therapeutic potential to generate hemato-endothelial progenitor (HEP) cells.

Co-administration of chemotherapy along with auto-SCT leads to a decrease in the level of regulatory T-cells. In response to the dysregulated immune system, biological characteristics of mesenchymal SCs (MSCs) contribute to hematopoietic reconstitution and an efficient HSC engraftment.24,25 On the other hand, bone marrow derived MSCs are other components of hematopoietic niche.26 Therefore, this review assessed different types of SCs that are utilized as the source and as support of SC transplantation. In addition, we also summarized the role of allogeneic and auto-SCT in the treatment of various types of leukemia.

The involvement of ESCs is the new therapeutic insights having a regenerative potential to restore impaired tissue or cells.27 ESCs are the source of SCs for cellular transplantation therapies; however, they may also lead to uncontrolled cell proliferation which also results in the development of cancers.28 The challenges of using these cells are their characteristic features of chromosomal abnormality and mutation during in vitro.29 Regard to this, c-MYC oncogene may be expressed that results in cancer cells than their cellular therapeutic significant.29 They require a safety concern due to their teratoma formation.30 Although they have teratoma effect, ESCs have a significant role in the transplantation process.28 Human ESCs (hESCs) serve as the source of development of cellular lineages through signaling pathways.13 Recently, protocols have been on the way to be designed to generate HSCs from pluripotent ESCs in vitro. The generation of HSCs from those pluripotent ESCs requires a transition from endothelial to hematopoietic progenitor cells to resolve HLAmismatching.21 The hematopoietic transcription factor Runx1 promotes the commitment of hematopoietic cellular lineages by activating the expression of Runx1a. NOTCH signaling enhances the transition state, while the TGF-signaling pathway inhibit it.31 Recently, generation of HSCs was achieved by Wang et al from hESCs andhumaniPSCs (). The commitment stages that had been examined by those scientists confirmed the synthesis of hematopoietic cells from hESCs.32 In support of this, recently the ESC gene SLL4was identified and used as a therapeutic target for leukemia. Because of its importance in the ESC fate, SALL4 expression need to be reactivated during the reprogramming process of mouse embryonic fibroblasts to be converted into iPSCs. Under normal condition, SALL4 is expressed highly in CD34+CD38 HSCs and llittle in CD34+CD38 + hematopoietic progenitor cells. Therefore, the main application behind this ESC gene product is as key player in hematopoietic differentiation. Consequently, downregulation of this gene could be considered a therapeutic option for leukemia.33

Role of different types of SCs in SC transplantation. MSCs were the nonhematopoietic source utilized to reduce GVHD (reduce risk of graft failure by secreting soluble factors with anti-inflammatory properties), efficient HSCs support to engraftment of transplant, hematologic reconstitution, and to improve the HSCT outcome. HSCs can be generated from the hematoendothelial transition process from HESCs to HiPSCs, and commonly from bone-marrow SCs, PBSCs, and umbilical cord blood. The pluripotent potential of VSELSCs also enables to generate HSCs.

Abbreviations: GVHD, graft-vs-host disease; HESCs, human embryonic SCs; HSCs, hematopoietic SCs; HSCT, hematopoietic SC transplantation; HiPSCs, human induced pluripotent SCs; MSCs, mesenchymal SCs; PBSC, peripheral blood SC; VSELSCs, very small embryonic-like SCs.

iPSCs were introduced as an alternative SC-based therapy method in 2006, by Takahashi and Yamanaka.34 Reprogramming of SCs through the integration of viruses with these cells induces differentiation capability in various tissue types.35 These are pSCs, which are generated from adult somatic cells through in vitro experimental investigation.36 They are synthesized in vitro by reprogramming mature mouse fibroblast cells through epigenetic modification.34 In human beings, production of iPSCs was started through the introduction of four genes SOX2, MYC, OCT4, and KLF4 into matured somatic fibroblasts37 and other human somatic cells.38 The genes are induced in these cells through the encoded retrovirus.39 The ability of iPSCs to expand into multicellular lineages enables them to be a potential SC-therapy method. Various types of patient-specific SCs have been synthesized from their expansion process in vitro.40 Research has revealed their cellular therapeutic significance in various hematologic malignancies, such as CML, MDS, AML,22 and BCR-ABLmyeloproliferative neoplasms.41 Donor blood cells are reprogrammed to iPSCs to generate patient-specific SCs.40 With specific forward-reprogramming protocols, iPSCs have the therapeutic potential to generate hematoendothelial progenitor cells. Lange et al demonstrate the possible generation of hematopoietic progenitor cells by combinatorial expression of transcription factors SCL, LMO2, GATA2, and ETV242 (). Moreover, researchers have been trying to generate hematopoietic progenitor cells from PSCs. Shan et al described possible strategies for generation of HSCs from human mesenchymal cells with hematopoietic potential (). They revealed the derivation or generation of hematopoietic progenitor cells from mouse PSCs using in vitro induction methods. Therefore, iPSCs can be have possible therapeutic potential in SCT; however, they present safety concerns, due to their teratoma formation.30 Allogeneic transplantation of bone marrow or umbilical cord reveals rejection, due to the effect of graft-vs-host disease (GVHD) and disease relapse, which restricts its applicability. In cases of auto-HSCT, there is no risk of rejection, but there remain leukemic cells that induce disease relapse. Collectively, these disadvantages of bone-marrow HSCT mandate alternative sources of HSCs aiming to reduce GVHD, disease relapse, and bone marrowfailure syndrome. Considering this, iPSCs represent a suitable source to generate HSCs in vitro with limited immunogenicity.43 These have a major advantage over bone-marrow and cord types, since their autologous transplantation from iPSCs does not induce GVHD.44

Bhartiya et al characterized VSELSCs as the true SCs and the subset of different SC population, such as HSCs, ovarian SCs and MSCs. They express the OCT4A antigenic marker in their nucleus.30 The pluripotency features of VSELSCs enhance their expansion in vitro using the pyrimidoindole-derivative molecule UM171,45 and in turn are utilized for expansion of CD34+ HSCs.46 VSELSCs are involved in homeostatic processes, because they are found in quiescent stage, and later they differentiate into ASCs. They differentiate into HSCs in vitro.23 VSELSCs can be generated from primordial germ cells and undergo further differentiation into HSCs47 (). Bone marrowderived VSELSCs may not have features characteristic of hematopoietic progenitor SCs, but they can retain hematopoietic features through external-stress growth factors.48 The transcriptional factors Oct4A), Nanog, and Rex1 are found in VSELSCs, but they are not expressed in HSCs.22 Treatment of immunocompromised ALL8 patients with granulocyte colonystimulating factorincreases mobilization of VSELSCs to the peripheral circulation.49 Dissemination of VSELSCs to the circulation promotes the regeneration of tissue.49 A recent investigation done by Serap et al hypothesized that achievement of effectiveHSCT may be associated with nonhematopoietic progenitor cells VSELSCs.22 The expression of transcription factors and pluripotent markers may contribute to their therapeutic potential in SC transplantation. Demonstrations on immunocompromised mice have shown that VSELSCs have a lower teratoma effect.47 Similarly, an investigation done on animal models showed that they have the capability to differentiate into HSCs.46

Bone marrowderived MSCs are important to regenerate injured tissue.50 Recently, MSCs have served as a new cellular therapy method in the field of regenerative medicine.13 They inhibit cancer-cell proliferation through secretion and inhibition of Dkk1- and Wnt-signaling pathways, respectively.51 Besides this, MSCs alter the immune system to regenerate damaged tissue and decrease inflammation.52 GVHD is one of the complications of both auto-SCT and allo-SCT during treatment.53 This posttransplantation complication is associated with immunologic intolerance.53 Indeed, MSCs have been shown to support the engraftment of autologously or allogeneically transplanted HSCs by secreting soluble factors or immunomodulators, such as TGF1 and HGF which inhibit the proliferation of CD4+ TH1, TH17, CD8+ T, and natural-killer cells, leading to prevention of GVHD.6,24,26 Therefore, GVHD that occurs after HSCT can be treated by coinfusion with MSCs.54 Bone marrowderived MSCs are components of the hematopoietic niche. Additionally, they have the capability to regulate the hematopoiesis process through interactionand communicating with HSCs and progenitor cells55 ().

Donor availability is a very important issue, particularly in patients from ethnic minorities. A haploidentical donor and CB allow allo-HSCT in the majority of transplant-eligible patients.UCB is a well-established cellular product source for hematopoietic reconstitution and transplantation.37 It is derived from fetal tissue and acts as a potential source of progenitor SCs to synthesize matured HSCs16 (). The lower complication rate of GVHD and less stringent HLA-matching requirements make it a valuable source of HSCs.56 It is more highly enriched with HSCs/progenitor cells than peripheral blood with regard to colony-forming unitgranulocyte/macrophage progenitors and CD34+-cell content.57

The effect of HLA mismatching is less severe in mismatched UCB transplantation than unrelated peripheral and bone marrowblood transplantation;58 therefore, higher numbers of mismatched donors may donate to save lives. Compatibility at the DRB1-allele and HLA-A and -B antigen level is better for UCB transplantation to be selected traditionally without consideration of HLA-C.59 UCB has significance for allo-HSCT transplantation, because it requires lower HLA matching than for unrelated donors.59 In AML, unrelated CB transplantation has failed, due to nonrelapse mortality.60 However, the cost of CB delaying engraftment and risk of infection are still challenges in its application for hematologic diseases, including leukemia.61,62

In cases of rapid requirement of allograft and absence of an HLA-matched donor, HLA-haploidentical SC transplantation is considered a therapeutic option.63 Peripheral and bone-marrow SCs can be donated from these family members if they have one common haplotype.64 HLA-haploidentical cells are considered an optional source for HSCT.65 In haploidentical transplantation, the graft contains lower of T-cell content to diminish GVHD.66 Outcomes of haploidentical HSCT may be affected by innate immune cells like T cells and natural-killer cells.67 In high-risk acute leukemia, the applicabilion of HLA-haploidentical HSCT is elevated.65 However, outcomes of nonrelapse mortality and GVHD may be increased from haploidentical HSCT with higher HLA mismatching including from partially related donors, as the content of T-cell is replete.68

A soft, gelatinous tissue, bone marrow is used as the source of peripheral HSCs.69 Researchers have argued that both bone marrow and peripheral blood are major sources of SCs. SCASCs generated from bone marrow are known as bone-marrow SCs,37 having clinical significance in restoring damaged cardiac tissue through gene therapy.70 Also, they can be a potential source for auto-HSCT..37 There is an improvement in GVHD in patients with bone-marrow SC transplantation compared to peripheral blood SCs (PBSCs).19 Bone marrowSC transplantation is utilized in various hematologic malignancies, such as AML, ALL, and CML. The use of bone-marrow transplantation from compatible donors is the most effective treatment for CML.71 Allogenic bone-marrow transplantation is an effective alternative treatment option for patients who are resistant to chemoradiation therapy and have a higher probability of relapse.72 The physician removes marrow from the donors hip bone using surgical procedures, including anesthesia, sterile needles, and syringes, and replaces the donated bone marrow within 46 weeks. As the level of T cell compare in both bone-marrow transplantation and PBSCs, the concentration of T cells is reduced in bone-marrow transplantation.19

Recent SC-transplantation protocols state that mobilization of HSCs from bone marrow to peripheral blood is an effective treatment method in the majority of transplanted patients.73 Although bone marrow is major source of SCs, a hematopoietic growth factor found in PBSCs showed that these are also another possible source of SCs.74 PBSCs from bone marrow are a valuable source in restoring hematologic disorders.69 The potential effect of PBSCs depends on hematopoietic development and enhancement of immunologic profiles, and hence they are a valuable source of HSCs to treat hematologic disorders. Peripheral blood CD34+ cells have hematopoietic potential for SCT.20 Javarappa et alpurified hematopoietic progenitor cells from CD4+ peripheral blood cellsafter which the cells differentiated into megakaryocytes and myeloid-lineage cells75 (). PBSCs serve as a valuable SC source if mobilization is supported by granulocyte colonystimulating factor.19 They are applicable in autolo-SCT in the treatment of multiple myeloma.76 The utilization of peripheral SCs as a source of SCs may induce the occurrence of GVHD.77 Even if they have such effects, the immune system has been enhanced, due to elevation of T-cell secretion. On the contrary, the elevation of T cells may also cause GVHD development;19 however, PBSC collection in children may expose them to metabolic complications, including hypocalcemia and hypoglycemia.78

The tight control in proliferation and differentiation of HSCs has significant value for the synthesis of blood cells.7 Multipotent HSCs are responsible for cell division and proliferation.79 Somatic mutation of T cells during DNA methylation and posttransplantation alteration are risk factors for ALL.8,80 CML is a hematologic disorder induced by reverse chromosomal translocation on t(9;22)(q34;q11)81 and BCRABL oncogene effects on proliferative myelogenous cells.82 Mutated gene BCRABL, has a tyrosine-kinase effect and induces the release of highly proliferative myelogenous cells from bone marrow.81 The MYC gene is another oncogene that induces gene expression and has a proliferative effect on hematopoietic progenitor cells.83 In addition to this gene, BCL2 is another mutated gene that inhibits programmed cell death. As such, cancerous cells proceed with their continued proliferation and leukemic cells are released from the tissue where they were generated.84 Hitzler et al reported that a mutation of the GATA1 gene in acute megakaryoblastic leukemia affects hematopoietic transcriptional factor. On the other hand, chromosomal translocation of t(7;11)(p15;p15) HSCs lead to the integration of genes, including HOXA9 and NUP98, which also leads to distortion in the transcriptional process of hematopoietic precursor cells.85 Aberration of the transcriptional process in these cells induces abnormal cell proliferation, which may lead to AML.85 Overproliferation of lymphoblasts within bone marrow can also result in the pathogenesis of ALL.8,49

Emphasis on the eradication of hematologic malignancies has shifted from cytotoxic chemotherapy to donors immune cells.86 HSCT is utilized by 20,000 people in the US every year.87 It is applicable in treating patients with rare diseases, such as AML,22 ALL,8 CML, Burkitts lymphoma, HL, and NHL,11 and other hematologic malignancies.88 Although it serves as an alternative treatment method, HSCT still has a relapse risk among 40%80% of recipients.89 Both auto-HSCT and allo-HSCTare the main alternative cellular therapeutic methods to treat leukemia. Auto-HSCT is the appropriate and applicable therapeutic option for multiple myeloma1,18 and HL.11 Charles et al explained that auto-HSCT was more frequently utilized by European and North American countries than allo-HSCT to treat myeloma. A lower mortality rate for myeloma is seen with auto-HSCT. Auto-HSCT is an established treatment approach if myeloma is at an acute stage, but for older patients it requires extra improvement.90 The occurrence of GVHD among myeloma patients who undergo allo-HSCT is 50% compared to 5%20% of occurrence of auto-SCTpatients91 (). As such, fewer GVHD effects have been seen in auto-SCT n treating multiple myeloma and HL.11 Furthermore, in HIV-related lymphoma, auto-HSCT is considered an applicable therapeutic option in both relapsed HL1 and relapsed NHL patients.18,92

Comparison of allogeneic and autologous stem-cell transplantation with hematologic disorders. Autologous stem-cell transplantation has been utilized as a treatment protocol to treat MM and HL, due to its initial response, low relapse sensitivity, and positive positron-emission tomography (+PET). Patients at higher risk or progress of AML are treated with allo-HSCT. Chronic phase 1 (CP1), TKI intolerance, and blast crisis enables allo-HSCT to be a standard treatment option for the treatment of CML. Allo-HSCT is also a treatment option for NHL patients presenting with complete remission 1 and 2 (CR1 and CR2) indications and also relapse after auto-HSCT. Although they have graft-vs-leukemic toxic effects, they are a significant alternative cell-based therapy to treat hematologic malignancies.

Abbreviations: ALL, acute lymphocytic leukemia; AML, acute myeloid leukemia; CML, chronic myeloid leukaemia; HL, Hodgkins lymphoma; MM, multiple myeloma; NHL, non-HL.

On the other hand, allo-HSCT is a curative treatment approach for severe AML93 It has been confirmed that hematologic toxicity is lower in these recipient patients. Allo-HSCT has also been used as a treatment option for acute lymphoid leukemia and multiple myeloma.1,23,94 Though alternative treatments remain undefined, it is a valuable treatment tool for hematologic malignancies. Reduced-intensity conditioning after allo-HSCT has been seen in Spain.95 The toxic effect of allo-HSCT is associated with graft-vs-leukemia reactions. Chronic myelogenous leukemia patients show lower relapse rate than other allogeneically transplanted leukemia patients.96 The therapeutic landscape of CML has shifted dramatically with developments tyrosine-kinase inhibitors (TKIs), which target the BCRABL1 hybrid oncoprotein and block the constitutive activity of tyrosine kinase. The course of CML is typically triphasic, with an early indolent chronic phase (CP), followed by an accelerated phase and a blast (crisis phase (BP).97,98 For selection of appropriate TKIs, of CML patients should be tested for BCRABL1 kinasedomain mutation (mutation profile), disease phase, and patient comorbidities. For example, if the patient has such mutations as Y253H, E255K/V, or F359C, physicians recommend dasatinib or bosutinib as TKI. On the other hand, if patients are in an advanced disease phase (BP) or CML-CP (with T315I mutation), third-generation ponatinib is preferred over imatinib.99103 However, allo-HSCT remains a therapeutic option for patients in CML-CP whose CML has progressed after at least two TKIs and after trialing ponatinib therapy (for T315I mutation) to reduce the CML burden, and for the effectiveness of the transplantation.99,100,102 An improvement in immunologic tolerance and lowered GVHD effect mean allo-HSCT is the only curative treatment option for CML-BP104 (). Similarly to CML, highly complicated and severe AML is effectively treated with allo-HSCT.22 Complications of AML may lead to higher mortality and morbidity rates, which may be due to chronic GVHD among patients >50 years old.105 Pediatric ALL patients presenting with indications of higher relapse risk are treated (10% of treatment) with allo-HSCT.106

ALL patients who develop high relapse risk are indications for treatment with allo-HSCT.107 Allo-HSCT is a standard treatment method for ALL patients who are at higher risk.108 The use of allo-HSCT has lower toxicity in young patients.86 Allo-HSCT has lower relapse risk than auto-HSCT in multiple myeloma.18 Graft-vs-tumor reactions in hematologic malignancies depend on the donors T cells and donor lymphocyte infusions. The decision to perform allo-HSCT depends mainly on reduced intensity conditioning.109 Researchers haverecommended that the use of allo-HSCT should depend on strong clinical data; however, 28%49% of allo-HSCT patients develop relapse risks for disease.110 Moreover, allo-HSCT has been widely applied as a therapeutic option in both HL and NHL.11

SCs play a major role in cell-based therapy to treat both hematologic and nonhematologic malignant disorders. They are mainly involved in the application of transplantation. Adult SCs (bone-marrow SCs), PBSCs, and UCB are the major potential sources of HSCs used during SC transplantation. Similarly, apart from ethical issues associated with disruption of inner cell mass, ESCs and ELSCs are also sources of HSCs as a therapeutic option to be utilized in SC transplantation. The generation of HSCs from iPSCs through hematopoieticendothelial transition will be therapeutic options during times of inadequate availability of compatible donors. On the other hand, non-HSCs and MSCs are possible to use as coinfusion to support engraftment of transplants, hematologic reconstitution, and manage GVHD posttransplantation. Auto-HSCT and allo-HSCT are the major cellular therapeutic options to treat leukemia. The lower relapse risk, blast crisis, TKI-intolerant patients in the CP and at higher risk of disease, and higher relapse risk are indications to utilize allo-HSCT rather than auto-HSCT to treat different types of leukemia. Likewise, primary refractory sensitivity to relapse and positive PET are basic indications to prefer auto-HSCT to allo-HSCT in treating both multiple myeloma and HL. Therefore, allo-HSCT is a more applicable standard cellular therapeutic option than auto-HSCT for many classes of leukemia.

The authors acknowledge Mrs Yonas Akalu for proofreading, language editing, and grammatical corrections to improve this review article.

Allo-HSCT, allogeneic hematopoietic stemcell transplantation; auto-HSCT, autologous HSCT; CML, chronic myeloid leukemia; GVHD, graft-versus-host disease; ESCs, embryonic SCs; iPSCs, induced pluripotent SCs;MSCs, mesenchymal SCs; PBSCs, peripheral blood SCsVSELSCs, very small embryonic-like SCs.

All authors made a significant contribution to the work reported, whether in conception, study design, execution, acquisition of data, analysis, interpretation, or all those areas; took part in drafting, revising, or critically reviewing the article; gave final approval to the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

The authors declare that they have no competing interests.

48. !!! INVALID CITATION !!!

See original here:
Role of Stem-Cell Transplantation in Leukemia Treatment

Lugano 2014 criteria for assessing FDG-PET/CT in lymphoma …

Drug Des Devel Ther. 2017; 11: 17191728.

1Medical Affairs, Bioclinica, Inc., Princeton, NJ

1Medical Affairs, Bioclinica, Inc., Princeton, NJ

1Medical Affairs, Bioclinica, Inc., Princeton, NJ

2Medical Affairs, Sierra Oncology, Brisbane, CA

3Medical Affairs, Apexian Pharmaceuticals, Indianapolis, IN

4Radiology, University Radiology at RWJ University Hospital, New Brunswick, NJ

4Radiology, University Radiology at RWJ University Hospital, New Brunswick, NJ

5Radiology, Abington Hospital, Abington, PA, USA

1Medical Affairs, Bioclinica, Inc., Princeton, NJ

1Medical Affairs, Bioclinica, Inc., Princeton, NJ

1Medical Affairs, Bioclinica, Inc., Princeton, NJ

2Medical Affairs, Sierra Oncology, Brisbane, CA

3Medical Affairs, Apexian Pharmaceuticals, Indianapolis, IN

4Radiology, University Radiology at RWJ University Hospital, New Brunswick, NJ

5Radiology, Abington Hospital, Abington, PA, USA

An operationalized workflow paradigm is presented and validated with pilot subject data. This approach is reproducible with a high concordance rate between individual readers (kappa 0.73 [confidence interval 0.590.87; P=<0.0001]) using a 5-point scale to assess [18F] labeled fluorodeoxyglucose metabolic activity in lymphomatous lesions. These results suggest an operationally practical 5-point scale workflow paradigm for potential use in larger clinical trials evaluating lymphoma therapeutics.

Keywords: lymphoma, Lugano criteria, molecular imaging, oncology trials

Lymphoma, typically categorized as either non-Hodgkins lymphoma (NHL) or Hodgkin lymphoma (HL), is the most common hematological malignancy in the US and accounts for approximately 5% of all newly diagnosed cancers (according to the National Cancer Institute [NCI], 2016). In 2016 in the US, approximately 72,580 new cases of NHL and 8,500 new cases of HL were diagnosed.1,2

While classified under the general heading of lymphoma, NHL and HL, as well as subtypes within each histologic category, may differ in surface protein expression, histologic appearance, cell of origin, clinical evolution, response to treatment, and other features. These differences are yielding important insights into the natural biology of lymphoma, as well as potential markers for diagnostic and therapeutic development. A compelling example is the successful development of CD20-targeted therapy for management of a broad variety of lymphomatous and hematologic diseases.3

Similarly, there are a number of newer diagnostic imaging approaches available, one of which includes [18F] fluorodeoxyglucose (FDG) positron emission tomography (PET) imaging, to better distinguish the lymphoma subtypes. This approach visually assesses the metabolic activity of lymphoma by three-dimensionally measuring the uptake distribution post-administration of FDG.4 In addition to identifying the presence and distribution of disease, FDG-PET imaging, particularly when combined with high quality computed tomography (CT) imaging (PET/CT), has also been shown to be a very effective tool for assessing response to treatment.5

Different sub-types of lymphomas exhibit varying degrees of FDG-avidity that correlate with the aggressiveness of the individual lymphoma.6 Previous investigations have established that NHL exhibits a varying FDG-avidity range from 40% to 100%, depending on the lymphoma subtype, while HL exhibits a much narrower FDG-avidity range of 97% to 100% ().7 Although the use of FDG-PET/CT for the assessment of lymphoma, particularly at the end of treatment (EOT), is supported by published literature, creating a standardized clinically practical methodology for the assessment of lymphoma by FDG-PET/CT continues to be a challenge.8,9

Modified Lugano 5-point scale (5PS)

The purpose of this paper is to define a proposed operational workflow to improve the efficiency and reproducibility of evaluating FDG-avid lymphomas using PET/CT, following the most current published criteria for assessing treatment response in clinical trials.10 The workflow methodology for evaluating FDG non-avid lymphomas using CT criteria will not be included in this manuscript.

In 1999, the NCI Lymphoma International Working Group (IWG) first published imaging and clinical response guidelines for NHL, commonly known as Cheson 1999 criteria.11 These guidelines formed a standardized approach for assessing the presence of NHL, and measuring response to therapeutic intervention, by evaluating imaging and clinical data. The imaging aspects of the Cheson 1999 criteria were primarily based on CT technology which was widely incorporated in clinical trials at that time. The Cheson 1999 criteria guidelines were then updated in 2007, when the IWG published revised response criteria for malignant lymphoma.12 The revised Cheson 1999 criteria, more commonly known as the Cheson 2007 criteria, were developed to address limitations of the Cheson 1999 criteria and to incorporate bone marrow (BM) immunohistochemistry, flow cytometry, and the increased use of FDG-PET imaging as a recognized and effective modality for visualizing the presence and distribution of lymphoma. As a result of incorporating FDG-PET, the response designation of complete response/unconfirmed permitted in the Cheson 1999 criteria was eliminated for FDG-avid histologies which converted from FDG-positive to FDG-negative following treatment. In the Cheson 2007 criteria, these lesions which changed from FDG-positive to FDG-negative following treatment, regardless of residual size on CT, were designated as a complete response. While these changes represented marked improvements to the Cheson 1999 criteria, the Cheson 2007 guidelines did present some challenges to the interpretation of lymphoma progression or response to treatment. Specifically, there was significant potential for ambiguity in the interpretation of lesion positivity due to a dichotomous (ie, positive vs negative) PET response criteria which was based on a subjective interpretation of what represented FDG background (ie, blood pool vs adjacent regions) and the degree of significantly discernible uptake, compared to the background.

Despite the challenges, the Cheson 2007 criteria remained the standard for evaluating HL and NHL until 2014 when the most recent revised criteria were published.10 The evolution of this revised criteria was based on the need to define tumor FDG-avidity with greater objectivity and reproducibility. These new criteria were the direct outgrowth of integrating the previously defined Deauville criteria with the input of investigators at follow-up International Workshop Conferences in 2011 and 2013.13

The goal of the Lugano 2014 guidelines was to revise the Cheson 2007 criteria, in order to reduce ambiguity and achieve more consistent therapeutic response assessments for patients enrolled in clinical trials evaluating treatment for lymphoma. The most significant aspects of the new guidelines pertain to three major components:

the predominant use of FDG-PET/CT in the assessment of FDG-avid lymphoma, while CT remains the designated standard for assessment of non-FDG-avid lymphomas;

the replacement of the dichotomous evaluation of FDG uptake (positive vs negative) with a 5-point scale (5PS) assessment for interim and EOT analyses;

the premise that all FDG-avid disease (for applicable lymphomatous indications) present in the individual patient is included in each time point (TP) analysis.

Other updates in the Lugano 2014 criteria include:

the discontinuation of routine BM biopsies in HL and FDG-avid NHL;

the modification of the Ann Arbor staging method;

the recommendation to reduce the total number of routine follow-up surveillance scan procedures.

The three major components, along with the other modifications to the prior guidance, are intended to help achieve a more uniform and consistent assessment necessary for multiple TP assessments in clinical trials.

The incorporation of FDG-PET as the predominant imaging modality for measuring the distribution and extent of disease in FDG-avid lymphomas represents a major paradigm shift, as this approach moves away from a pure anatomic size-based response into a physiologic response assessment based on tumor metabolism. This approach should allow for a more accurate early assessment of lymphoma tumor treatment response, however, there is still some controversy in the literature regarding the use of interim PET assessment of treatment response in the clinical trial setting.14,15 While the new criteria should reduce the subjective variability which has existed in regards to determination of FDG-PET lesion positivity, this observation has yet to be documented in any multi-center lymphoma clinical trials.

The Lugano 2014 criteria, as defined in the article by Cheson et al, were used as the basis for our approach.10 Our goal was to develop a reproducible and time-efficient operational paradigm, utilizing the Lugano 2014 criteria, which could be routinely employed in clinical drug trials assessing FDG-avid lymphoma. The Lugano 2014 criteria was studied by the authors and modifications were incorporated into the workflow in order to operationalize this approach, as described in the following section.

At present, FDG-PET/CT is generally accepted as the preferred procedure for the clinical staging of FDG-avid lymphomas.16,17 In recognition of the wide-spread utilization of FDG-PET/CT and the supporting literature, the IWG recommends that this modality be routinely employed in clinical trials assessing subjects with FDG-avid lymphomatous disease. In addition to the FDG-PET imaging, a contrast-enhanced CT scan should be included at baseline for accurate measurement of lesion size, separation of bowel from lymphadenopathy, and differentiation of vascular structures from lymph nodes. Another significant modification to the staging criteria is the integration of a 5PS to achieve a more accurate assessment of the degree of FDG avidity at baseline and during follow-up, as it relates to the evaluation of treatment response and progression of disease ().

The 5PS ranges from a score of 1 (where no uptake is discernible in the lesion) to a score of 5 (where the uptake in the lesion is markedly increased compared to the uptake in the liver parenchyma). A single 5PS score, which represents the most FDG-avid (ie, metabolically intense) area of disease (across all index and non-index lesions), is assigned for each TP. The designation of X in the Lugano 2014 5PS has been removed, since under the proposed operational workflow, the readers are trained to provide a comment in their assessment if there are new areas of observed uptake that are unlikely to be lymphoma.

The assessment of BM according to the Lugano 2014 criteria is also very different from the Cheson 2007 criteria, since BM biopsy (BMB) is no longer required for all patients with FDG-avid lymphomas. Disease involvement in BM can now, in most cases, be solely evaluated using FDG-PET imaging; however, confirmation by BMB is still recommended in certain cases. Some of these include patients with certain FDG-avid lymphoma subtypes, cases of negative focal FDG BM activity with additional discordant clinical data, and cases of persistent focal FDG BM activity.

At the baseline imaging assessment, whenever possible all sites of lymphomatous disease are selected (as described in ) and should represent the patients overall FDG-avid tumor burden. The most effective implementation of the methodology for response assessment in clinical trials described in this manuscript, requires consistency of FDG-PET/CT image acquisition performed at multiple sites. Consensus guidelines for FDG-PET/CT image acquisition have been published by experts in the field, and should be incorporated into any clinical trial paradigm.18 Correlation of the FDG-avid sites on CT imaging should be performed to confirm lesion size and morphology, and differentiate sites of disease from bowel and vascular structures. Finally, a 5PS score (as previously described) is assigned to the baseline TP to represent disease avidity on the FDG-PET imaging. The baseline assessment workflow is summarized in . When assessing post-baseline imaging TPs, the same method used at baseline is employed.

Proposed baseline assessment workflow.

Abbreviations: CT, computed tomography; PET, positron emission tomography; 5PS, 5-point scale; SUVmax, maximum standardized uptake value.

Although the Lugano 2014 criteria represent a major advance in the assessment of FDG-avid lymphomas, there are a number of specific modifications to consider when optimizing the criteria for use in multi-center clinical trials. Our proposed approach is summarized in the following sections.

At baseline, a maximum of six sites with most metabolically active FDG-avid disease (classified as index [or target] lesions) should be selected which, when possible, include the largest lesions most representative of the patients overall tumor burden. When possible, index lesions should be chosen from disparate regions of the body and include mediastinal and retroperitoneal areas of disease. These lesions must meet the minimum size requirement of being >15 mm in longest diameter (LDi) for nodal disease, or >10 mm in LDi for extranodal lesions. The LDi and shortest diameter should be recorded for each index lesion. All other disease, consisting of up to ten individual or grouped sites, should be selected at baseline as non-index (or non-target) disease. These can include nodal or extranodal lesions or groups of lesions which are not measurable (or measurable beyond the six sites chosen to be followed as index lesions). In addition, non-index disease can include markedly diffuse FDG uptake in the liver or spleen and marked focal FDG uptake in the BM. All selected sites of disease should be followed throughout the course of treatment. Although the PET criteria in Lugano 2014 for FDG-avid lymphomas do not specifically require the designation of index and non-index disease and size measurements on CT, this approach allows investigators to follow all disease in a logical manner, where the PET findings can be easily correlated with CT imaging and clinical observations. This methodology ensures that all sites of disease, which are reflective of the patients overall tumor burden, are accounted for in each TP assessment.

Our approach specifies that each designated index and non-index CT lesion should be correlated to the corresponding and co-registered PET lesion. A visual assessment using the 5PS should then be performed on the most metabolically active lesion out of all index and non-index disease. In addition, a quantitative standardized uptake value (SUV) measurement, which represents the maximum SUV (SUVmax), should also be documented for this lesion. The SUVmax will be used to calculate the change in uptake compared to post-baseline TPs.

At each on-study TP, the index and non-index lesions identified at baseline are assessed on the PET/CT exam. The most metabolically active lesion is again assessed using the 5PS approach and the SUVmax of that lesion is determined. Of note, it is possible that the most metabolically active lesion identified on-study, when a subject is undergoing treatment, may be different from the most metabolically active lesion which had been identified at the baseline TP. The on-study SUVmax measurement is then utilized to perform the on-study response assessment. The proposed on-study operational approach is illustrated in .

On-study PET response workflow.

Abbreviations: PET, positron emission tomography; 5PS, 5-point scale; FDG, [18F] fluorodeoxyglucose; SUVmax, maximum standardized uptake value; CT, computed tomography.

The SUVmax of the most metabolically active lesion at each on-study TP is compared to the most metabolically active lesion at baseline in order to quantify changes in FDG uptake and obtain a percent change in SUVmax. An on-study Lugano 5PS score of 1, 2 or 3 is considered complete metabolic response at both interim and EOT, whereas a score of 4, 5 represents a different response outcome depending on the measured change in FDG uptake () and the type of TP being evaluated (ie, an interim or EOT TP). At interim, a score of 4 or 5 with a decrease of >25% in SUVmax is considered to be a significant decline in FDG uptake, representative of a partial metabolic response. A score of 4 or 5 with an increase of >50% is considered a significant increase in FDG uptake, representative of progressive metabolic disease (PMD), and a change metric between 25% decrease and 50% increase in FDG uptake is considered to be no significant change in FDG uptake, representative of no metabolic response. At EOT, a score of 4 or 5 is representative of treatment failure (TF) regardless of any significant change in SUVmax. These threshold metrics may be modified in the context of different clinical trial requirements.

Determination of Lugano PET-based on-study response

In frontline therapy lymphoma trials, where a finite number of drug treatment cycles is frequently part of the study design, the recommendation is to use both interim and EOT assessment methods. Conversely, in relapsed and/or refractory lymphoma trials, it is recommended to only use interim assessment methods, as continuation of therapy can be based on a wide range of factors. In this paper, the focus is on the use of an interim assessment method; however, when accounting for an EOT analysis, the main difference is that the term TF is incorporated in the Lugano guidelines as a descriptor for patients who have demonstrated persistent FDG lesion uptake. This term can be confusing when used along with the term PMD. In our proposed workflow, both TF and PMD are classified as one category labeled as PMD. It is important to note that, depending on the type of therapy being evaluated in a particular oncology trial, different change metric thresholds and response categories may be used.

For example, if five lesions are being followed and only one is observed to have markedly increased uptake compared to the liver, then the overall 5PS score for that TP is 5, regardless of the uptake in the other four lesions. Within this 5PS approach, a score of 1, 2, and 3 is generally considered to be PET-negative and values of 4 and 5 would be classified as PET-positive; however, in certain situations (specifically, in response-adaptive trials assessing de-escalation therapy) a 5PS score of 3 may be viewed as PET-positive and therefore considered to be an inadequate treatment response (). Note: the classification of a 5PS of 3 as PET-positive should be prospectively defined prior to the commencement of reads, preferably during development of the trial protocol.

Lugano operational workflow example.

Notes: (A) A 50-year-old male with NHL. CT (left image) reveals diffuse adenopathy in the neck and mediastinum (white arrows). PET (middle image) reveals marked FDG uptake (5PS of 5) in neck and mediastinum (black arrows) confirmed on fused PET/CT (right image). (B) Interim treatment follow-up CT (left image) at 8 weeks reveals significant residual adenopathy (white arrow). Follow-up PET (middle image) still assessed as marked uptake above liver (5PS of 5), demonstrates a significant decrease in FDG uptake with residual activity in the mediastinum (black arrow) which is also confirmed on the PET/CT (right image). The overall findings are consistent with a significant partial metabolic response.

Abbreviations: NHL, non-Hodgkins lymphoma; CT, computed tomography; PET, positron emission tomography; FDG, [18F] fluorodeoxyglucose; 5PS, 5-point scale.

In order to validate the proposed Lugano workflow, a pilot study cohort consisting of 12 NHL patients with a total of 34 imaging TPs was evaluated. The objective of this validation was to determine if the proposed Lugano workflow is a feasible method to improve the reproducibility and efficiency amongst readers evaluating the radiographic response in lymphoma patients.

The study cohort consisted of 12 well-documented, NHL patients, eight male, four female, ranging in age from 40 to 80 years, who were a subset of patients enrolled in an Institutional Review Board (IRB)-approved early-phase, commercially-sponsored, clinical trial.19 All patients signed written informed consents acknowledging all aspects of the clinical trial including an independent review of their imaging data. The participating IRBs included Schulman Associates IRB, St John Hospital and Medical Center IRB, and New England IRB. All of the patients had documented FDG-avid disease. Three of the authors, all experienced independent radiology reviewers (RA, LS, FT), blindly assessed all FDG-PET/CT scans for each patient. The reviewers conducted their evaluations using a modified 5PS () according to the modified Lugano10 response assessment criteria for FDG-avid lymphomas and the proposed operational workflow described in this paper. Specifically, the reviewers were instructed to categorize all lymphomatous disease visualized on FDG-PET/CT into one of two groups. The six most dominant lesions (labeled as index 001006) which were representative of the patients overall tumor burden were identified on the baseline CT and PET images. These index lesions were measured for anatomic size on CT and evaluated for metabolic activity on the PET images. The remainder of the patients tumor burden was assigned by location to a maximum of ten single (or grouped) lesion sites (labeled as non-index 200209). Baseline lesions were considered positive when they met the criteria for a 5PS of 4 or 5 (ie, uptake moderately or markedly > liver).

At on-study TPs, CT index and non-index lesions were assessed for continued presence of disease, however, no size measurements or change metrics were required. PET index and non-index lesions were again assessed using the on-study workflow (). The change metric at each on-study TP was calculated by the following formula:

%SUVmax=(SUVmaxTPxSUVmaxScreeningSUVmaxScreening)100Note:TPx=TimepointX

New lesions (labeled as 300302) were required to meet the minimum anatomic size criteria (>15 mm) on CT and were also required to be FDG-avid on PET (ie, 5PS of 4 or 5).

The overall concordance rate between the three reviewers was determined. A 5PS of either 1, 2 or 3 (PET-negative) was considered concordant across readers, as was a score of 4 or 5 (PET-positive). Reader discordance was observed when the 5PS assessment recorded by readers differed between PET-positive and PET-negative at a given TP.

In order to evaluate inter-reader reliability, Fleiss kappa, an extension of Scotts pi to more than two observers and nominal categories, was calculated for the Lugano TP 5PS assessments of three readers who independently reviewed multiple FDG-PET imaging series.20

All three reviewers assessed all patients at all individual TPs using the Lugano TP 5PS (). The three independent reviewers were in concordance in 97 out of 102 TPs assessed, which equates to an overall 95% concordance rate. The kappa statistic for 5PS agreement () was 0.73 (confidence interval 0.590.87; P=<0.0001) using the Fleiss kappa statistic methodology, indicative of an overall good to excellent correlation between the three readers. Furthermore, two out of the three reviewers were in concordance at all TPs.

Reviewer results Lugano time point 5PS assessment

The incorporation of the Lugano 2014 criteria for the assessment of lymphoma patients response to therapy represents an important paradigm shift. In particular, the use of FDG-PET/CT imaging as the dominant imaging technique for the evaluation of FDG-avid lymphomas, allows for the pathophysiologic assessment of tumor metabolic activity in the ongoing evaluation of lymphoma patients.

There are a number of issues that must be considered when implementing a workflow paradigm for the Lugano criteria. These include the proper selection of representative disease, lesion size thresholds for index and new lesions, and ensuring that proper reader training is provided prior to trial commencement.

The optimum approach is to have each reader select all FDG-avid lesions present at the baseline TP. In situations where a reader chooses to select and follow fewer lesions from the total number of FDG-avid lesions, there may be a higher risk of discordance between the assessment by a reader who chooses to select and follow a larger representative number of lesions. This is particularly true at on-study TPs where there may be a difference in the 5PS assessment between individual readers. In this situation, the difference between reader assessments may be spurious due to the lack of complete lesion selection by one of the readers. For example, if one reader selects one index lesion and no non-index lesions while another reader selects four index lesions and three non-index lesions, there is a high probability that there may be a discrepancy in the PET 5PS response assessment between the two readers.

It is also essential to establish a minimum size for the selection of index lesions at baseline and the identification of new lesions at post-baseline TPs in order to ensure optimum reproducibility between individual readers. At baseline, a minimum size threshold for selecting index lesions will facilitate a higher level of reader harmonization with respect to selection of representative disease. At on-study TPs, a minimum size threshold for new lesions is also necessary for optimal reader concordance. For example, if one reader selects a new lesion which does not meet a minimum size criteria, the response assessment may result in PMD designation, whereas another reader who did not believe the same lesion to be significant, would end up with a different response assessment.

Comprehensive reader training for an individual lymphoma clinical trial using the Lugano 2014 criteria, should be based on the presumption that the readers already have in-depth experience and knowledge of the radiographic assessment of lymphomatous disease and the Lugano 2014 criteria. The specific training material for an individual clinical trial should include ample clinical case examples and test case examples, to ensure that each reader adequately understands the overall workflow guidelines and any individual study-specific rules. Ideally, a discussion of lessons learned and known pitfalls should also be included in the training session(s). The overall goal of the training process is to achieve optimal reader harmonization and concordance which is reproducible on both an inter- and intra-reader level. For example, in this pilot validation study, the 5PS discordance noted between readers occurred most frequently between a score of 3 (> mediastinum, liver) and 4 (moderately > liver). This observation emphasizes the importance of training readers to be aware of the subtle differences in discerning FDG uptake in lesions compared to the background activity in the liver.

The approach taken in this validation study was to categorize all FDG-avid lesions as either index or non-index. This approach allows for the correlation of the FDG-PET assessments with the separate lesion size measurements on CT imaging, which is particularly helpful in clinical trials which require independent CT and PET assessments. In studies that do not require a separate CT analysis with a classification of index and non-index disease, it is possible to assess PET scans in a different manner, which is beyond the scope of this paper. The workflow presented here is an operational scheme that can be utilized for single-center or multi-center clinical trials which include both CT and FDG-PET imaging requirements. The proposed approach has inherent flexibility, which allows further modification to address the specific goals and/or issues of an individual clinical trial or pharmacologic therapy.

Regardless of the approach taken, monitoring total tumor burden response at the cellular level is essential, and the process implemented to apply the Lugano 2014 criteria should result in an assessment method that more accurately aligns with a patients clinical outcome. This is in contrast to the Cheson 2007 guidelines, where a limited number of representative lesions are selected and assessed using a simple dichotomous (ie, positive vs negative) scale.

Another potential challenge with the implementation of the Lugano 2014 criteria is in immunotherapy oncology clinical trials, where the observation of increased metabolic activity may be mistakenly interpreted as PMD. In these trials, the proper assessment of possible transient metabolic flare, which may be visualized on FDG-PET/CT scans at interim TPs during treatment, needs to be considered. One possible solution to this challenge is to raise the threshold for assessing PMD to allow for greater changes in immune-related FDG metabolic activity. An alternative approach for controlling against sudden increases in FDG uptake which may be due to immune-related metabolic activity, is to delay the confirmation of PMD until a subsequent imaging TP (approximately 612 weeks after the initial observation of PMD) is submitted and the initial assessment of PMD can be either confirmed or not confirmed by the reader. Additional recommendations for handling immune-related response assessments are discussed in a recent publication.21

The workflow paradigm presented in this paper represents an operationalized method which can be utilized in single- and multi-center lymphoma clinical trials employing the Lugano 2014 PET criteria. The pilot validation data presented in this paper, confirm that the proposed workflow is a useful and reproducible methodology to achieve consistent imaging assessment results with a high level of concordance across readers. The proposed paradigm is a work-in-progress which will require validation in a larger multi-center clinical trial, to further solidify the operational workflow as an assessment standard for clinical trials investigating therapies for PET-avid lymphomas.

Disclosure

RLVH, RS, JGW, JAS and MON are full time employees at Bioclinica Inc; RA, FT and LS are reader consultants for Bioclinica Inc; BK is a full time employee of Sierra Oncology and RM is a full time employee at Apexian Pharmaceuticals. The authors report no other conflicts of interest in this work.

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The people cloning their pets – BBC.com

"People ask me, 'Why is it so expensive?' and I tell them because there are so many complicated steps involved in the whole process," says Rodriguez. "It's definitely an emotional reason for pet clients. They want to be able to carry on that strong emotional bond that they have with the pet."

The industry has since expanded elsewhere in the globe. Sooam Biotech in South Korea offer dog cloning services, as well as Sinogene in China.

However, many scientists remain uncomfortable about the whole premise. Lovell-Badge argues that there is "no justification" for pet cloning as while the resulting animals will be genetically identical, they will not have the same behavioural characteristics and personalities as all creatures are a product of both genes and their environment.

"People really want their pet that knows them and knows certain tricks and so forth," says George Church, professor of genetics at Harvard Medical School. "In that sense, it's a little bit taking advantage of people's grief."

Reviving extinct species

In the years that followed Dolly's cloning, the central question was whether scientists would ever extend the technology to humans, and the many moral and ethical issues that would invoke.

But while a human embryo was successfully cloned in 2013, the process of creating an entire human being has never been attempted because of the likely public outcry. Chinese scientists did clone the first primates in January 2018, long-tailed macques Zhong Zhong and Hua Hua, but there are currently no suggestions that this work will continue into further primate species.

Instead, most funding is being devoted to using cloning to resurrect animals on the verge of extinction. Efforts are underway to clone both the giant panda and the northern white rhino a species for which there are just two animals left on the planet while in the last two years, ViaGen have cloned the black footed ferret and Przewalski's horse, both of which are endangered.

Church is leading the most ambitious project, a quest to revive the woolly mammoth, a species that last lived some 4,000 years ago. His de-extinction company Colossal has already raised 11m ($14.5m) in funding to support the idea, which will involve creating an elephant-mammoth hybrid through taking skin cells from Asian elephants and using cloning technology to reprogram them with mammoth DNA.

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The people cloning their pets - BBC.com

Therapeutic feline and canine cancer vaccine – Open Access Government

Canine cancer bear substantial similarities with their human counterparts[1-4]. Treatment of pets that get solid tumours will typically consist of surgery, chemotherapy and sporadically radiation, or a combination of these. Unfortunately, these treatments are not always effective.

In humans, experimental cancer treatments have had a slow but sure advance into the clinics and have given many patients new hope. Especially, treatment methods related to immunotherapy have been on the rise for the past decade.

Despite the documented clinical success of human immunotherapy, the opportunities to apply these treatments on companion dogs in clinical settings are few or non-existent in Nordic countries. As the number of insured pets in these countries increases so does the prospect that experimental treatments will also be affordable for pet owners.

Recent research on pet cancers shows that cancer immunotherapy can have life-prolonging effects and is often associated with fewer side effects (for the overview of literature see the provided reviews and the references therein)[4,5]. We are therefore developing new therapies for companion dogs (and cats) that will combine our expertise in human immunotherapy and translational research with the newfound knowledge of canine cancer at the molecular level.

Alvacan (Figure) is our product line of therapeutic cancer vaccines that combines the best of classical cellular immunotherapy with recombinant DNA/RNA technology.

The treatments that we are developing are tailored for each individual patient and will serve as a supplement to standard cancer surgery and chemotherapy. We are currently testing two immunotherapy treatments that can be administered at the local veterinary clinic.

What we need is a patients blood and if possible, a cancer tissue sample that is typically obtained through surgery (Figure).The administration of vaccines and patient follow up will continue in the selected partner clinics. These vaccines will be affordable for the typical pet owner in Nordic countries.

As a part of our vaccine research, we have created a biobank of living tissues and cell lines from canine and feline solid tumours. This collection serves as a base for our research and can be available for other researchers through collaboration with us or commercialisation of our material. We have already successfully adapted our previously described human methods to work with canine and feline biobanking and cell cultures [6-10].

For each primary cancer cell line, isolated from patient biopsies, we will attempt to establish a cell line that is enriched for cancer stem cells (CSCs). CSCs are believed to be cellular drivers of carcinogenesis. One of the hallmarks of CSCs is self-renewal. We have previously extensively studied stemness and growth properties in a series of primary CSC lines [10]. Our biobank comprises currently 180 samples of 80 canine and feline patients and these numbers are growing day by day.

By the end of this year, we expect to have doubled the number of patient samples. Our collection of living tissues and cell lines includes intracranial, mammary, and testicular solid tumours, sarcomas and many other less prevalent cancers.

We will also map molecular profiles of canine tumours using the previously established techniques tested in human cancer [10]. Once such information is available, we can develop more advanced targeted treatments. By comparing molecular profiles from many cancer patients, we can form a more general picture of the disease and develop treatments with a broader effect.

The need for animal models that translate to human immunity is a primary challenge of human cancer immunotherapy[11]. A better understanding of canine carcinogenesis is therefore one of the main goals of our research. This project has excellent translational potential and will not only be beneficial for cancer-suffering pets, but also humans.

We are also studying gene expression regulation in canine cancer. Targeted proteomics and gene expression analysis is conducted according to methods that we previously established in humans[10]. There are currently only a few bioinformatic tools that apply to canine genomes, transcriptomes and proteomes. The number of public canine molecular profiles is also far behind that for human and murine counterparts.

Our goal is to generate molecular data profiles and design bioinformatic tools that will speed up this type of research and contribute to the information exchange between research organisations and communities. We intend to generate many canine molecular cancer profiles and create new tools for data analysis. Based on a better understanding of molecular drivers of canine carcinogenesis we are also planning on building next-generation diagnostic tools for canine cancer. We are going to combine molecular profiles with clinical and imaging data to design machine learning and AI tools that will enable better diagnostics and improve medication efficiency.

Literature list

About the author

Biljana Stangeland. PhD is an Executive Director, Chief Scientific Officer, and co-founder of Alv B AS (https://alvb.no/), a Norwegian biotech start-up. Biljana has more than 25 years of academic research behind her and over five years as a Lead Data Scientist in the private sector.

Please note: This is a commercial profile

2019. This work is licensed under CC-BY-NC-ND.

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Therapeutic feline and canine cancer vaccine - Open Access Government

Chemotherapy for Non-Hodgkin’s Lymphoma: What to Know – Healthline

Non-Hodgkins lymphoma (NHL) is a type of cancer that affects white blood cells, known as lymphocytes. In NHL, cancer cells tend to spread to parts of the lymphatic system throughout the body, like the lymph nodes.

An estimated 4 percent of people in the United States who receive a cancer diagnosis have NHL. If a doctor diagnoses NHL in you or a loved one, they will likely recommend chemotherapy for treatment. Chemotherapy is the use of medications to treat rapidly dividing cells, such as cancer cells.

Choosing a chemotherapy regimen depends on several factors:

Most people will receive a combination of chemotherapy drugs to treat NHL. There are many different types of NHL and many different drugs and combinations that doctors use to treat specific types. Well review some of the common drugs and how they work.

Many types of chemotherapy drugs are available to treat NHL. Each works slightly differently to target and ideally kill cancerous cells or keep them from multiplying.

But chemotherapy can affect healthy cells, too, causing side effects. Certain groups of chemotherapy drugs may have unique side effects. These are things a doctor will consider before coming up with an appropriate regimen.

Chemotherapy drugs used to treat NHL usually fall into one of the following groups:

Alkylating agents work by damaging the genetic material (DNA) that tells a cancerous cell to replicate.

Examples of alkylating agents doctors prescribe to treat NHL include:

While all chemotherapy drugs have side effects, alkylating agents may come with an increased risk of bone marrow damage. Research has also linked some alkylating agents to pulmonary fibrosis.

Platinum drugs are a form of alkylating agent. When inside the body, they form platinum complexes that keep cancer cells from replicating.

Examples of platinum drugs include:

Platinum drugs have some unique side effects.

Up to 40 specific side effects are known to occur with platinum drugs, but some are unique. Some platinum drugs, particularly oxaliplatin, have been observed to cause nerve damage.

Antimetabolites are medications that interfere with the typical parts of a cancerous cells genetic material. They scramble the code that helps DNA copy itself, so the cancerous cells cannot multiply.

Examples of antimetabolites used to treat NHL include:

One of the main side effects of antimetabolites is a low white blood cell count (leukopenia).

Purine analogs are an antimetabolite drug category. They have a similar structure to purines, which can be a building block of certain genetic material.

Examples of purine analogs used to treat NHL include:

Anthracyclines are antitumor antibiotics. These are not the same as the antibiotics we use to treat infections. These drugs bind to DNA to keep it from copying itself.

The types of anthracyclines doctors prescribe to treat NHL include:

Anthracyclines can cause heart damage in higher doses.

Doctors may prescribe other medications to treat NHL that may not fall into a specific category. Examples of these medications include:

If your doctor prescribes these or other medications, you can ask how they work to help treat your cancer type and what combinations may be most effective.

Doctors usually treat NHL with a combination of chemotherapy drugs. One such option for treating some of the most common types of NHL is R-CHOP. R-CHOP is an acronym for five drugs:

Corticosteroids are not a chemotherapy drug, but they may be part of your treatment. For NHL, doctors prescribe them to reduce inflammation and boost the effectiveness of your chemotherapy drugs.

Examples of corticosteroids used to treat NHL include:

Doctors often prescribe chemotherapy drugs for NHL in cycles. This means a person may take a medication for a short time, followed by a rest period.

Most chemotherapy drugs are taken either by mouth or by an intravenous (IV) line.

Typically, a doctor may prescribe several doses of chemotherapy drugs to be given over several weeks. After this time, you may undergo imaging tests, such as a PET scan or CT scan, to see if the drugs are working well.

If the initial chemotherapy treatment was ineffective or not fully effective, a doctor might recommend another chemotherapy regimen or different therapies.

If lymphomas have developed in the spinal area, doctors may give some chemotherapy drugs by intrathecal chemotherapy. This is when they insert a small, thin needle through the spinal column to get the medication directly to the spinal fluid.

Doctors may also use intrathecal chemotherapy to prevent lymphomas from developing in the spinal area.

The side effects of chemotherapy for NHL depend on what chemotherapy type a doctor prescribes. Its important to understand the side effects of the specific chemotherapy drugs you may be taking.

Some side effects that may commonly occur related to chemotherapy drugs include:

Some chemotherapy drugs are known to have specific effects. Examples of these known side effects include damage to the:

A doctor will consider the impact of these side effects when deciding on dosage.

Sometimes, NHL will not respond to chemotherapy. When this is the case, a doctor may recommend alternative treatments. These will depend on exactly what NHL type you have and how advanced your cancer is.

Treatment examples include:

Researchers are also studying new treatment types regularly to determine if there are other, more effective methods to treat NHL.

Advancements in chemotherapy drugs and how doctors can combine them have meant better outcomes for people with NHL. The earlier the NHL stage is detected, the better a persons 5-year survival rate is.

If your doctor has prescribed a chemotherapy regimen for you, they should explain how the drugs work to help your body deal with cancer.

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Chemotherapy for Non-Hodgkin's Lymphoma: What to Know - Healthline

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