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News Article | December 5, 2016
Site: www.eurekalert.org

SAN DIEGO, CA (December 5, 2016)--Researchers from Columbia University Medical Center and NewYork-Presbyterian reported that 8 out of 12 patients with relapsed and/or chemotherapy refractory acute myeloid leukemia (AML) or other blood cancers responded to a regimen including the chemotherapy drugs thioguanine and decitabine. Results from this small phase I study were reported at the American Society of Hematology's annual conference. "Outcomes are typically poor for older patients with advanced blood cancers, and new therapies are desperately needed to help patients with these cancers achieve remission," said Mark Frattini, MD, PhD, associate professor of medicine at Columbia University Medical Center (CUMC) and blood cancer specialist at NewYork-Presbyterian. "While our study was small, the response we saw in this phase I, dose-escalating trial was encouraging." Previously, Frattini and colleagues had used a proprietary chemosensitivity screening assay to demonstrate that combining thioguanine and decitabine--chemotherapy drugs that are commonly used as single agents to treat patients with AML--restored therapeutic efficacy in leukemia cells from patients with relapsed and/or refractory disease. In this study, the researchers tested the efficacy of the combination therapy in 12 older patients (median age of 67 years) with relapsed or chemotherapy refractory AML or chronic myelomonocytic leukemia, including 6 patients whose disease progressed after being treated previously with decitabine as a single agent. Of these, 11 patients completed the first treatment cycle, and 6 completed a second cycle, with a median of 3 rounds of treatment. Eight of the 11 evaluable patients responded to the combination therapy, including 6 who achieved a complete remission (5 in complete remission with incomplete count recovery). In addition, all of the patients who had progressed after prior treatment with decitabine alone responded to the combination therapy, demonstrating that the combination could overcome disease resistance to decitabine. Chemosensitivity assay results, obtained before treatment, accurately predicted each patient's response to the combination therapy. After treatment with the combination therapy, 4 of the responders went on to have a stem cell transplant. "The goal of chemotherapy for patients with relapsed and/or refractory AML and other blood cancers is to achieve a remission that enables them to undergo a potentially curative stem cell transplant," said Dr. Frattini. "With our phase I results, we have shown that this combination therapy can get some patients--including those who failed to respond to or progressed after previous chemotherapy treatment with a single agent such as decitabine--to that point. The next challenge for hematologic oncologists is to reduce morbidity and mortality associated with stem cell transplantation." After the study, 2 of the patients who had a stem cell transplant died from transplant-related toxicity, and another relapsed. One patient has remained in remission for more than 2 years. The study is titled, "Final Results of a Phase I Trial of a Pharmacodynamically Conceived Thioguanine/Decitabine Combination in Patients with Advanced Myeloid Malignancies." The other contributors are: Daniel J. Lee (Columbia University Medical Center, New York, NY), Todd L. Rosenblat (CUMC), Mark Lawrence Heaney (CUMC), Joseph G. Jurcic (CUMC), Azra Raza (CUMC), Kristina Gazivoda (CUMC), Katherine Harwood (CUMC), Ryan Shelton (CUMC), Hakim Djaballah (Institut Pasteur Korea, Seoul, Republic of Korea), Joseph M. Scandura (Weill Cornell/NewYork-Presbyterian, New York, NY), and Anthony Letai (Dana-Farber Cancer Institute, Boston, MA). The study was supported by an award from the Herbert Irving Comprehensive Cancer Center at Columbia University Medical Center. Dr. Jurcic's research is funded by Astellas. Dr. Letai receives funding from and is a consultant for from Astra-Zeneca, Tetralogic, and AbbVie. The researchers declare no additional conflicts of interest. Columbia University Medical Center provides international leadership in basic, preclinical, and clinical research; medical and health sciences education; and patient care. The medical center trains future leaders and includes the dedicated work of many physicians, scientists, public health professionals, dentists, and nurses at the College of Physicians and Surgeons, the Mailman School of Public Health, the College of Dental Medicine, the School of Nursing, the biomedical departments of the Graduate School of Arts and Sciences, and allied research centers and institutions. Columbia University Medical Center is home to the largest medical research enterprise in New York City and State and one of the largest faculty medical practices in the Northeast. The campus that Columbia University Medical Center shares with its hospital partner, NewYork-Presbyterian, is now called the Columbia University Irving Medical Center. For more information, visit cumc.columbia.edu or columbiadoctors.org. NewYork-Presbyterian is one of the nation's most comprehensive healthcare delivery networks, focused on providing innovative and compassionate care to patients in the New York metropolitan area and throughout the globe. In collaboration with two renowned medical school partners, Weill Cornell Medicine and Columbia University College of Physicians & Surgeons, NewYork-Presbyterian is consistently recognized as a leader in medical education, groundbreaking research and clinical innovation. NewYork-Presbyterian has four major divisions: NewYork-Presbyterian Hospital is ranked #1 in the New York metropolitan area by U.S. News and World Report and repeatedly named to the magazine's Honor Roll of best hospitals in the nation; NewYork-Presbyterian Regional Hospital Network is comprised of leading hospitals in and around New York and delivers high-quality care to patients throughout the region; NewYork-Presbyterian Physician Services connects medical experts with patients in their communities; and NewYork-Presbyterian Community and Population Health features the hospital's ambulatory care network sites and operations, community care initiatives and healthcare quality programs, including NewYork Quality Care, established by NewYork-Presbyterian, Weill Cornell and Columbia. NewYork-Presbyterian is one of the largest healthcare providers in the U.S. Each year, nearly 29,000 NewYork-Presbyterian professionals deliver exceptional care to more than 2 million patients. For more information, visit http://www. and find us on Facebook, Twitter and YouTube.


News Article | February 27, 2017
Site: www.eurekalert.org

(PRINCETON, N.J., Feb. 27, 2017) - Bristol-Myers Squibb Company (NYSE:BMY) today announced that Columbia University Medical Center and Peter MacCallum Cancer Centre (Peter Mac) have joined the International Immuno-Oncology Network (II-ON), a global peer-to-peer collaboration between Bristol-Myers Squibb and academia that aims to advance Immuno-Oncology (I-O) science and translational medicine to improve patient outcomes. Launched in 2012 by Bristol-Myers Squibb, the II-ON was one of the first networks to bring academia and industry together to further the scientific understanding of I-O, and has expanded from 10 to 15 sites including more than 250 investigators working on over 150 projects across 20 tumor types. The II-ON has generated cutting-edge I-O data that have informed the development of new I-O agents, yielded publications and produced some of the earliest findings on a variety of biomarkers and target identification and validation. "Bristol-Myers Squibb has long believed the future of cancer research is dependent on investments in science and partnerships. We formed the II-ON to facilitate innovation in I-O science and drug discovery by providing a streamlined framework for peer-to-peer collaboration among global cancer research leaders," said Nils Lonberg, Head of Oncology Biology Discovery at Bristol-Myers Squibb. "The significant discoveries generated by the II-ON over the past five years have not only informed our robust early I-O pipeline, but also serve to advance the entire field. We are proud to collaborate with Columbia University Medical Center and Peter Mac, and together with the entire II-ON will continue to lead pioneering research and heighten our collective understanding of the science behind I-O." Through the II-ON, Bristol-Myers Squibb is collaborating with leading cancer research institutions around the world to generate innovative I-O science, launch biology-driven trials and seek out cutting-edge technologies with the goal of translating research findings into clinical trials and, ultimately, clinical practice. "I-O research may be transforming the way we treat cancer," said Charles G. Drake, MD, PhD, Professor of Medicine at Columbia University Medical Center and Director of Genitourinary Oncology and Associate Director for Clinical Research at the Herbert Irving Comprehensive Cancer Center at New York-Presbyterian/Columbia. "The II-ON offers a tremendous opportunity to work smarter and faster along with our colleagues to address fundamental scientific questions in I-O." "We believe the collective knowledge and research power of the II-ON will generate groundbreaking findings in I-O with the potential to improve outcomes for people affected by cancer," said Professor Joe Trapani, Executive Director Cancer Research and Head of the Cancer Immunology Program at Peter MacCallum Cancer Centre, Melbourne, Australia. Building on the success of the II-ON, Bristol-Myers Squibb has invested in several other models of scientific collaboration with academic partners across the globe, including the Global Expert Centers Initiative (GECI) and the Immuno-Oncology Integrated Community Oncology Network (IO-ICON). "We believe a one-size-fits-all research approach does not facilitate innovation," said Lonberg. "Our tailored collaborations with academic centers expand our research capabilities and accelerate our collective ability to deliver potentially life-changing results for patients." The II-ON, formed in 2012, is a global peer-to-peer collaboration between Bristol-Myers Squibb and academia advancing the science of Immuno-Oncology (I-O) through a series of preclinical, translational and biology-focused research objectives. The research in the collaboration is focused on three fundamental scientific pillars: understanding the mechanisms of resistance to immunotherapy; identifying patient populations likely to benefit from immunotherapy; and exploring novel combination therapies that may enhance anti-tumor response through complementary mechanisms of action. The II-ON facilitates the translation of scientific research findings into drug discovery and development, with the goal of introducing new treatment options into clinical practice. In addition to Bristol-Myers Squibb, the II-ON currently comprises 15 leading cancer research institutions, including: Clinica Universidad Navarra, Dana-Farber Cancer Institute, The Earle A. Chiles Research Institute (Providence Health & Services), Institut Gustave Roussy, Istituto Nazionale per lo Studio e la Cura dei Tumori "Fondazione G. Pascale", Bloomberg-Kimmel Institute for Cancer Immunotherapy at the Johns Hopkins Kimmel Cancer Center, Memorial Sloan Kettering Cancer Center, National Cancer Center Japan, The Netherlands Cancer Institute, The Royal Marsden NHS Foundation Trust and The Institute of Cancer Research, University College London, The University of Chicago, West German Cancer Center/University Hospital Essen, and now Columbia University Medical Center and Peter MacCallum Cancer Centre. Bristol-Myers Squibb: At the Forefront of Immuno-Oncology Science & Innovation At Bristol-Myers Squibb, patients are at the center of everything we do. Our vision for the future of cancer care is focused on researching and developing transformational Immuno-Oncology (I-O) medicines that will raise survival expectations in hard-to-treat cancers and will change the way patients live with cancer. We are leading the scientific understanding of I-O through our extensive portfolio of investigational and approved agents - including the first combination of two I-O agents in metastatic melanoma - and our differentiated clinical development program, which is studying broad patient populations across more than 20 types of cancers with 12 clinical-stage molecules designed to target different immune system pathways. Our deep expertise and innovative clinical trial designs uniquely position us to advance the science of combinations across multiple tumors and potentially deliver the next wave of I-O combination regimens with a sense of urgency. We also continue to pioneer research that will help facilitate a deeper understanding of the role of immune biomarkers and inform which patients will benefit most from I-O therapies. We understand making the promise of I-O a reality for the many patients who may benefit from these therapies requires not only innovation on our part, but also close collaboration with leading experts in the field. Our partnerships with academia, government, advocacy and biotech companies support our collective goal of providing new treatment options to advance the standards of clinical practice. Bristol-Myers Squibb is a global biopharmaceutical company whose mission is to discover, develop and deliver innovative medicines that help patients prevail over serious diseases. For more information about Bristol-Myers Squibb, visit us at BMS.com or follow us on LinkedIn, Twitter, YouTube and Facebook. This press release contains "forward-looking statements" as that term is defined in the Private Securities Litigation Reform Act of 1995 regarding the research, development and commercialization of pharmaceutical products. Such forward-looking statements are based on current expectations and involve inherent risks and uncertainties, including factors that could delay, divert or change any of them, and could cause actual outcomes and results to differ materially from current expectations. No forward-looking statement can be guaranteed. Forward-looking statements in this press release should be evaluated together with the many uncertainties that affect Bristol-Myers Squibb's business, particularly those identified in the cautionary factors discussion in Bristol-Myers Squibb's Annual Report on Form 10-K for the year ended December 31, 2016 in our Quarterly Reports on Form 10-Q and our Current Reports on Form 8-K. Bristol-Myers Squibb undertakes no obligation to publicly update any forward-looking statement, whether as a result of new information, future events or otherwise.


PRINCETON, N.J.--(BUSINESS WIRE)--Bristol-Myers Squibb Company (NYSE:BMY) today announced that Columbia University Medical Center and Peter MacCallum Cancer Centre (Peter Mac) have joined the International Immuno-Oncology Network (II-ON), a global peer-to-peer collaboration between Bristol-Myers Squibb and academia that aims to advance Immuno-Oncology (I-O) science and translational medicine to improve patient outcomes. Launched in 2012 by Bristol-Myers Squibb, the II-ON was one of the first networks to bring academia and industry together to further the scientific understanding of I-O, and has expanded from 10 to 15 sites including more than 250 investigators working on over 150 projects across 20 tumor types. The II-ON has generated cutting-edge I-O data that have informed the development of new I-O agents, yielded publications and produced some of the earliest findings on a variety of biomarkers and target identification and validation. “Bristol-Myers Squibb has long believed the future of cancer research is dependent on investments in science and partnerships. We formed the II-ON to facilitate innovation in I-O science and drug discovery by providing a streamlined framework for peer-to-peer collaboration among global cancer research leaders,” said Nils Lonberg, Head of Oncology Biology Discovery at Bristol-Myers Squibb. “The significant discoveries generated by the II-ON over the past five years have not only informed our robust early I-O pipeline, but also serve to advance the entire field. We are proud to collaborate with Columbia University Medical Center and Peter Mac, and together with the entire II-ON will continue to lead pioneering research and heighten our collective understanding of the science behind I-O.” Through the II-ON, Bristol-Myers Squibb is collaborating with leading cancer research institutions around the world to generate innovative I-O science, launch biology-driven trials and seek out cutting-edge technologies with the goal of translating research findings into clinical trials and, ultimately, clinical practice. “I-O research may be transforming the way we treat cancer,” said Charles G. Drake, MD, PhD, Professor of Medicine at Columbia University Medical Center and Director of Genitourinary Oncology and Associate Director for Clinical Research at the Herbert Irving Comprehensive Cancer Center at New York-Presbyterian/Columbia. “The II-ON offers a tremendous opportunity to work smarter and faster along with our colleagues to address fundamental scientific questions in I-O.” “We believe the collective knowledge and research power of the II-ON will generate groundbreaking findings in I-O with the potential to improve outcomes for people affected by cancer,” said Professor Joe Trapani, Executive Director Cancer Research and Head of the Cancer Immunology Program at Peter MacCallum Cancer Centre, Melbourne, Australia. Building on the success of the II-ON, Bristol-Myers Squibb has invested in several other models of scientific collaboration with academic partners across the globe, including the Global Expert Centers Initiative (GECI) and the Immuno-Oncology Integrated Community Oncology Network (IO-ICON). "We believe a one-size-fits-all research approach does not facilitate innovation,” said Lonberg. “Our tailored collaborations with academic centers expand our research capabilities and accelerate our collective ability to deliver potentially life-changing results for patients." The II-ON, formed in 2012, is a global peer-to-peer collaboration between Bristol-Myers Squibb and academia advancing the science of Immuno-Oncology (I-O) through a series of preclinical, translational and biology-focused research objectives. The research in the collaboration is focused on three fundamental scientific pillars: understanding the mechanisms of resistance to immunotherapy; identifying patient populations likely to benefit from immunotherapy; and exploring novel combination therapies that may enhance anti-tumor response through complementary mechanisms of action. The II-ON facilitates the translation of scientific research findings into drug discovery and development, with the goal of introducing new treatment options into clinical practice. In addition to Bristol-Myers Squibb, the II-ON currently comprises 15 leading cancer research institutions, including: Clinica Universidad Navarra, Dana-Farber Cancer Institute, The Earle A. Chiles Research Institute (Providence Health & Services), Institut Gustave Roussy, Istituto Nazionale per lo Studio e la Cura dei Tumori “Fondazione G. Pascale”, Bloomberg-Kimmel Institute for Cancer Immunotherapy at the Johns Hopkins Kimmel Cancer Center, Memorial Sloan Kettering Cancer Center, National Cancer Center Japan, The Netherlands Cancer Institute, The Royal Marsden NHS Foundation Trust and The Institute of Cancer Research, University College London, The University of Chicago, West German Cancer Center/University Hospital Essen, and now Columbia University Medical Center and Peter MacCallum Cancer Centre. Bristol-Myers Squibb: At the Forefront of Immuno-Oncology Science & Innovation At Bristol-Myers Squibb, patients are at the center of everything we do. Our vision for the future of cancer care is focused on researching and developing transformational Immuno-Oncology (I-O) medicines that will raise survival expectations in hard-to-treat cancers and will change the way patients live with cancer. We are leading the scientific understanding of I-O through our extensive portfolio of investigational and approved agents – including the first combination of two I-O agents in metastatic melanoma – and our differentiated clinical development program, which is studying broad patient populations across more than 20 types of cancers with 12 clinical-stage molecules designed to target different immune system pathways. Our deep expertise and innovative clinical trial designs uniquely position us to advance the science of combinations across multiple tumors and potentially deliver the next wave of I-O combination regimens with a sense of urgency. We also continue to pioneer research that will help facilitate a deeper understanding of the role of immune biomarkers and inform which patients will benefit most from I-O therapies. We understand making the promise of I-O a reality for the many patients who may benefit from these therapies requires not only innovation on our part, but also close collaboration with leading experts in the field. Our partnerships with academia, government, advocacy and biotech companies support our collective goal of providing new treatment options to advance the standards of clinical practice. Bristol-Myers Squibb is a global biopharmaceutical company whose mission is to discover, develop and deliver innovative medicines that help patients prevail over serious diseases. For more information about Bristol-Myers Squibb, visit us at BMS.com or follow us on LinkedIn, Twitter, YouTube and Facebook. This press release contains “forward-looking statements” as that term is defined in the Private Securities Litigation Reform Act of 1995 regarding the research, development and commercialization of pharmaceutical products. Such forward-looking statements are based on current expectations and involve inherent risks and uncertainties, including factors that could delay, divert or change any of them, and could cause actual outcomes and results to differ materially from current expectations. No forward-looking statement can be guaranteed. Forward-looking statements in this press release should be evaluated together with the many uncertainties that affect Bristol-Myers Squibb’s business, particularly those identified in the cautionary factors discussion in Bristol-Myers Squibb’s Annual Report on Form 10-K for the year ended December 31, 2016 in our Quarterly Reports on Form 10-Q and our Current Reports on Form 8-K. Bristol-Myers Squibb undertakes no obligation to publicly update any forward-looking statement, whether as a result of new information, future events or otherwise.


Expert in immunotherapy will hold several key positions at NewYork-Presbyterian/Columbia NEW YORK, NY--(Marketwired - November 02, 2016) - Dr. Charles G. Drake has joined NewYork-Presbyterian/Columbia University Medical Center (CUMC) as director of genitourinary oncology and associate director for clinical research at the Herbert Irving Comprehensive Cancer Center, effective October 1. A nationally recognized expert in immunotherapy, Professor Drake will also serve as co-director of Columbia's Cancer Immunotherapy Program and on the faculty of CUMC. "Charles is one of the top minds in immunotherapy and in prostate cancer research and therapies," said Dr. Gary Schwartz, chief of the Division of Hematology/Oncology at NewYork-Presbyterian/Columbia University Medical Center, associate director for clinical research at the Herbert Irving Comprehensive Cancer Center, and Clyde '56 and Helen Wu Professor of Oncology (in Medicine). "By bringing him on, NewYork-Presbyterian/Columbia is establishing itself as an emerging powerhouse in immunotherapy, which will allow us to unlock the mysteries of our immune system so we can bring new hope to patients with prostate and other genitourinary malignancies." Dr. Drake is a physician-scientist with a Ph.D. in immunology, whose work focuses on understanding and fighting advanced-stage cancers with the immune system. He is known for rapidly incorporating discoveries made in the research lab into innovative clinical trials, including anti-tumor vaccines. His most recent work has focused on the body's immunological response to radiation therapy and how immunotherapy and radiation therapy can be used in concert to treat cancer. "Immunotherapy represents a new frontier in prostate cancer. We're also looking at how it can be used synergistically with traditional therapies, both in prostate cancer as well as in other tumor types," said Dr. Drake. "It is truly an honor to join NewYork-Presbyterian/Columbia, which has shown a deep commitment to building a world-class clinical and translational program in immunotherapy across the spectrum of cancers." Prior to joining NewYork-Presbyterian/Columbia, Dr. Drake served as the co-director of the Cancer Immunology Program at Johns Hopkins Kimmel Cancer Center. He was also a professor of oncology, urology, and immunology. Clinically, he served as a co-director of the Prostate Cancer Multi-Disciplinary Clinic and in the laboratory he developed a novel transgenic model of prostate cancer, in which a unique antigen is expressed exclusively in the prostate gland and in prostate tumors. Earlier in his Hopkins career, he was an associate professor in the Department of Oncology and an assistant professor of medical oncology at the institution's Kimmel Cancer Center. Dr. Drake was active in teaching, leading a small group in the medical school immunology course for many years. His research has been published in prestigious journals such as the New England Journal of Medicine, Cancer Research, the Journal of Clinical Investigation, and the Journal of Clinical Oncology. Dr. Drake received both his bachelor's degree in electrical engineering and his master's degree in biomedical engineering from Rutgers University. He completed a Ph.D. program at the National Jewish Center for Immunology and Respiratory Medicine at the University of Colorado Health Sciences Center, and later earned his M.D. from the University of Colorado as part of the MSTP program. He did his internship and residency in internal medicine on the Osler Medical Service of Johns Hopkins Hospital, and did his medical oncology fellowship training in the Johns Hopkins Department of Oncology. NewYork-Presbyterian is one of the nation's most comprehensive healthcare delivery networks, focused on providing innovative and compassionate care to patients in the New York metropolitan area and throughout the globe. In collaboration with two renowned medical school partners, Weill Cornell Medicine and Columbia University College of Physicians & Surgeons, NewYork-Presbyterian is consistently recognized as a leader in medical education, groundbreaking research and clinical innovation. NewYork-Presbyterian has four major divisions: NewYork-Presbyterian Hospital is ranked #1 in the New York metropolitan area by U.S. News and World Report and repeatedly named to the magazine's Honor Roll of best hospitals in the nation; NewYork-Presbyterian Regional Hospital Network is comprised of leading hospitals in and around New York and delivers high-quality care to patients throughout the region; NewYork-Presbyterian Physician Services connects medical experts with patients in their communities; and NewYork-Presbyterian Community and Population Health features the hospital's ambulatory care network sites and operations, community care initiatives and healthcare quality programs, including NewYork Quality Care, established by NewYork-Presbyterian, Weill Cornell and Columbia. NewYork-Presbyterian is one of the largest healthcare providers in the U.S. Each year, nearly 29,000 NewYork-Presbyterian professionals deliver exceptional care to more than 2 million patients. For more information, visit www.nyp.org and find us on Facebook, Twitter and YouTube. Columbia University Medical Center provides international leadership in basic, preclinical, and clinical research; medical and health sciences education; and patient care. The medical center trains future leaders and includes the dedicated work of many physicians, scientists, public health professionals, dentists, and nurses at the College of Physicians and Surgeons, the Mailman School of Public Health, the College of Dental Medicine, the School of Nursing, the biomedical departments of the Graduate School of Arts and Sciences, and allied research centers and institutions. Columbia University Medical Center is home to the largest medical research enterprise in New York City and State and one of the largest faculty medical practices in the Northeast. For more information, visit Columbia University Medical Center or Columbia University Medical Center Doctors.


Objective Response Rate (ORR) of 31%, One Confirmed Complete Response (CR) and Ten Confirmed Partial Responses (PRs) ORLANDO, Fla., Feb. 17, 2017 (GLOBE NEWSWIRE) --  Immunomedics, Inc., (NASDAQ:IMMU) (“Immunomedics” or “the Company”) today announced that sacituzumab govitecan (IMMU-132) is active in patients with metastatic urothelial cancer (UC) and has the potential to become a second line or later treatment to platinum-based or immuno-oncology therapy for these patients. “With larger numbers than the initial report, I remain impressed with the safety and efficacy results produced by sacituzumab govitecan in a difficult-to-treat patient population that had a median of two prior therapies and had extensive metastatic disease,” commented Dr. Scott T. Tagawa, the Richard A. Stratton Associate Professor in Hematology and Oncology, and an Associate Professor of Clinical Medicine and of Clinical Urology at Weill Cornell Medicine and an oncologist at NewYork-Presbyterian, who presented the results at the GU conference. “While patients with metastatic UC usually respond well to initial therapy with a platinum-containing regimen, few options are available after they become refractive. Second-line immune checkpoint-inhibitor (IO) therapy was recently approved by the FDA, such as atezolizumab and nivolumab, with expected approval of pembrolizumab as well. Although responders to the new IO therapy may do well for a prolonged period of time, about three-fourths do not respond and overall median PFS is less than 2.5 months and median OS less than 13 months have been reported,” added Dr. Tagawa, who has served as a consultant to Immunomedics. In the ongoing Phase 2 study with sacituzumab govitecan in metastatic UC, the ORR among 36 assessable patients was 31% (11/36), including one confirmed CR and ten confirmed PRs. The median duration of response for these ten patients was 7.5 months (95% confidence interval [CI], 4.4 to 12.9 months), with one patient having a PR for more than 18 months and continuing therapy. Overall, 69% of patients showed tumor shrinkage from baseline with sacituzumab govitecan therapy, and 14 patients are still under therapy. For the 41 intention-to-treat patients, median PFS was 7.2 months (95% CI, 6.7 to 11.7 months) and median OS was 15.5 months (95% CI, 8.9 to 17.2 months). Of the twelve patients with progression after prior IO therapy and chemotherapy, there were one unconfirmed PR and six patients with stable disease following sacituzumab govitecan treatment. The Company announced on February 10, 2017 that an exclusive global licensing agreement was entered into with Seattle Genetics (NASDAQ:SGEN), providing Seattle Genetics worldwide rights to develop, manufacture and commercialize sacituzumab govitecan in multiple indications, including UC. “We are pleased with these promising results, especially the long-term control of advanced disease in patients who failed multiple prior therapies, and look forward to working closely with Seattle Genetics to bring this important investigational product to cancer patients expeditiously,” stated Cynthia L. Sullivan, President and Chief Executive Officer of Immunomedics. Ms. Sullivan added, “We remain on target to commence our Phase 3 randomized trial in patients with advanced triple-negative breast cancer in March, and are working diligently to complete the submission of our Biologics License Application to FDA for Accelerated Approval of this indication.” In addition to Dr. Tagawa, other clinical investigators participating in this study include Drs. Allyson J. Ocean, Bishoy Faltas, and Ana Molina, his colleagues at NewYork-Presbyterian and Weill Cornell Medicine, New York, NY;  Dr. Elaine Lam, University of Colorado Cancer Center, Aurora, CO; Drs. Philip Saylor and Aditya Bardia, Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, MA; Dr. Julio J. Hajdenberg, UF Health Cancer Center-Orlando Health, Orlando, FL; Dr. Alicia K. Morgans, Vanderbilt-Ingram Cancer Center, Nashville, TN; Drs. Kevin Kalinsky and Emerson Lim, NewYork-Presbyterian/Columbia University Medical Center-Herbert Irving Comprehensive Cancer Center, New York, NY; and Dr. Matthew D. Galsky, Icahn School of Medicine Mount Sinai, Tisch Cancer Institute, New York, NY. A total of 44 patients with metastatic UC had been enrolled into this open-label multicenter study. Sites of metastases included liver (N=9; 25%), lymph nodes (N=14; 39%), lungs (N=14; 39%, pelvis (N=9, 25%), and bone (N=4; 11%). Patients received a median of six doses (range, 1-50) of sacituzumab govitecan, which was administered at 8 or 10 mg/kg on days 1 and 8 of 3-week cycles. Despite repeated dosing, grade 3 or higher adverse events were limited to neutropenia (30%), febrile neutropenia (11%), fatigue (11%), and diarrhea (3%). Treatment response was assessed by computed tomography (CT) every 8 weeks. Patients with more than 30% tumor shrinkage required confirmation within 4 to 6 weeks after the initial response in accordance with by RECIST 1.1 for single-arm studies. About Immunomedics Immunomedics (the “Company”) is a clinical-stage biopharmaceutical company developing monoclonal antibody-based products for the targeted treatment of cancer, autoimmune disorders and other serious diseases. Immunomedics’ advanced proprietary technologies allow the Company to create humanized antibodies that can be used either alone in unlabeled or “naked” form, or conjugated with radioactive isotopes, chemotherapeutics, cytokines or toxins. Using these technologies, Immunomedics has built a pipeline of eight clinical-stage product candidates. Immunomedics’ portfolio of investigational products includes antibody-drug conjugates (ADCs) that are designed to deliver a specific payload of a chemotherapeutic directly to the tumor while reducing overall toxic effects that are usually found with conventional administration of these chemotherapeutic agents. Immunomedics’ most advanced ADCs are sacituzumab govitecan (IMMU-132) and labetuzumab govitecan (IMMU-130), which are in Phase 2 trials for a number of solid tumors and metastatic colorectal cancer, respectively. IMMU-132 has received Breakthrough Therapy Designation from the FDA for the treatment of patients with triple-negative breast cancer who have failed at least two prior therapies for metastatic disease. Immunomedics has a research collaboration with Bayer to study epratuzumab as a thorium-227-labeled antibody. Immunomedics has other ongoing collaborations in oncology with independent cancer study groups. The IntreALL Inter-European study group is conducting a large, randomized Phase 3 trial combining epratuzumab with chemotherapy in children with relapsed acute lymphoblastic leukemia at clinical sites in Australia, Europe, and Israel. Immunomedics also has a number of other product candidates that target solid tumors and hematologic malignancies, as well as other diseases, in various stages of clinical and preclinical development. These include combination therapies involving its antibody-drug conjugates, bispecific antibodies targeting cancers and infectious diseases as T-cell redirecting immunotherapies, as well as bispecific antibodies for next-generation cancer and autoimmune disease therapies, created using its patented DOCK-AND-LOCK® protein conjugation technology. The Company believes that its portfolio of intellectual property, which includes approximately 306 active patents in the United States and more than 400 foreign patents, protects its product candidates and technologies. For additional information on the Company, please visit its website at www.immunomedics.com. The information on its website does not, however, form a part of this press release. Important Additional Information Immunomedics, Inc. (the “Company”), its directors and certain of its executive officers will be deemed to be participants in the solicitation of proxies from Company stockholders in connection with the matters to be considered at the Company’s 2016 Annual Meeting. The Company has filed a definitive proxy statement and form of WHITE proxy card with the U.S. Securities and Exchange Commission (the “SEC”) in connection with any such solicitation of proxies from Company stockholders. COMPANY STOCKHOLDERS ARE STRONGLY ENCOURAGED TO READ THE DEFINITIVE PROXY STATEMENT (INCLUDING ANY AMENDMENTS AND SUPPLEMENTS), THE ACCOMPANYING WHITE PROXY CARD AND ANY OTHER RELEVANT DOCUMENTS THAT THE COMPANY FILES WITH THE SEC WHEN THEY BECOME AVAILABLE BECAUSE THEY WILL CONTAIN IMPORTANT INFORMATION. Information regarding the identity of participants, and their direct or indirect interests, by security holdings or otherwise, is set forth in the proxy statement and other materials filed by the Company with the SEC.  Stockholders will be able to obtain the proxy statement, any amendments or supplements to the proxy statement and other documents filed by the Company with the SEC for no charge at the SEC’s website at www.sec.gov. Copies will also be available at no charge at the Company’s website at www.immunomedics.com, by writing to Immunomedics, Inc. at 300 The American Road, Morris Plains, New Jersey 07950, or by calling the Company’s proxy solicitor, MacKenzie Partners, Inc. at (212) 929-5500, or by calling Dr. Chau Cheng, Senior Director, Investor Relations & Corporate Secretary, (973) 605-8200, extension 123. Forward-Looking Statements This release, in addition to historical information, may contain forward-looking statements made pursuant to the Private Securities Litigation Reform Act of 1995. Such statements, including statements regarding clinical trials (including the funding therefor, anticipated patient enrollment, trial outcomes, timing or associated costs), regulatory applications and related timelines, out-licensing arrangements (including the timing and amount of contingent payments under the licensing and development agreement with Seattle Genetics), forecasts of future operating results, potential collaborations, and capital raising activities, involve significant risks and uncertainties and actual results could differ materially from those expressed or implied herein. Factors that could cause such differences include, but are not limited to, the Company’s dependence on business collaborations or availability of required financing from capital markets, or other sources on acceptable terms, if at all, in order to further develop our products and finance our operations, new product development (including clinical trials outcome and regulatory requirements/actions), the risk that we or any of our collaborators may be unable to secure regulatory approval of and market our drug candidates, risks associated with the outcome of pending litigation and competitive risks to marketed products, and the Company’s ability to repay its outstanding indebtedness, if and when required, as well as the risks discussed in the Company’s filings with the Securities and Exchange Commission. The Company is not under any obligation, and the Company expressly disclaims any obligation, to update or alter any forward-looking statements, whether as a result of new information, future events or otherwise.


News Article | January 29, 2016
Site: www.biosciencetechnology.com

A comprehensive analysis of the molecular characteristics of gliomas—the most common malignant brain tumor—explains why some patients diagnosed with slow-growing (low-grade) tumors quickly succumb to the disease while others with more aggressive (high-grade) tumors survive for many years. The multinational study suggests a new way of classifying gliomas that may have a significant impact on patient management and may lead to the development of more targeted therapies. The paper, co-led by researchers from Columbia University Medical Center (CUMC), USA, Ribeirão Preto Medical School (FMRP) at the University of São Paulo (USP), Brazil, and The University of Texas MD Anderson Cancer Center, Houston, Texas, USA, was published in the journal Cell. Currently, pathologists determine if a glioma is low-grade or high-grade based on the tumor tissue’s appearance under the microscope. “While this approach is generally good at distinguishing between gliomas that are clearly very aggressive and those that are relatively slow-growing, it misses the mark in a significant percentage of cases, leading to inappropriate treatment,” said co-senior author Antonio Iavarone, M.D., professor of neurology and pathology and cell biology (in the Institute for Cancer Genetics) at CUMC and a member of the Herbert Irving Comprehensive Cancer Center (HICCC) at NewYork-Presbyterian /Columbia University Medical Center. “Instead, by looking at the molecular makeup of these tumors, we now have a much more precise way of predicting which tumors are more likely to grow rapidly and can prescribe treatments accordingly.” Other researchers have attempted to classify gliomas according to their genetic characteristics. One study found that tumors with mutations in a gene called IDH were significantly less aggressive than those without the mutation, known as IDHwildtype tumors. However, these findings did not fully explain why some patients with IDHmutant tumors fare worse than expected and some with IDHwildtype tumors fare better than expected. Other studies suggested that a glioma’s level of DNA methylation, an epigenetic process that cells use to control gene expression, might explain a tumor’s aggressiveness, but the evidence was inconclusive. In this study, Dr. Iavarone and his colleagues analyzed 1,122 high and low grade glioma samples from the Cancer Genome Atlas, looking for epigenetic changes in the tumors’ DNA. The researchers found that the best predictor of progression in an IDHmutant glioma—the less-aggressive variety—is its level of DNA methylation. Among IDHmutant gliomas, those with a high degree of DNA methylation progressed more slowly. However, tumors with less DNA methylation, about 6 percent of the total, progressed very quickly. “Based on their appearance under the microscope, these aggressive tumors looked very much like the other IDHmutant tumors,” said Dr. Iavarone. “But from a disease prognosis standpoint, they progressed quite similarly to the more lethal subset of IDHwildtype gliomas,” said Dr. Iavarone. Among those with IDHwildtype gliomas—the most aggressive type—a small subset (about 6 percent) had relatively favorable clinical outcomes. The molecular characteristics of this group were similar to those of pilocytic astrocytomas, a childhood brain tumor with a relatively favorable survival rate. “The present study advances the understanding of the glioma division by correlating each subtype of DNA methylation with a distinct clinical outcome,” said co-senior author Houtan Noushmehr, Ph.D., professor of epigenomics and bioinformatics at University of São Paulo and director of the OMICs and Bioinformatics lab at FMRP at Ribeirão Preto, São Paulo. “We discovered low grade and high grade gliomas mixed together within these different epigenetic subtypes. This was an unexpected finding and allowed us to further understand the progression of gliomas within the different subtypes,” said Dr. Noushmehr. “This research has expanded our knowledge of the glioma somatic alteration landscape and emphasized the relevance of DNA methylation profiles as a method for clinical classification,” said senior co-author Roel Verhaak, Ph.D., associate professor of bioinformatics and computational biology MD Anderson. “These findings are an important step forward in our understanding of glioma as discrete disease subsets, and the mechanism driving glioma formation and progression.” The paper also identified several previously unrecognized genetic alterations that may contribute to glioma development, highlighting potential new targets for drug therapy. “This study, which focused on tumor classification, does not point to specific therapies for glioma,” said Dr. Iavarone. “But our findings will help clinicians identify subsets of patients with IDHmutant tumors who need to be treated more aggressively and those with IDHwildtype tumors who can be spared aggressive treatment.”


News Article | November 10, 2016
Site: www.prweb.com

The Society for Immunotherapy of Cancer’s (SITC) 31st Annual Meeting & Associated Programs (SITC 2016) kicked off on November 9 with an exciting program aimed at basic, translational and clinical researchers interested in novel immune-based agents and combinations. The New Cancer Immunotherapy Agents in Development session featured brief, rapid-fire presentations on clinical and pre-clinical studies of novel target molecules, drug mechanisms of action and combination approaches. A lively extended panel discussion among leaders from industry, government and academia followed, helping attendees bring these data into context at a time when clinicians are eager for new therapeutic options for patients. Combination immunotherapy approaches, especially those including blockade of the PD-1/PD-L1 immune checkpoint pathway, dominated both the clinical and pre-clinical sessions. Many of the combination strategies presented aimed to augment the antitumor immune response either by stimulating the patient’s own immune response or by blocking inhibitory signals that limit immune system activity. Other clinical agents targeted the other side of the equation – the tumor microenvironment — rather than the patient’s immune system. In combination with immune checkpoint inhibitors, these agents combat evasion strategies used by the tumor to exclude immune cell involvement. Clinical data for two monotherapy approaches were also presented, including a novel adoptive cellular therapy based on modified NK cells, and an agent designed to recruit immune cells to the site of the tumor, inflaming “cold” tumors to improve clinical outcomes. The pre-clinical session showcased creative strategies to mobilize antitumor immunity, including two different bispecific antibodies targeting T cells. One of the agents functioned to generate a more potent antitumor response by binding to a tumor antigen and simultaneously inducing T cell activation by clustering the T cell costimulatory molecule 4-1BB. In the other approach, researchers highlighted a bispecific antibody that remains inert until activated by factors specific to the tumor microenvironment, as a means of limiting systemic toxicities. In a different strategy, investigators modified the immune-stimulating properties of an attenuated Listeria monocytogenes platform to facilitate tumor antigen recognition. Aiming to build on the success of injected immune checkpoint inhibitors but make treatment less invasive, an oral checkpoint inhibitor was presented, as were various novel combinations of innate immune activators, or novel immune checkpoint molecules with PD-1/PD-L1 pathway blockers. One promising approach to overcome tumor cells’ ability to evade attack by the T cells engineered to recognize them (CAR T cells) was the development of a CAR T cell modified to express “decoy” PD-1 receptors, thereby avoiding the need for repeated anti-PD-1 injections. Leading the Strategic Considerations of Combinations and Biomarkers in New Agent Development session, Charles G. Drake, MD, PhD (Columbia University Herbert Irving Comprehensive Cancer Center) focused on different immunotherapy combination strategies, including dual immunotherapy approaches and combinations of immunotherapy with conventional therapies. Dr. Drake emphasized the mechanistic basis for the clinical efficacy of particular combinations and explained how this information can inform the development of rational combinations in the future. Opening the extended panel discussion, the multidisciplinary panel members and attendees were invited to consider the implications of the fact that more than 800 combination immunotherapy approaches are currently in clinical trials. Panel discussants were uniformly optimistic about the influx of potential new treatment strategies. “The enormous number of clinical trials with multiple combination agents will help identify what works and what is safe, and the new technologies being applied to these efforts will tell us how it works,” said Gordon J. Freeman, PhD (Dana-Farber Cancer Institute). The optimization of drug development and the integration of biomarkers into clinical decision-making were also identified as critical to ensuring that only the most promising trials are selected to move forward. ABOUT SITC Established in 1984, the Society for Immunotherapy of Cancer (SITC) is a non-profit organization of medical professionals dedicated to improving cancer patient outcomes by advancing the development, science and application of cancer immunotherapy and tumor immunology. SITC is comprised of influential basic and translational scientists, practitioners, healthcare professionals, government leaders and industry professionals around the globe. Through educational initiatives that foster scientific exchange and collaboration among leaders in the field, SITC aims to one day make the word “cure” a reality for cancer patients everywhere. Learn more about SITC, our educational offerings and other resources at sitcancer.org and follow us on Twitter, LinkedIn, Facebook and YouTube. # # #


Klein U.,Herbert Irving Comprehensive Cancer Center | Dalla-Favera R.,Herbert Irving Comprehensive Cancer Center | Dalla-Favera R.,Columbia University
Seminars in Cancer Biology | Year: 2010

Chronic lymphocytic leukemia (CLL), an incurable disease of the elderly, stands out as unique among the malignancies derived from mature B lymphocytes. The histology, immunophenotype, immunoglobulin variable region (IgV) gene somatic hypermutation status, and the pattern of genetic alterations of the tumor cells are markedly distinct from that of any other B-cell tumor. Most notably, CLL cases can have somatically mutated as well as unmutated IgV genes which largely correlate with a favorable and unfavorable clinical prognosis, respectively. Moreover, recent evidence suggests that 6% of the normal elderly population develops a monoclonal B-cell lymphocytosis (MBL) that appears as the precursor to CLL in 1-2% of cases. Over the last decade, global gene expression profile analysis was instrumental in defining CLL as a malignancy originating from the oncogenic transformation of a common cellular precursor that resembles an antigen-experienced B cell. These findings were complemented by the realization that all CLL, independent of their IgV gene somatic mutation status, express B-cell receptors (BCRs) that show evidence of antigen-experience. Indeed, the BCRs of CLL cases among different individuals can be similar to the extent that one was able to define subsets of stereotyped receptors based on the homology in the antigen-binding regions. Together, these observations strongly support the notion that antigen plays a critical role in CLL pathogenesis. This role is complemented by genetic alterations that, analogous to most cancer types, represent the initiating pathogenetic event. In fact, CLL cases display recurrent genetic aberrations including trisomy 12 and monoallelic or biallelic deletion/inactivation of chromosomal regions 17p, 11q and 13q14. However, virtually all CLL cases lack balanced reciprocal chromosomal translocations, the genetic hallmark of germinal center (GC)-derived lymphomas. The most frequent genetic aberration in CLL, deletion of chromosomal region 13q14, was recently shown to have a specific role in CLL pathogenesis. This region encodes a tumor suppressor locus comprising a microRNA cluster embedded in a long sterile RNA gene, whose deletion in the mouse leads to lymphoproliferative syndromes recapitulating the human CLL-associated spectrum, including MBL, CLL and B-cell non-Hodgkin lymphoma (B-NHL). This review will focus on the cellular origin of CLL, its relationship to the mechanisms of generating CLL-associated genetic lesions and on the role of the 13q14 deletion in CLL pathogenesis as emerging from the analysis of a newly generated mouse model. andcopy; 2010 Elsevier Ltd.


Acharyya S.,Columbia University | Acharyya S.,Herbert Irving Comprehensive Cancer Center | Massague J.,Sloan Kettering Cancer Center
Cell Research | Year: 2016

It is becoming increasingly clear that leukocytes dynamically regulate cancer progression and metastasis, and among leukocytes, granulocytic cells abundantly accumulate in metastatic organs; however, their function in metastasis remains controversial. In a recent report in Nature, Wculek and Malanchi clarify the role of mature neutrophils as mediators of metastatic initiation and provide a targeted approach to prevent the pro-metastatic activity of neutrophils in breast cancer models.


Paoluzzi L.,Columbia University | Scotto L.,NYU Langone Medical Center | Marchi E.,NYU Langone Medical Center | Zain J.,NYU Langone Medical Center | And 2 more authors.
Clinical Cancer Research | Year: 2010

Purpose: Romidepsin and belinostat are inhibitors of histone deacetylases (HDACI). HDACIs are known to induce cell death in malignant cells through multiple mechanisms, including upregulation of death receptors and induction of cell cycle arrest. They are also known to be prodifferentiating. Mantle cell lymphoma (MCL) is an aggressive subtype of non-Hodgkin lymphoma characterized by the t(11;14) (q13;q32) translocation leading to the overexpression of cyclin D1. Experimental Design: Assays for cytotoxicty including mathematical analysis for synergism, flow-cytometry, immunoblottings, and a xenograft severe combined immunodeficient beige mouse model were used to explore the in vitro and in vivo activity of romidepsin and/or belinostat alone or in combination with the proteasome inhibitor bortezomib in MCL. Results: In vitro, romidepsin and belinostat exhibited concentration-dependent cytotoxicity against a panel of MCL cell lines. Both HDACI showed strong synergism when combined with the proteasome inhibitor bortezomib in MCL. An HDACI plus bortezomib also induced potent mitochondrial membrane depolarization and apoptosis, whereas no significant apoptosis was observed in peripheral blood mononuclear cells from healthy donors with the combination. These events were associated with a decrease in cyclin D1 and Bcl-XL, and an increase in accumulation of acetylated histone H3, acetylated α-tubulin, and Noxa in cell lines. In a severe combined immunodeficient beige mouse model of MCL, the addition of belinostat to bortezomib enhanced efficacy compared with either drug alone. Conclusions: Collectively, these data strongly suggest that HDACI such as romidepsin or belinostat in combination with a proteasome inhibitor could represent a novel and rationale platform for the treatment of MCL. ©2010 AACR.

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