Theater Benefits to Fund Cancer Research
Our Theater Benefits offer the chance to attend a dinner at a premier New York restaurant, followed by tickets to a successful or highly anticipated Broadway show. Guests also have the opportunity to hear first-hand from the scientists themselves about the impact of Damon Runyon funding.
Fall Theater Benefit: Hamilton
On September 16, 2015, see this year's most highly anticipated show on Broadway and support cancer research! Following an amazing sold-out run at The Public Theater, Lin-Manuel Miranda's critically acclaimed Hamilton will move to Broadway this summer. From the creative team behind the Tony Award-winning In the Heights comes a wildly inventive musical about the scrappy young immigrant who forever changed America: Alexander Hamilton. Lin-Manuel Miranda takes the stage as the unlikely founding father determined to make his mark on a new nation as hungry and ambitious as he is.Don't miss out! See one of Broadway's most buzzed about shows while supporting new generations of innovative cancer researchers. Hamilton Theater Benefit Wednesday, September 16, 2015 Dinner / 5:30pm Performance / 8:00pm Richard Rodgers Theatre 226 West 46th Street (between Broadway and 8th Avenue) Tickets are $600. For more information or to reserve your Theater Benefit tickets today, please call at 212.455.0501 or email email@example.com.
March 30, 2015 > New drug combination promising for treating aggressive breast cancer in brain
Carey K. Anders, MD (Damon Runyon Clinical Investigator ’12-’15), and C. Ryan Miller, MD, PhD (Damon Runyon Clinical Investigator ’09-’12) of UNC Lineberger Comprehensive Cancer Center, Chapel Hill, and colleagues, reported that they identified a drug treatment strategy that can improve survival for a particularly aggressive breast cancer sub-type (triple negative breast cancer) after it has spread to the brain. They demonstrated, in a mouse model of this cancer, that a combination of the drugs carboplatin and a PARP inhibitor improved survival. The researchers hope that these findings will lead to a clinical trial that would allow researchers to test this treatment strategy in patients. These results were published in the journal Molecular Cancer Therapeutics.
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March 26, 2015 > Blocking cellular mechanism may make chemotherapy more effective
Maximilian W. Popp, PhD (HHMI-Damon Runyon Fellow ’12-’15) and colleagues at the University of Rochester, Rochester, discovered that stopping a cellular quality-control mechanism can make chemotherapy more effective. This mechanism is called NMD (nonsense-mediated mRNA decay). The researchers found that exposing breast cancer cells to a molecule that inhibits NMD prior to treatment with doxorubicin, a drug used to treat leukemia, breast, bone, lung and other cancers, speeds cancer cell death. The results provide insights that could lead to new treatment strategies for cancer patients in the future. These findings were published in the journal Nature Communications.
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March 25, 2015 > Genetics underlying rare blood cancer identified
Eirini Papapetrou, MD, PhD (Damon Runyon-Edward P. Evans Foundation Innovator ’13-’16) of Icahn School of Medicine at Mount Sinai, New York, reported the results of a technique called cellular reprogramming that takes mature blood cells from patients with myelodysplastic syndrome (MDS) and reprograms them back into stem cells to study the genetic origins of MDS. MDS is a rare blood cancer that can progress into acute leukemia; its causes are not well understood. Her team was able to define a region on chromosome 7 that is critical to MDS and identify candidate genes in the region that may underlie the disease. The findings were published in the journal Nature Biotechnology.
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March 24, 2015 > Metformin and Vitamin D3 show promise in colorectal cancer prevention
Li Li, MD, PhD (Damon Runyon Clinical Investigator ’01-’06), of Case Western Reserve University, Cleveland, and colleagues, demonstrated that a combination of the diabetes drug metformin and vitamin D3 work together to prevent colorectal cancer in two animal models. They plan to advance these findings to develop clinical trials in humans. These results were reported in the journal Cancer Prevention Research.
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March 19, 2015 > American Association for Cancer Research names recipient of prestigious award
William C. Hahn, MD, PhD (Damon Runyon Fellow ’98-’99) of the Dana-Farber Cancer Institute, Boston, will be honored with the 39th annual AACR-Richard and Hinda Rosenthal Memorial Award. He is being recognized for his seminal contributions to the understanding of the mechanisms underlying cancer initiation, maintenance, and progression. His work has defined new paradigms and has provided a foundation for novel therapeutic approaches that are being tested in the clinic. He will receive the award at the AACR Annual Meeting 2015 in April.
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Annual Breakfast to Support Cancer Research
Held at a premier New York City location, our Annual Breakfast is an entertaining cancer fundraising event that gives guests the chance to learn about the important work of our scientists and network with well known New Yorkers – all before the work day starts.
Thank you to those who joined us on Tuesday, May 5, 2015, for the Damon Runyon Cancer Research Foundation's Annual Breakfast. The Foundation honored Dmitri Stockton, President and CEO of GE Asset Management, and recognized GE Asset Management for its longstanding partnership with the Foundation to invest in new generations of innovative researchers. John Elway, legendary quarterback and Executive Vice President of Football Operations and General Manager for the Denver Broncos, joined us to talk about his family's experience with cancer and the importance of funding future research leaders. Guests also heard from two Damon Runyon scientists, Moritz F. Kircher, MD, PhD, of Memorial Sloan Kettering Cancer Center and Angela J. Waanders, MD, of the Children's Hospital of Philadelphia, who discussed their current projects and the importance of supporting cutting edge cancer research.
March 5, 2015 > Genome-wide screen gives insight on cancer metastasis and tumor evolution
Sidi Chen, PhD (Damon Runyon-Dale F. Frey Scientist ‘15, Damon Runyon Fellow ’12-’15) and Feng Zhang, PhD (Damon Runyon-Rachleff Innovator ’12-’14), of the Broad Institute and MIT’s David H. Koch Institute for Integrative Cancer Research, Cambridge, used CRISPR-Cas9 gene-editing technology to systematically target every gene in the genome in an animal model. The study revealed genes involved in tumor evolution and metastasis, including some well-known tumor suppressor genes as well as novel genes not previously linked to cancer. The work was published in the journal Cell.
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Industry and Academic Researchers Gather for Innovative Accelerating Cancer Cures Research Symposium
Accelerating Cancer Cures is a unique collaboration between Damon Runyon, a prestigious cancer charity that supports cutting-edge early career cancer researchers, and leading biopharmaceutical companies. The goal of this multi-million dollar initiative is to rebuild the ranks of specially trained physician-scientists who conduct both the innovative laboratory research necessary to identify new therapeutics and the clinical trials to bring these new treatments to patients. By collaborating on this initiative with their competitors in the marketplace, the companies involved demonstrate their shared commitment to driving the next generation of breakthroughs in cancer prevention, diagnosis and treatment.
Richard B. Gaynor, MD, Senior Vice President of Global Development/Medical Affairs for Lilly Oncology, Damon Runyon Board member, and Chair of Accelerating Cancer Cures, opened the meeting by welcoming its attendees and stressing the urgency of collaboration between academia and industry at this crucial moment in cancer research. Jedd D. Wolchok, MD, PhD, Chief of the Melanoma and Immunotherapeutics Service and Lloyd J. Old Chair in Clinical Investigation at Memorial Sloan Kettering Cancer Center, delivered a keynote address about his groundbreaking work identifying and developing new immunotherapies for advanced melanoma and other cancers. Participants also heard research presentations from selected Damon Runyon scientists and enjoyed industry roundtable discussions on bridging the gap between academia and industry. Lorraine Egan, President and CEO of Damon Runyon, provided opening remarks.
”It is extraordinary that industry competitors have come together to address a major obstacle to developing new treatments for cancer patients,” said Damon Runyon Cancer Research Foundation President and CEO, Lorraine Egan. “Through Accelerating Cancer Cures, we are ensuring that the best young physician-scientists can continue to be the critical link between the research lab and the patients.”
Gaynor added, “This is an exciting time in cancer research with major discoveries in both genetics and immunology leading to innovative cancer therapies. Today we heard presentations from young investigators who are at the forefront of these discoveries bringing novel insights from the laboratory into the clinic. The efforts of the Damon Runyon Foundation and programs like Accelerating Cancer Cures are helping to make the hope of new cancer therapies a reality.”
Scientists from the nation’s leading research institutions, including Stanford University School of Medicine, Memorial Sloan Kettering Cancer Center, Weill Cornell Medical College, Huntsman Cancer Institute of the University of Utah, Mayo Clinic, City of Hope, and the Dana-Farber Cancer Institute attended the symposium to hear presentations on a diverse range of promising research, from novel new mechanisms to identify drug targets to genomic approaches to understanding drug resistance, and to brainstorm about creative approaches to speed new treatments to cancer patients.
Accelerating Cancer Cures is supported by some of the world’s leading companies including:Eli Lilly and Company, Celgene, Genentech, Merck, Pfizer, and Takeda Pharmaceuticals International Co. For more information, visit www.damonrunyon.org/accelerate.
100% of all donations to the Foundation are used to support scientific research. Its administrative and fundraising costs are paid from its Damon Runyon Broadway Tickets Service and endowment.
For more information visit http://www.damonrunyon.org.
February 2, 2015 > New pathway for slowing BRCA tumor growth
Agnel Sfeir, PhD (Damon Runyon-Rachleff Innovator ‘13-‘15) and colleagues at New York University School of Medicine, New York, reported that inhibiting the action of a particular enzyme called polymerase theta, or PolQ, dramatically slows the growth of tumor cells containing BRCA1 and BRCA2 genetic mutations. This could have an impact on breast and ovarian cancers. The findings were published in the journal Nature.
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Damon Runyon Cancer Research Foundation Grants Prestigious Fellowship, Breakthrough Scientist Awards
Grants totaling $3.76M give early career investigators independence to pursue novel ideas
New York, NY (January 30, 2015) – The Damon Runyon Cancer Research Foundation, a non-profit organization focused on supporting innovative early career researchers, named 15 new Damon Runyon Fellows at its fall Fellowship Award Committee review. The recipients of this prestigious, four-year award are outstanding postdoctoral scientists conducting basic and translational cancer research in the laboratories of leading senior investigators across the country. The Fellowship encourages the nation's most promising young scientists to pursue careers in cancer research by providing them with independent funding ($208,000 each for basic scientists, $248,000 for physician-scientists) to work on innovative projects.
The Committee also named six new recipients of the Damon Runyon-Dale F. Frey Award for Breakthrough Scientists. This award provides additional funding to scientists completing a prestigious Damon Runyon Fellowship Award who have greatly exceeded the Foundation's highest expectations and are most likely to make paradigm-shifting breakthroughs that transform the way we prevent, diagnose and treat cancer. Each awardee will receive $100,000 to be used toward their research.
Recipients of the Damon Runyon-Dale F. Frey Award for Breakthrough Scientists:
Angela N. Brooks, PhD (Damon Runyon Fellow ‘12-‘15)
Dana-Farber Cancer Institute, Boston
Dr. Brooks is developing computational and experimental approaches to study genomic changes that give rise to cancer. She designed a powerful new computational tool that she used to analyze data from The Cancer Genome Atlas; she identified and characterized specific genetic alterations in lung adenocarcinoma tumors that disrupt a process called splicing. Her goal for the future is to expand her computational analysis to build a database of splicing alterations in many different cancers and to apply these genomic studies to understudied human populations.
Sidi Chen, PhD (Damon Runyon Fellow ‘12-‘15)
Massachusetts Institute of Technology, Cambridge
Dr. Chen aims to understand the relationship between small RNAs (microRNAs) and cancer. Small RNAs are important regulators of genetic networks inside the cell; perturbation of these networks can lead to malignant cell growth. He is studying the role of microRNAs in tumor metastasis, or spread, in models of lung and liver cancers and will validate his findings using clinical and genomic data from human patients. His goal is to accelerate the development of more effective diagnostics and therapeutics for cancer by targeting microRNAs.
Robert K. McGinty, MD, PhD (Damon Runyon Fellow ‘12-‘16)
Pennsylvania State University, University Park
Dr. McGinty is examining the structure and function of enzymes called methyltransferases. His structural biology approach has already revealed unexpected roles for certain of these enzymes. As these enzymes are commonly misregulated in human leukemias, an understanding of their normal function may provide insight into novel platforms for drug development.
Michael J. Smanski, PhD (Damon Runyon Fellow ‘12-‘14)
University of Minnesota, Saint Paul
Dr. Smanski seeks to develop a new platform for accelerating the discovery of anticancer agents from natural sources. He will use "gene cluster" sequence information from microbes to produce anticancer agents in the laboratory. His ultimate goal is to demonstrate that this technique can be used to rapidly produce drug-like molecules in a highly efficient manner.
Angela J. Waanders, MD, MPH (Damon Runyon-Sohn Pediatric Cancer Fellow ‘12-‘15)
Children's Hospital of Philadelphia, Philadelphia
Dr. Waanders is committed to developing more effective treatments for the many children diagnosed with brain tumors each year. Mutations in BRAF, an oncogene that can drive cancer growth, are prevalent in pediatric astrocytomas. Her research has shown that different BRAF mutations identified in these tumors respond differently to targeted BRAF treatments and suggests that combination therapies may be highly effective. Her continued studies will be the basis for moving novel, targeted treatment strategies into the clinic to treat the children afflicted by this devastating cancer.
Arun P. Wiita, MD, PhD (Damon Runyon Fellow ‘12-‘14)
University of California, San Francisco
Dr. Wiita is using emerging technologies to study response to chemotherapy in multiple myeloma. He aims to characterize the genetic changes that underlie development and progression of the disease, and determine how these changes may predict sensitivity to chemotherapy. His goal is to use this information to enable more effective individualized chemotherapeutic regimens for cancer patients.
November 2014 Damon Runyon Fellows:
Anupam K. Chakravarty, PhD [HHMI Fellow], with his sponsor Daniel F. Jarosz, PhD, at Stanford University School of Medicine, Stanford, is investigating heritable physical structures, called higher order assemblies, formed upon overexpression of RNA binding proteins. These proteins are consistently overexpressed in multiple cancers. His research will illuminate the mechanism of assembly formation and its role in altering gene regulation, thereby suggesting novel avenues to potential therapeutic intervention.
Matthew R. Clay, PhD [HHMI Fellow], with his sponsor David R. Sherwood, PhD, at Duke University, Durham, is studying how cells in their natural environment move across basement membranes-the extracellular matrix of proteins that surrounds tissues. Basement membrane "breaching" is the first step of cell invasion, which underlies cancer metastasis. These studies will uncover fundamental mechanisms that govern cell invasion and drive the deadly progression of cancers.
Ronald J. Hause, PhD, with his sponsor Jay A. Shendure, MD, PhD, at the University of Washington, Seattle, is developing new experimental and analytical methods to better understand, interpret and predict how genetic mutations affect individuals' risks for cancers and responses to chemotherapy. He will use a combination of genomic, biochemical, and machine learning approaches to investigate and model the effects of all possible mutations of a gene involved in chemotherapeutic drug response and relate these results to patient outcome.
Kai Mao, PhD, with his sponsor Gary Ruvkun, PhD, at Massachusetts General Hospital, Boston, is studying the cell's cytoskeleton, which provides the physical structure and shape of a cell. The cytoskeleton is an attractive target for cancer chemotherapy because of its central function in mitosis or cell division, but these chemotherapeutic agents have very high toxicity. He hypothesizes that the next generation of chemotherapy will benefit from the inhibition of these toxin response pathways.
Rand M. Miller, PhD, with his sponsor Tarun M. Kapoor, PhD, at The Rockefeller University, New York, is interested in understanding the mechanisms by which cancers become resistant to chemotherapeutic agents. Many cancers acquire resistance to drugs by overproducing molecular "pumps" called multidrug resistance proteins, which actively export the toxic drug molecules out of cells. Using a variety of chemical techniques, he will investigate how these pumps mediate drug resistance in cancers, as well as their roles in the maintenance of healthy cellular function.
Sigrid Nachtergaele, PhD, with her sponsor Chuan He, PhD, at The University of Chicago, Chicago, is investigating the roles of a chemical modification of mRNA called methylation. Many enzymes that add and remove RNA modifications impact developmental processes and cancer proliferation, but how they are regulated remains a mystery. She aims to identify the mechanisms by which mRNA methylation alters gene expression and eventually results in altered cell signaling and growth.
Thomas Norman, PhD, with his sponsor Jonathan Weissman, PhD, at the University of California, San Francisco, is investigating the role that "epigenetic" differences play in cancer cells' ability to develop drug resistance. These epigenetic changes result in altered gene expression. He will use a new technique called CRISPRi to systematically tune the expression of different parts of the genome and measure their effects on drug resistance. He hopes that these studies will identify new avenues for reducing resistance and expand our knowledge of the role epigenetic factors play in leukemia and other cancers.
Magdalena E. Potok, PhD [HHMI Fellow], with her sponsor Steven E. Jacobsen, PhD, at University of California, Los Angeles, is investigating how gene expression is controlled by heterochromatin (the physically compacted form of DNA) and genomic instability. In certain plants, reduction in a chemical mark on the chromatin, called H3K27me1, results in heterochromatin decompaction, abnormal gene expression and the production of extra DNA from certain regions. Extra copies of DNA are a sign of genomic instability often observed in cancers.
William Razzell, PhD [HHMI Fellow], with his sponsor Jennifer A. Zallen, PhD, at Memorial Sloan Kettering Cancer Center, New York, is using cell biological, molecular genetic, and biophysical approaches to understand how cell-derived mechanical forces contribute to tumorigenesis through the modulation of cellular signaling pathways. He will focus on one pathway that is responsive to mechanical forces, the Hippo pathway, which prevents excessive tissue growth during development.
David W. Taylor, PhD, with his sponsor Eva Nogales, PhD, at the University of California, Berkeley, is studying the structural biology of bacterial CRISPR-Cas surveillance complexes, which have been adopted as versatile genome engineering tools. He aims to decipher the principles by which these complexes function and to apply them for cancer research and therapeutics.
Albert Tsai, PhD, with his sponsor Robert H. Singer, PhD, at HHMI Janelia Farm Research Campus, Ashburn, is studying a process called translation, by which messenger RNAs (mRNAs) are decoded into proteins. A hallmark of cancer cells is distorted patterns of protein production, leading to uncontrolled growth and invasive behavior. He is using novel microscope technology to image live cells in real-time and developing techniques to image individual protein molecules during their synthesis, thereby linking the time, location and amount of protein production to individual mRNAs.
Jeanine L. Van Nostrand, PhD, with her sponsor Reuben J. Shaw, PhD, at the Salk Institute, La Jolla, aims to understand how signaling pathways involved in the energetic and metabolic stress responses prevent cancer. She will generate models harboring specific mutations that prevent the stress response, and evaluate the effects of these mutations on lung cancer development.
Aaron D. Viny, MD, with his sponsor Ross L. Levine, MD, at Memorial Sloan Kettering Cancer Center, New York, is studying the oncogenic role of abnormalities in the cohesin complex-a group of proteins that function to align and stabilize sister chromatids (copies of the chromosomes) during cell division. Mutations within several proteins in this complex have been identified in solid tumors and hematologic malignancies, particularly acute myeloid leukemia, the most common adult leukemia.
Jonathan R. Whicher, PhD, with his sponsor Roderick MacKinnon, MD, at The Rockefeller University, New York, focuses on a cellular structure called the voltage-gated potassium channel Eag1, which can promote tumor growth and is aberrantly expressed in many types of cancer including breast, colon, prostate, lung, and liver. He is determining the structure and mechanism of Eag1 in order to elucidate how Eag1 promotes cancer growth, with the eventual goal of developing Eag1 modulators as potential anti-cancer therapies.
Andrew L. Wolfe, PhD, with his sponsor Ramon Parsons, MD, PhD, at the Icahn School of Medicine at Mount Sinai, New York, studies PTEN, an anti-cancer protein that opposes cell growth and can induce cancer cells to die. Loss of PTEN protein has been detected in nearly every form of cancer and is associated with drug resistance and poor clinical outcome. A new, longer form of PTEN, called PTEN-L, was recently discovered. He aims to answer fundamental questions about the mechanism and function of PTEN-L, which will characterize the expression and regulation of this important anti-cancer protein for the first time.
To accelerate breakthroughs, the Damon Runyon Cancer Research Foundation provides today's best young scientists with funding to pursue innovative research. The Foundation has gained worldwide prominence in cancer research by identifying outstanding researchers and physician-scientists. Twelve scientists supported by the Foundation have received the Nobel Prize, and others are heads of cancer centers and leaders of renowned research programs. Each of its award programs is extremely competitive, with less than 10% of applications funded. Since its founding in 1946, the Foundation has invested over $287 million and funded more than 3,460 young scientists. This year it will commit over $15 million in new awards to brilliant young investigators.100% of all donations to the Foundation are used to support scientific research. Its administrative and fundraising costs are paid from its Damon Runyon Broadway Tickets Service and endowment.
January 27, 2015 > Identification of two genes that trigger ovarian cancer
Terry Magnuson, PhD (Fellowship Award Committee Member), William Y. Kim, MD (Damon Runyon Clinical Investigator ‘09-‘14), and colleagues at the University of North Carolina, Chapel Hill, created the first mouse model of ovarian clear cell carcinoma using data from The Cancer Genome Atlas. Specific types of mutation of the genes ARID1A and PIK2CA gave rise to ovarian cancer 100 percent of the time. These mutations led to the overproduction of Interleukin-6 (IL-6), a type of protein called a cytokine that is crucial for cell signaling that triggers inflammation. They demonstrated that a known drug can suppress tumor growth. The findings were published in the journal Nature Communications.
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January 21, 2015 > Nanoparticles for detecting cancer cells
Moritz F. Kircher, MD, PhD (Damon Runyon-Rachleff Innovator ‘14-‘16) and colleagues at Memorial Sloan Kettering Cancer Center, New York, reported development of a new type of nanoparticle called "nanostars," which accumulate in tumor cells and scatter light, making the tumors easily visible with a special camera. The nanoparticles cannot enter noncancerous cells in the body, so only the cancer cells light up. The scientists hope that this may one day enable improved identification of tumor margins during surgery, microscopic metastases, and even precancerous cells with high precision. The findings were reported in the journal Science Translational Medicine.
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December 31, 2014 > Novel system for 3D culture of pancreatic cancer
Christine Iok In Chio, PhD (Damon Runyon Shirley Stein Fellow ‘13-‘17) of Cold Spring Harbor Laboratory, and colleagues, developed a 3D “organoid” culture system for pancreatic cancer that enables growth of pancreatic tissue not only from laboratory mouse models, but also from human patient tissue, offering a path to personalized treatment approaches in the future. The study was published in the journal Cell.
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December 10, 2014 > New connection established between cell metabolism and stem cell identity
Lydia Finley, PhD (Damon Runyon Jack Sorrell Fellow ‘13-‘17) of Memorial Sloan Kettering Cancer Center, New York, and colleagues, demonstrated that stem cells can rewire their metabolism to enhance a mechanism that helps them avoid committing to a specific fate; in turn, this improves stem cells’ ability to renew themselves. She showed that the nutrients a stem cell uses, and how it uses them, can contribute to a cell’s fate by influencing gene expression through epigenetic modifications. This newly established link between metabolism and stem cell fate improves our understanding of development and regeneration, and, of cancer. These results were published in the journal Nature.
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December 9, 2014 > Genetic link to treatment-related cognitive decline in children with leukemia
Peter D. Cole, MD (Damon Runyon-Sohn Pediatric Cancer Fellowship Award Committee, Damon Runyon Clinical Investigator ‘03-‘08) of Albert Einstein College of Medicine, Bronx, and colleagues, reported that common variations in four genes related to brain inflammation or cells' response to damage from oxidation may contribute to the problems with memory, learning and other cognitive functions seen in children treated for acute lymphoblastic leukemia (ALL). The findings suggest it may be possible to screen ALL patients for their risk of long-term treatment-related effects on memory, attention and learning and studying potential interventions. These results were presented at the 56th annual meeting of the American Society of Hematology.
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December 8, 2014 > Highly disorganized gene regulation linked to chronic lymphocytic leukemia
Catherine J. Wu, MD (Damon Runyon Clinical Investigator ‘07-‘12) and colleagues at Dana-Farber Cancer Institute, Boston, found that in patients with chronic lymphocytic leukemia (CLL), treatment produced shorter remissions if the tumor tissue showed signs of highly disorganized methylation, chemical modifications on the DNA that regulate gene expression. The findings demonstrate that such disorganization can actually benefit tumors and render them less vulnerable to anti-cancer drugs. The study was published in the journal Cancer Cell.
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December 6, 2014 > New immunotherapy effective for Hodgkin’s lymphoma as well as melanoma
John M. Timmerman, MD (Damon Runyon Clinical Investigator ‘05-‘10) of University of California, Los Angeles, Gordon J. Freeman, PhD (Damon Runyon Fellow ‘79-'81), of Dana-Farber Cancer Institute, Boston, and colleagues, reported that an immunotherapy drug called Opdivo/nivolumab, which inhibits the PD-1 pathway, is effective in treatment of relapsed or refractory Hodgkin's lymphoma. In a Phase I clinical trial of 23 patients with Hodgkin's lymphoma treated with the drug, the rate of progression-free survival was 86%. The results were presented at the 56th Annual Meeting of the American Society of Hematology (ASH) and published in The New England Journal of Medicine. The US FDA subsequently approved the drug for treatment of metastatic melanoma and also granted it Breakthrough Therapy Designation in relapsed Hodgkin's lymphoma.
November 19, 2014 > Genetic mutations predict response to immunotherapy
Jedd D. Wolchok, MD, PhD (Damon Runyon-Lilly Clinical Investigator ‘03-‘08) and colleagues at Memorial Sloan Kettering Cancer Center, New York, reported a key discovery that explains why some patients respond to Yervoy/ipilimumab, an immunotherapy drug, while others do not. They found that the cancer cells from patients who respond to the drug carry a high number of genetic mutations--some of which make tumors more visible to the immune system, and therefore easier to fight. In the future, the researchers hope to develop a diagnostic test to detect the mutations in melanoma patients, which could help doctors to make more effective treatment decisions. This study was published in The New England Journal of Medicine.
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