March 26, 2009
Six members of the Damon Runyon circle were selected to become Early Career Scientists of the prestigious Howard Hughes Medical Institute (HHMI):
Howard Y. Chang, MD, PhD (Damon Runyon Scholar ‘06-‘08, Sponsor ‘05-‘07), Stanford University, Stanford
Neil Hunter, PhD (Damon Runyon Scholar ‘04-‘06), University of California, Davis
Susan M. Kaech, PhD (Damon Runyon Fellow ‘99-‘02), Yale University, New Haven
Christopher M. Sassetti, PhD (Damon Runyon Fellow ‘01-‘03), University of Massachussetts Medical School, Worcester
Kristin Scott, PhD (Current Sponsor), University of California, Berkeley
Jennifer A. Zallen, PhD (Damon Runyon Fellow ‘00-‘03), Memorial Sloan-Kettering Cancer Center, New York
50 of the best early career investigators were chosen from more than 200 institutions nationwide for this six-year appointment to the institute, which gives them time and resources ($1.5 million) to focus on their boldest ideas.
March 23, 2009
Ronald Levy, MD (Damon Runyon Board and Innovation Award Committee Member) of the Stanford University School of Medicine, Stanford, was selected to receive the 2009 King Faisal International Prize in Medicine. Dr. Levy developed the concept that a drug made from an antibody could be used to fight cancer. His work led to the development of Rituxan, the first commercial antibody to treat cancer, which was approved by the FDA in 1997 for treatment of lymphoma. This class of drug is now part of the standard treatment for a wide range of cancers, including breast, colon and lung cancers.
Joseph A. Califano, III, MD (Damon Runyon-Lilly Clinical Investigator ‘01-‘06) and colleagues at The Johns Hopkins’ Kimmel Cancer Center, Baltimore, reported that the chemical process of demethylation activates a significant number of cancer genes, particularly in head and neck and lung cancers. The researchers identified the role of a gene called BORIS, which acts as a “master regulator” to direct gene demethylation. The reverse process, hypermethylation, was previously shown to lead to cancer formation; some cancer patients are currently treated with demethylating drugs. One potential consequence of these new findings is that demethylating drugs may actually cause additional cancers as a side effect. This work was published in the journal PLoS One.
March 20, 2009
Peter D. Cole, MD (Damon Runyon-Lilly Clinical Investigator ‘03-‘08) of Albert Einstein College of Medicine, Bronx, is the communicating author of a new report from the Children’s Oncology Group, which conducted a phase II study to examine a drug combination of gemcitabine and vinorelbine (GV) in children or young adults with relapsed/refractory Hodgkin’s lymphoma disease. The report indicates a positive response for GV, compared with either drug alone. This study was published in the Journal of Clinical Oncology.
Nathanael S. Gray, PhD (Damon Runyon-Rachleff Innovator ‘08-‘10) of the Dana-Farber Cancer Institute, Boston, and colleagues, reported studies of a highly potent and selective inhibitor of the mTOR kinase. The inhibitor, Torin1, impairs cell growth and proliferation to a far greater degree than the immunosuppressant and anti-cancer agent Rapamycin (also an mTOR inhibitor). Torin1 may be a promising agent for inhibition of mTOR-dependent tumors. This work was published in the Journal of Biological Chemistry.
March 16, 2009 > Gene expression signature discovered for metastatic prostate cancer
A team of researchers led by Phillip G. Febbo, MD (Damon Runyon-Lilly Clinical Investigator '05-'10) of Duke University, Durham, reported the discovery of a gene expression “signature” that may predict therapeutic response of men with a type of metastatic prostate cancer (called hormone refractory or castration resistant). This genomic signature is currently being tested in clinical trials for its potential to help individualize and improve therapy for these patients. Elahe A. Mostaghel, MD, PhD (Damon Runyon-Genentech Clinical Investigator '08-'11) of the Fred Hutchinson Cancer Research Center, Seattle, also contributed to this study.
March 15, 2009 > 2009 Novitski Prize in genetics research
Rodney J. Rothstein, PhD (Former Fellowship Award Committee Member) of Columbia University, New York, was awarded the 2009 Novitski Prize for his pioneering work in gene targeting. He contributed fundamental ideas that now enable scientists to knock out genes and to knock in specific mutations. The Novitski Prize is awarded for innovative experimental approaches and extraordinary creativity in solving a significant problem in genetics research.
March 12, 2009
Scott A. Armstrong, MD, PhD (Damon Runyon-Lilly Clinical Investigator '03-'08) of the Children’s Hospital Boston, and colleagues, reported the role of the Homeobox class gene HOXA9 in human leukemias that contain rearrangements in the mixed lineage leukemia gene (MLL). The researchers demonstrated that suppression of HOXA9 induces apoptosis (cell death) and arrests cell proliferation; these findings suggest that targeting the HOXA9 pathway may be a novel therapeutic option for treatment of MLL-rearranged leukemia. This work was published in the journal Blood.
March 10, 2009
Ronald A. DePinho, MD (Former Fellowship Award Committee Member and Sponsor) of the Dana-Farber Cancer Institute and Harvard Medical School, Boston, was awarded the 4th Annual Albert Szent-Györgyi Prize for Progress in Cancer Research. He won the prize for his groundbreaking discoveries in cancer research, including linking the tumor suppressor gene p53 to the process of apoptosis (programmed cell death). His research findings have resulted in advances across many areas of science. The prize was established in honor of Dr. Albert Szent-Györgyi (Damon Runyon Grantee '73), recipient of the 1937 Nobel Prize.
February 18, 2009
Hai Yan, MD, PhD (Damon Runyon Scholar '05-'07) of Duke University Medical Center, Durham, and colleagues discovered novel mutations that are associated with malignant glioma, a type of brain tumor. Mutations in two genes, isocitrate dehydrogenase 1, gene 1 and 2 (IDH1 and IDH2) appear to play different roles in glioma: firstly, IDH mutations are the earliest genetic changes that start glioma progression. However, patients with later-stage tumors who had mutations in the IDH genes survive longer than those who lacked the mutations. These genes could become therapeutic targets for treatment of malignant glioma. These findings were published in the New England Journal of Medicine.
February 11, 2009
Jedd D. Wolchok, MD, PhD (Damon Runyon-Lilly Clinical Investigator '03-'08) of Memorial Sloan-Kettering Cancer Center, New York, and Cassian Yee, MD (Damon Runyon-Lilly Clinical Investigator '01-'06) of Fred Hutchinson Cancer Research Center, Seattle, are featured in the Forbes story "Cancer Miracles" describing recent successes in harnessing the immune system for treatment of cancer.
February 9, 2009
Howard Y. Chang, MD, PhD (Kenneth G. and Elaine A. Langone Scholar '06-'08) of Stanford University, Stanford, was selected to receive the first Vilcek Prize for Creative Promise in biomedical science. The awards from the Vilcek Foundation are presented to recognize the successes of foreign-born individuals, 38 years old or younger, in the fields of biomedical science and the arts. Dr. Chang's research focuses on how cells determine their identity and how disruption of this process plays a role in cancer metastasis. His findings may suggest new approaches for the treatment of malignant tumors.
February 8, 2009
Rama Ranganathan, MD, PhD (Fellowship Award Committee Member) of University of Texas Southwestern, Dallas, was selected to receive one of three 2009 annual awards from the Academy of Medicine, Engineering and Science of Texas for outstanding young investigators. He was recognized for his work in the field of systems biology, an approach to understanding how vast networks of molecules and cells work together in an organism. This is essential to understanding healthy development as well diseases such as cancer.
February 1, 2009
Albert C. Koong, MD, PhD (Damon Runyon-Lilly Clinical Investigator '02-'07) of the Stanford University School of Medicine, Stanford, and colleagues identified the critical role of Connective tissue growth factor (CTGF/CCN2) in pancreatic tumor growth and progression. Tumor cells expressing high levels of this factor exhibit rapid growth and are resistant to cell death. Their results suggest that CCN2 represents a viable therapeutic target for the treatment of pancreatic cancer. These data were published in the journal Cancer Research.
John L. Rinn, PhD (Damon Runyon-Rachleff Innovator '09-'11, Damon Runyon Fellow '05-'07) of the Broad Institute, Harvard Medical School and Beth Israel Hospital, Boston, and colleagues reported the discovery of nearly 1,600 novel RNA molecules called lincRNAs. Members of this new class of RNAs, “long intervening noncoding RNAs,” are highly conserved in both sequence and chromatin signature but do not encode proteins. Using new computer analysis tools, the researchers are predicting the function of lincRNAs in critical biological processes. Certain lincRNAs are associated with disruption of the p53 tumor suppressor gene, suggesting a potential role in cancer. In the future, this work could lead to novel diagnostic markers and therapeutic targets for cancer. These findings were published in the prestigious journal Nature.
January 28, 2009
Two members of the Damon Runyon Cancer Research Foundation circle were awarded by the National Academy of Sciences for their exceptional scientific achievements:
Cornelia I. Bargmann, PhD (Current Sponsor, Former Fellowship Award Committee Member) at The Rockefeller University, New York
Roger W. Hendrix, PhD (Damon Runyon Fellow '70-'73) at the University of Pittsburgh, Pittsburgh
January 26, 2009
Laura A. Banaszynski, PhD (Angelo Family Fellow '08-'11) of The Rockefeller University, New York, is the recipient of the 2009 Nobel Laureate Signature Award For Graduate Education In Chemistry granted by the American Chemical Society. She was nominated by her graduate thesis adviser, Stanford University chemical and systems biology professor Thomas J. Wandless, for the excellence of her dissertation research which focused on defining the molecular interactions between the immunosuppressant drug and anticancer agent rapamycin and its complex with FK506 binding protein (FKBP12) and the enzyme mTOR. Her findings may be useful towards developing rapamycin analogs with more potent anticancer activity.
January 19, 2009
Julien Sage, PhD (Damon Runyon Scholar '05-'07) of Stanford University, Stanford, and colleagues, identified a role for the tumor suppressor genes Rb and p130, in lung cancer (adenocarcinoma). They reported that loss of p130 accelerated death in a mouse model of lung cancer (containing an activated version of the K-Ras oncogene); loss of Rb increased the efficiency of lung cancer initiation and progression leading to rapid death. These results demonstrate a cooperative effect between loss of Rb/p130 and activation of K-Ras in lung adenocarcinoma development. These findings were published in the journal Oncogene.
January 10, 2009
Andrew T. Chan, MD, MPH (Damon Runyon Clinical Investigator '08-'11) of Massachussetts General Hospital, Boston, and colleagues performed a study of insulin levels in patients diagnosed with nonmetastatic colorectal cancer between 1991 and 2004. High insulin levels indicate excess energy in the body, which can result from obesity, sedentary lifestyle, and poor dietary pattern. The researchers found that increased levels of insulin-related proteins in the blood of colorectal cancer patients were associated with increased risk of cancer recurrence and mortality. These findings were published in the Journal of Clinical Oncology.
January 5, 2009
Albert C. Koong, MD, PhD (Damon Runyon-Lilly Clinical Investigator '02-'07) and colleagues at Stanford University Medical Center, Stanford, identified a mechanism by which metastasis occurs. A protein called lysyl oxidase (LOX) is found at high levels in cancer cells; inhibiting LOX expression decreases tumor cell invasion and metastasis in a mouse model of breast cancer. In this study, the researchers found that this effect occurs because a particular type of cell, the CD11b cell, cannot function without LOX. In breast cancer metastasis, LOX attracts CD11b cells to the lung; these cells weaken the lung tissue to create an “entry point” for arriving breast cancer cells. The researchers plan to design a clinical trial to study the effect of blocking LOX activity in humans with primary cancers.
January 1, 2009 > Protein could be target for head and neck squamous cell carcinoma
Christine H. Chung, MD (Damon Runyon-Lilly Clinical Investigator '05-'10) of the Vanderbilt University School of Medicine, Nashville, and colleagues, identified a critical function of Protein Kinase Cα (PKCα) and microRNA miR-15a in regulating tumor cell growth in head and neck squamous cell carcinoma (SCCHN), a type of head and neck cancer. The researchers demonstrated that agents that block PKCα decrease tumor growth in animal models, indicating that this protein may be a promising target for treatment of SCCHN. These findings were published in the journal Cancer Research.
January 1, 2009
A team of researchers led by John M. Pagel, MD, PhD (Damon Runyon-Lilly Clinical Investigator '05-'10) and Frederick R. Appelbaum, MD (Clinical Investigator Award Committee Member) of the Fred Hutchinson Cancer Research Center, Seattle, reported the success of radiotherapy directed against specific proteins found on the surface of leukemia cells. When used for the treatment of leukemia, this technique, called “pretargeted radioimmunotherapy,” may allow intensification of therapy while minimizing toxicity to non-cancerous cells. These results were published in the journal Cancer Research.