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Valerie Horsley, PhD (Damon Runyon Fellow ‘04-‘07) of Yale University, New Haven, and Georgios Skiniotis, PhD (Damon Runyon Fellow ‘04-‘07) of University of Michigan, Ann Arbor, were named recipients of the Presidential Early Career Award for Scientists and Engineers, the highest honor bestowed by the United States government on science and engineering professionals in the early stages of their independent research careers.
Jean Y. Tang, MD, PhD (Damon Runyon Clinical Investigator ‘11-‘14) of Stanford University School of Medicine, and colleagues, reported the success of a newly approved drug, vismodegib/Erivedge, in dramatically shrinking basal cell carcinoma (BCC) skin cancers and preventing new ones from forming in patients with basal cell nevus syndrome, a rare genetic condition that causes dozens to thousands of skin cancers on each patient’s body.
Robert H. Vonderheide, MD, PhD (Damon Runyon-Lilly Clinical Investigator ‘00-‘05) and colleagues at University of Pennsylvania School of Medicine, Philadelphia, reported that the drug daclizumab (Zenapax) improved the survival of breast cancer patients taking a cancer vaccine by 30 percent (seven months), compared to those patients not taking the drug. Daclizumab, approved for use in preventing transplant rejection, targets Tregs (regulatory T cells) that normally prevent the immune system from detecting and attacking tumors.
A team of scientists from the Broad Institute, Cambridge, and Dana-Farber Cancer Institute, Boston, led by Matthew L. Meyerson, MD, PhD (Damon Runyon Fellow ‘95-‘98) and Todd R. Golub, MD (Innovation Award Committee Member, Board Member) sequenced the whole genomes of 25 metastatic melanoma tumors. Analysis of these sequences indicated that the rates of genetic mutation rose along with chronic sun exposure in patients. As expected, the scientists detected known mutations in genes that regulate cell growth.
Election to the National Academy of Sciences is one of the highest honors that can be earned by a U.S. scientist. In recognition of their distinguished and continuing achievements in original biomedical research, three Damon Runyon alumni were inducted this May:
Rachel D. Green, PhD (Fellow ‘93-‘96, Current Innovation Award Committee, Fellowship Sponsor), Investigator, Howard Hughes Medical Institute, and Professor, Johns Hopkins University School of Medicine, Baltimore
MCL1 encodes a protein that helps keep cells alive (anti-apoptotic); it is frequently overexpressed in cancer. Joseph T. Opferman, PhD (Damon Runyon Fellow ‘01-‘04) and colleagues at St. Jude Children’s Research Hospital, Memphis, reported that different forms of MCL-1 reside in distinct locations in the cell’s mitochondria and exhibit separable functions. One form is anti-apoptotic, while a newly identified form that works inside the mitochondria is involved in energy production and is probably essential for tumor cell survival.
Sujun Hua, PhD (Damon Runyon Fellow ‘10-‘13), Costas A. Lyssiotis, PhD (Damon Runyon Fellow ‘10-‘13), Ji-Hye Paik, PhD (Damon Runyon Fellow ‘06-‘08) and colleagues at Dana-Farber Cancer Institute, Boston, discovered a new role for the Kras oncogene in controlling cell metabolism. They reported that a genetic mutation in Kras linked to initiation of pancreatic cancer also manipulates metabolic pathways to support tumor growth and progression.
Guo Wei, PhD (Damon Runyon Fellow ‘05-‘08), Todd R. Golub, MD (Innovation Award Committee Member, Board Member) and colleagues at Dana-Farber Cancer Institute and The Broad Institute, Cambridge, used chemical genomics to identify compounds that decrease activity of MCL1, a protein that helps keep cells alive (anti-apoptotic) and is frequently overexpressed in cancer. In addition, the researchers found that high expression of another gene, BCL-xL, confers resistance to MCL1 repression.
Scott A. Armstrong, MD, PhD (Damon Runyon-Lilly Clinical Investigator ‘03-‘08) of Dana-Farber Cancer Institute and Children’s Hospital Boston, and colleagues, reported the role of a protein called β-catenin in chronic myeloid leukemia (CML) stem cells. They demonstrated that reducing β-catenin in combination with treatment with Gleevec/imatinib decreases CML stem cells in mice, without harming healthy cells. These findings, published in the journal Cell Stem Cell, suggest that this combination therapy may prevent recurrence of AML disease in patients.
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