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James E. Bradner, MD (Damon Runyon-Rachleff Innovator ‘11-‘13) of Dana-Farber Cancer Institute, Boston, and colleagues, discovered a set of powerful gene regulators -“super-enhancers” that control cell state and identity. Important for gene control in healthy cells, super-enhancers are co-opted by cancer cells to overexpress oncogenes that lead to aggressive tumors. Treatment of multiple myeloma tumor cells with the drug JQ1 blocked the super-enhancer of the MYC oncogene and resulted in tumor growth arrest.
Oren J. Becher, MD (Damon Runyon Clinical Investigator ’12-’15) of Duke University, Durham, Laura A. Banaszynski, PhD (Angelo Family Fellow ‘08-‘11) of The Rockefeller University, New York, and colleagues, reported results that, for the first time, link a mutated histone protein to a rare brain stem cancer in children called diffuse intrinsic pontine gliomas (DIPG). This histone typically silences expression of certain genes; when the histone is mutated in DIPG, cancer-promoting genes are aberrantly turned on.
Renier J. Brentjens, MD, PhD (Damon Runyon-Lilly Clinical Investigator ‘06-‘11) and colleagues at the Memorial Sloan-Kettering Cancer Center, New York, reported the success of immunotherapy treatment of adults with acute lymphoblastic leukemia (ALL). Patients were treated with their own T immune cells, which had been genetically modified to target and attack the cancer cells. The treatment induced rapid remissions in these patients.
Elaine V. Fuchs, PhD (Damon Runyon Board Member, Damon Runyon Fellow ‘77-‘79) of The Rockefeller University, New York, is one of three recipients of the Robert J. and Claire Pasarow Foundation Medical Research Awards in Cancer Research. She is honored for her extraordinary achievement, creativity and distinction in the field of skin stem cells. Matthew P. Scott, PhD (Damon Runyon Fellowship Sponsor) of Stanford University School of Medicine, Stanford, is also a recipient of the award.
Jean Y. Tang, MD, PhD (Damon Runyon Clinical Investigator ‘11-‘14) of Stanford University School of Medicine, Stanford, and colleagues, reported that women who take aspirin regularly have a reduced risk of developing melanoma. Overall the risk is reduced by over 20 percent. The findings, based on a study of nearly 60,000 women aged 50 to 79, suggest the anti-inflammatory effects of aspirin may help protect against this type of skin cancer. The study was published in the journal Cancer.
Catherine J. Wu, MD (Damon Runyon Clinical Investigator ‘07-‘12), Matthew L. Meyerson, MD, PhD (Damon Runyon Fellow ‘95-‘98), and colleagues at Dana-Farber Cancer Institute, Boston, and the Broad Institute, Cambridge, demonstrated how genetic mutations evolve over time in chronic lymphocytic leukemia (CLL) cells. The researchers used next-generation gene-sequencing technology to monitor genetic changes in tissue samples from cancer patients, demonstrating that subsets of cells in each tumor contain different genetic makeup.
David G. Kirsch, MD, PhD (Damon Runyon-Rachleff Innovator ‘08-‘10), and colleagues at Duke University Medical Center, Durham, reported that epidermal growth factor (EGF) speeds the recovery of blood-making hematopoietic stem cells after exposure to radiation. Mice with high levels of EGF were protected from radiation damage. EGF may be able to accelerate the recovery of the blood system in cancer patients treated with chemotherapy or radiation. The study was published in the journal Nature Medicine.
Adam de la Zerda, PhD (Damon Runyon Fellow ‘11-‘12) of Stanford University, Stanford, was named to the Forbes Magazine “30 Under 30” list in Science and Healthcare for 2012. Adam is applying nanotechnology and novel medical imaging to look inside tumors and gather information on cellular changes that drive cancer progression. Those on this list “represent the entrepreneurial, creative and intellectual best of their generation.”
Jing Yang, PhD (Damon Runyon Fellow ‘00-‘03) and colleagues at the University of California, San Diego School of Medicine, La Jolla, demonstrated how cancer cells control a developmental process known as epithelial-to-mesenchymal transition (EMT) to metastasize, breaking free and spreading to other parts of the body, where they proliferate and grow into secondary tumors.