He has demonstrated that loss of ASXL1 results in increased expression of genes that are known to promote development of AML. Preliminary data suggests that ASXL1 regulates expression of key genes by affecting proteins called histones. In a mouse model, loss of ASXL1 alone results in a phenotype remarkably similar to human MDS. Moreover, when ASXL1 loss is combined with other genes known to promote chronic leukemia in mice, an acute leukemia develops that hastens death of the mice. His overall goal is to gain a more thorough understanding of ASXL1 function and to ultimately test approved as well as novel targeted therapeutics for treatment of MDS and AML.
Dr. Abdel-Wahab works under the mentorship of Ross L. Levine, MD, at Memorial Sloan-Kettering Cancer Center, New York, New York.
Himisha Beltran, MD [Damon Runyon-Gordon Family Clinical Investigator]
Many prostate cancers initially respond to treatments that block the hormone testosterone, thus halting tumor growth. These treatments block testosterone by targeting a molecule called the androgen receptor (AR). However, patients often develop resistance to these drugs, giving rise to an aggressive AR-independent form of prostate cancer. Often under-recognized, AR-negative neuroendocrine prostate cancer (NEPC) currently represents approximately 25% of advanced prostate cancers. The clinical diagnosis is most often made when the cancer has metastasized, especially to liver and brain, and is associated with a low prostate specific antigen (PSA) level. The poor prognosis of NEPC is, in part, due to an incomplete understanding of the molecular events underlying its development.
By utilizing valuable tissue resources and state-of-the-art technologies, Dr. Beltran seeks to comprehensively evaluate
|Contact: Yung S. Lie|
Damon Runyon Cancer Research Foundation