D. Joseph Jerry
Research areas include tumor suppressor genes and the cellular basis for susceptibility to breast cancer.
The p53 tumor suppressor protein is a major focus of the laboratory because its genome surveillance activity can be enhanced by hormonal stimuli and it contributes to the protective effect of pregnancy. Although estrogen stimulates proliferation, it also potentiates the p53-mediated apoptosis. The estrogen receptor beta appears to be important in mediating the protective effects of estrogen. We have also shown that Activin, which is elevated during pregnancy, is a potent inhibitor of stem cells in the mouse and reduces the incidence of mammary tumors. The frequent mutation of p53 in breast cancer reflects its critical role. However, in mice bearing mutations in p53, the incidence of mammary tumors differs dramatically. Naturally-occurring variants in homology-directed DNA repair have revealed a profound role for this pathway in determining risk of mammary tumors. We are also determining gene expression profiles premalignant breast lesions. These studies provide the basis for diagnostic tests defining which patients are at high risk and should consider treatments while also providing insights into the molecular basis for premalignancy in the human breast.
Learn more at www.umass.edu/vasci/faculty/jerry/jerry.html
- MS Purdue University
- PhD The Pennsylvania State University
- Postdoctoral training: Jackson Laboratory, Bar Harbor, Maine; Baylor College of Medicine, Houston, Texas