Jun 19, 2009 -- Dr. Marina Holz, assistant professor of biology at Yeshiva University’s Stern College for Women, was recently awarded a one-year $30,000 grant from the Wendy Will Case Cancer Fund to research the role of the mTOR (mammalian target of rapamycin) /S6 Kinase 1 (S6K1) genetic pathway in breast cancer. Holz, a resident of Greenwich, CT, is interested in identifying genetic and molecular differences between normal and cancer cells that would allow scientists to design targeted therapies. The $30,000 grant follows a previous grant of $75,000 grant from the Elias Genevieve and Georgiana Atol Charitable Trust to research the molecular mechanisms of the S6K1 gene. She recently published a research paper that provides a biochemical explanation as to why a two-drug regimen is effective for some breast cancer patients. While the paper in the Journal of Biological Chemistry is laudable for its contribution to advances in breast cancer treatments, it is also noteworthy for its co-authorship by four Stern students, most of whom are now recent graduates, including lead author Rachel Yamnik ’08SCW. “It’s exciting to get undergraduates interested in biology, biomedicine and science—and now they all have a productive research experience they can use to advance their careers,” said Holz, who is also an assistant professor of molecular pharmacology at Albert Einstein College of Medicine. As a post-doctoral researcher during the summer of 2006, Holz had two Stern students—Yamnik and Nilly Brodt ’08SCW—join her for an internship at Harvard Medical School, from which she received her PhD. When Holz was recruited to Stern in 2007, the students continued their research with her. They were joined by current Stern S. Daniel Abraham Honors student Alla Digilova and Daphne Davis ’09SCW, who are also listed as co-authors of the paper. (The sixth co-author, Chris Murphy, was a technician in Stern’s biology department.) Yamnik is now a full-time research fellow in Holz’s lab and Brodt begins medical school in the fall. In the paper, the researchers show that S6K1 activates the estrogen receptor (ER), causing breast cancer cells to proliferate—as many as 60 percent of breast cancers test positive for ER. Doctors treat ER-positive cancers with anti-estrogen therapy—usually tamoxifen—but resistance to therapy develops in most cases. The drug rapamycin, which is already FDA-approved for other clinical applications, is known to target S6K1, so the Stern study suggests that a combination of rapamycin and tamoxifen is effective for patients who “carry the double mutation of too much S6 and too much ER,” Holz said. When Holz presented the study at the 31st Annual San Antonio Breast Cancer Symposium last December, she said, “clinicians were very excited because it explained why some patients respond to the combination of rapamycin and tamoxifen, and others don’t."