Now that screening for genes that predispose a woman to breast cancer is routinely available, women at an increased risk are looking for ways to keep themselves healthy. Insoo Bae, PhD, a junior faculty member of the Lombardi Comprehensive Cancer Center at Georgetown University Medical Center received a $2 million research award from Susan G. Komen for the Cure to do just that.
Bae, an assistant professor of oncology, has developed a new methodology for studying the interaction between environmental carcinogens and genetic risk for breast cancer, a project aimed at developing novel prevention strategies for women who are genetically predisposed to breast cancer.
The age-old question of nature versus nurture in the field of psychology also applies in oncology: is a cancer caused by an inherited genetic predisposition or by exposure to environmental carcinogens” Bae?s clear response to the question is ?both.?
Instead of separating out the differences between the two, he is worried about the dangerous combination of both factors together. Specifically, Bae wants to find out what combinations of genetic predisposition and carcinogen exposure are most likely to cause cancer. To do this, Bae developed a new technique for studying the environment-gene interaction .
Komen awarded its grant to Bae so he can test this methodology for the BRCA1 mutation, one of the few inherited mutations known to predispose women to breast cancer. Bae will examine a range of environmental carcinogens ? such as cigarette smoke, alcohol, and dietary factors ? to identify those agents that increase the probability that BRCA1 defective cells will become cancerous.
The impact of this research is far-reaching. With more knowledge about environment-gene interactions, physicians will be able to make personalized recommendations for women with BRCA1 mutations, and basic scientists will be able to identify new molecular mechanisms that contribute to breast carcinogenesis. Bae also plans to develop preventive agents that will protect women against cellular damage.