Spotlight for Former MIT SRP Program Trainee | Dr. Jennifer Kay
Spotlight for Former MIT SRP Program Trainee | Dr. Jennifer Kay
Mar 27, 2024
Dr. Jennifer Kay received a Bachelor of Science in Chemical Engineering from the University of Pittsburgh followed with a Ph.D. in Biological Engineering at MIT working in the Engelward and Samson Labs. Following her postdoctoral fellowship with the MIT SRP, she is currently a Research Scientist at Silent Spring Institute. During her tenure at MIT and with SRP, she conducted animal-based research to examine the key biological outcomes caused by exposure to N-nitrosodimethylamine (NDMA), an environmental contaminant. In particular, she studied the impact of DNA repair capacity on responses to NDMA to identify genetic susceptibility factors. Research in gene-environment interactions, as with Dr. Kay’s work, could offer insights into biological mechanisms of disease, which in turn could provide strategies in public health protection. Also, as a critical member of the SRP team, Dr. Kay was the lead for the Research Translation Core, building communication bridges with internal and external stakeholders to advance a holistic approach with SRP projects.
At Silent Spring Institute, Dr. Kay and her colleagues focus on identifying chemicals that may promote breast cancer. Globally, breast cancer has surpassed lung cancer to become the most common cancer diagnosis, predominantly impacting women. The need for investigating environmental chemicals that increase breast cancer risk is even more pressing as cancer is affecting more young people (ages 15-39 according to National Cancer Institute data: Abbott, Brianna. “Cancer is Hitting More Young People.” Wall Street Journal, 12 January 2024, pgs. A1 and A9). The concern is heightened because screening for many types of cancer, including breast cancer, tends to start at a later age for most people.
Combing through multiple international and U.S. agency databases, the Silent Spring team aimed to identify chemicals that have experimental evidence suggesting they could increase breast cancer risk. Specifically, they looked at chemicals that cause mammary tumors in animal studies, increase certain hormones (estrogen or progesterone), or activate the estrogen receptor, which is present in breast cells. They focused on chemicals that increase estrogen and progesterone signaling in particular because these hormones are well established to increase breast cancer risk. After searching through many databases for these targeted biological endpoints, the study yielded 921 chemicals that have the potential of initiating the development of breast cancer.
Knowing that DNA damage can also promote cancer, the team scoured additional databases to identify the mammary carcinogens and endocrine disruptors that damage DNA, finding 420 chemicals on their list were also genotoxic. They demonstrated that chemicals producing mammary tumors in laboratory animals also tend to display DNA damaging and hormone-disrupting traits, supporting the use of mechanistic data for endocrine activity and genotoxicity to flag breast cancer hazards.
The importance and relevance of this study goes beyond a better understanding of endocrine disruptors in relation to breast cancer risk. This study also provides added insights for regulators to include biological mechanisms in assessing chemicals for a more comprehensive evaluation of exposure. To that end, the work spearheaded by Dr. Kay can lead to better public health protection for women.
