September 26, 2024

Jennifer Kay, Ph.D., was an MIT SRP Center trainee before becoming a research scientist at Silent Spring Institute. (Image courtesy of Silent Spring Institute)
Cancer studies often focus on treatments after diagnosis, but toxicologist Jennifer Kay, Ph.D., is determined to stop cancer at its source.
“I’m more interested in what causes tumors in the first place,” Kay said. “How can we figure out what chemicals cause those changes to prevent exposures and reduce cancer burdens?”
Kay, a former NIEHS Superfund Research Program (SRP) trainee, is now a research scientist at Silent Spring Institute. She became interested in cancer research as a biological engineering doctoral student at the Massachusetts Institute of Technology (MIT).
DNA Damage and Repair
Mentored by Bevin Engelward, Sc.D., Kay used novel mouse models in her dissertation research to understand how inflammation contributes to DNA damage and, eventually, cancer.
Later, as a postdoctoral researcher at the MIT SRP Center, co-founded by Engelward, she investigated DNA damage and repair following exposure to NDMA, or N-nitrosodimethylamine, a chemical historically dumped into unlined pits at the site of a former chemical manufacturing facility in Wilmington, Massachusetts.

Kay presents her NDMA and DNA damage research at an MIT SRP Center external advisory board meeting. (Photo courtesy of Jennifer Kay)
“We were studying how this chemical causes cancer using animal models,” Kay said. “Ultimately, we wanted to understand how people’s exposure to this chemical might have contributed to a childhood cancer cluster in their community.” (In 2021, the Massachusetts Department of Public Health published findings showing an association between in utero exposure to NDMA and childhood cancer.)
That work laid the foundation for a pivotal study in cancer research. Working with the MIT SRP Center team, Kay examined how mouse cells responded to NDMA exposure based on the activity of an enzyme called AAG, vital to repairing damaged DNA.

As a postdoc at the MIT SRP Center, Kay also led the center’s Research Translation Core and ran a blog that described many of the center’s key research, engagement, and translation activities. (Photo courtesy of MIT SRP)
“Some people have high levels of this enzyme activity, and some people have low levels,” Kay explained. “By investigating what happens at either extreme, we could see that people with lower levels of this repair enzyme are at much higher cancer risk.”
“Screening for AAG activity in humans could allow us to identify people exposed to NDMA who may be at a greater risk for developing cancer,” she added. “This could help inform studies of both cancer treatment and prevention.”
In 2021, NIEHS SRP recognized Kay for her breakthrough findings and research translation efforts with the Karen Wetterhahn Memorial Award, which celebrates early career researchers for excellence in science, outreach, and mentorship.
Hormonal Signaling and Breast Cancer
At Silent Spring Institute, a nonprofit dedicated to uncovering environmental causes of breast cancer, Kay’s research has grown to focus on preventing breast cancer, the second most common cancer in women.
“Rising rates of breast cancer are likely tied to environmental factors that could be changed if we understood what they were, and if we could do something to prevent them,” Kay said.
She has also expanded her research to consider how hormonal signaling interacts with DNA damage and repair in breast cancer development.
“MIT gave me a strong background in DNA damage, mutagenesis, and carcinogenesis,” Kay said. “But I’ve done a lot of work to teach myself about how hormones interact with DNA damage processes to increase cancer risk.”
For example, in one study, Kay used publicly available data on various chemicals known to cause DNA damage and analyzed their effects on estrogen and progesterone signaling. The two hormones are crucial for regulating normal breast development but can also influence breast cancer risk. She found that a large proportion of chemicals that cause tumors in various mammals also activate estrogen and progesterone signaling.
“This tells us that doing these screening assays to look for chemicals that increase hormone production or activate hormone receptors is likely a good way to flag chemicals as potential breast cancer risk factors,” Kay said.
A Focus on Prevention
NIEHS recently funded a new project that will enable Kay to build upon her findings.
“The work I’m doing now is trying to get at the question of how DNA damage and increased hormonal signaling work together,” Kay said. “The goal is to identify chemicals that do those things so that we can reduce exposures that might increase breast cancer risk.”
Ultimately, Kay hopes to reduce peoples’ suffering by limiting their exposure to known carcinogens.
“I’m not equipped to be a physician, but I strongly feel people should not get sick from just living their regular lives,” she said. “So, what am I equipped to succeed at? Research. I want to take everything that I’m good at and turn it into something that helps keep people from getting sick.”