A new study from the University of Michigan sheds light on the genetic roots of a deadly form of ovarian cancer and points toward a potential new treatment strategy.
The research, published in the Proceedings of the National Academy of Sciences, focuses on high-grade serous carcinoma—the most common and aggressive type of ovarian cancer.
This cancer typically starts in the fallopian tubes, spreads quickly to the ovaries and other pelvic organs, and is usually diagnosed at a late stage when current treatments often stop working.
Scientists have long known that high-grade serous carcinoma is genetically complex, involving many unstable genetic changes. One gene that has drawn attention is CDK12. The new study shows that CDK12 acts as a tumor suppressor, meaning it normally helps keep cancer from forming. When this gene is turned off, tumors grow more aggressively, and the disease worsens faster.
The research team developed a new mouse model that closely mimics human disease. They started with a model created by Dr. Kathleen Cho in which three tumor-suppressing genes were already turned off in the fallopian tube (the equivalent of the human site where this cancer starts).
The scientists then added a fourth gene, CDK12, to the mix. Mice with this four-gene inactivation developed more aggressive tumors, confirming CDK12’s important protective role.
“This is the first time we’ve seen clear evidence in a mouse model that CDK12 helps prevent this cancer. Without it, the cancer gets worse faster, and survival drops,” said Dr. Arul Chinnaiyan, co-lead author and director of the Michigan Center for Translational Pathology.
Importantly, the researchers found that when CDK12 is turned off, the immune system responds by sending T cells (a type of immune cell) to the tumor. This raised an exciting possibility: combining a drug that targets CDK12’s effects with immune checkpoint inhibitors, a type of immunotherapy that helps the immune system attack cancer.
To build on this, the team looked at another gene, CDK13, which works closely with CDK12. They tested a drug that targets and degrades both CDK12 and CDK13 in the mouse model.
When combined with immunotherapy, this approach significantly slowed down tumor growth. This combination therapy could represent a promising new path for treating women with this form of ovarian cancer.
“Currently, when patients with this cancer become resistant to chemotherapy, the next steps are mostly trial and error,” said Dr. Cho. “There are few effective treatment options. That’s why this discovery is so important—it gives us a specific target and a clear direction for developing better therapies.”
The study also bridges cancer research in ovarian and prostate cancer. CDK12 is known to play a role in about 7% of advanced prostate cancers and about 3% of high-grade tubo-ovarian cancers. Chinnaiyan’s team previously found similar results in prostate cancer, and now this new work suggests that drugs targeting CDK12 and CDK13 could work in both cancers.
Several CDK12/13 inhibitors are already in development, including one created by the Michigan team. The next goal is to move this research into clinical trials so it can be tested in patients.
In summary, this study not only deepens understanding of a key genetic driver of high-grade ovarian cancer but also offers a potential treatment route—using CDK12/13 degraders in combination with immunotherapy—to improve outcomes for patients facing this aggressive disease.
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The research findings can be found in PNAS.
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