Why ovarian cancer keeps coming back — and how 鶹ýӳ researchers hope to stop it
A new study identifies how treatment-resistant cells survive chemotherapy, pointing to a potential strategy for preventing frequent, deadly relapses.

For many women diagnosed with ovarian cancer, the most difficult battle begins after initial treatment appears to work.
High-grade serous ovarian cancer (HGSOC) is the most common and deadliest form of the disease, accounting for approximately 75% of total ovarian cancer cases. Chemotherapy is often effective in shrinking initial tumors and sending the disease into remission, but roughly three-quarters of patients with advanced cases within five years.
Now, 鶹ýӳ researchers led by Carrie House, associate professor of biology in the , have made an important discovery that could lead to new strategies for preventing these deadly relapses.
Researchers have long known that a small population of therapy-resistant cancer cells survives chemotherapy, but exactly how those cells persist and drive relapses has remained unclear.
In , however, House and her collaborators identified a molecular pathway and a specific protein that enable the chemotherapy-resistant cells to withstand treatment, spread and regenerate tumors.
"It is all too common for ovarian cancer to respond well to initial chemotherapy, go quiet and then return with a vengeance," said House. “By understanding the cells that survive treatment and eventually spark relapse, we are working to stop the disease’s typical deadly progression in its tracks.”
The resilient cells can remain dormant, spread to new locations and eventually spawn new tumors that are often more resistant to therapy. House's laboratory focuses specifically on understanding exactly what allows those cells to persist.

The research team found that two particular proteins play distinct roles in helping ovarian cancer cells survive. One, called RelB, promotes production of a cell-surface protein found at especially high levels on the therapy-resistant stem-like cells responsible for relapses. In fact, more than 90% of cells collected from relapsed tumors carried the marker.
Importantly for patients being treated for the disease, the team demonstrated that disrupting the effects of the ReIB protein had a dramatic effect. By simultaneously reducing its activity and blocking the associated cell-surface protein, researchers eliminated the stress-tolerant stem-like cells, reduced tumor burden and significantly extended survival in preclinical models.
The team’s research found certain drugs — some of which are already in clinical trials for other cancers or diseases or in preclinical development — may be effective in blocking the treatment-resistant molecular pathway or in blocking the cell-surface protein interaction associated with relapse.
"Removing the cells responsible for rebuilding the tumors after chemotherapy or the proteins that help them spread may be the best thing we can do to improve long-term outcomes for patients," House said. "In a disease where relapse is common and statistically more deadly than initial onset, stopping that progression could have a massive impact and save many lives."
The study included researchers from 鶹ýӳ, , the National Cancer Institute and several other collaborating institutions. The research was supported by the and the .
House's lab studies the biology of ovarian and breast cancers, with a particular focus on cancer stem cells, drug resistance and the signals that allow tumors to progress and return after treatment. Her research combines advanced cell biology, genomics and animal models to identify new therapeutic targets that could prevent recurrent disease.
House’s findings add to 鶹ýӳ’s growing contributions to cancer research. In another recent study, 鶹ýӳ associate professor of biology Svasti Haricharan and an international team identified a potential way to reduce deaths from the deadliest form of breast cancer by using an existing FDA-approved therapy earlier in treatment for certain patients whose tumors are resistant to standard treatment.



