Researchers at the MUSC Hollings Cancer Center have developed a new ovarian cancer model that offers intriguing insights into the origins of serous uterine cancer. A recent study, led by Joe Delaney, Ph.D., and published in Cancer Research Communications, suggests that serous uterine cancer may actually begin in the fallopian tubes, making it metastatic by the time it’s found in the uterus.
While most uterine cancers have favorable survival rates—up to 95% for localized cases—serous uterine cancer has significantly poorer outcomes, with survival rates between 35% to 50% for early-stage cases. The new research offers evidence that this aggressive form of uterine cancer likely originates in the fallopian tubes, changing the way scientists understand its development.
The discovery came during the creation of a new model for ovarian cancer, which Delaney’s team had been working on for seven years. Their aim was to develop a model that represents the majority of ovarian cancer cases, as existing models only account for cancers caused by mutations in the PTEN or BRCA genes, which occur in a minority of patients.
The researchers used the MYC oncogene—linked to about 70% of human cancers—and targeted it specifically to the fallopian tubes, where most ovarian cancers are believed to begin. Surprisingly, the cancer signals appeared not only in the fallopian tubes and ovaries but also in the uterus, specifically in uterine epithelial cells.
“We were shocked to see cancer signals in the uterus because the oncogene was only targeted to the fallopian tubes,” said Delaney. This unexpected result led to the hypothesis that serous uterine cancer could start in the fallopian tubes, much like ovarian cancer.
The team’s findings are supported by previous studies. One study from McMaster University in Canada discovered that precancerous lesions in the fallopian tubes, known as serous tubal intraepithelial carcinoma (STIC), were present in both serous ovarian and uterine cancers. Another retrospective study in Sweden found lower rates of uterine cancer, particularly aggressive types, in women who had undergone tubal ligation, a procedure that blocks the fallopian tubes, potentially preventing cancer cells from migrating to the uterus.
Delaney’s lab plans to further test this theory by removing the fallopian tubes from mice and observing the rates of serous uterine cancer. The results of these experiments are expected in two years. In the meantime, the newly developed model has drawn interest from other researchers, who hope to use it to study high-grade serous ovarian cancer in women without gene mutations, as well as potential treatments.
This model may also serve as a breakthrough for uterine serous carcinoma research. Delaney speculated that they may have created the first accurate mouse model for this cancer, which could be reclassified as a metastatic ovarian cancer rather than a uterine cancer.
“This discovery was thrilling,” Delaney said. “It opens up new possibilities for understanding and treating both ovarian and uterine cancers, and it challenges long-standing assumptions about their origins.”
This new model is poised to have a significant impact on future research, potentially changing the way these cancers are studied and treated.
