Peritoneal ovarian cancer expands in the omentum without requiring mature adipocytes, according to research published in Nature Communications on Aug. 12, 2026. The findings challenge the prevailing model that omental fat cells are required to fuel metastatic ovarian tumor growth through direct lipid delivery.
Researchers led by Rachel L. Mintz and Gwendalyn J. Randolph at Washington University tested tumor expansion in mice congenitally lacking mature adipocytes across the peritoneal cavity. Across three distinct cancer models—ID8p53−/−Brca2−/−, BPPNM, and KPCA—ovarian tumors continued to preferentially seed adipose-associated regions despite the total absence of mature fat cells. The loss of mature adipocytes did not impair peritoneal tumor growth, whereas surgical removal of the adipocyte-free omentum significantly reduced tumor burden.
Single-cell transcriptomic analyses of murine and human tissues revealed that lipid-handling gene expression, including FABP4, is enriched in omental endothelial cells during steady-state conditions and in tumor-bearing tissue. Deleting FABP4 specifically in endothelial cells reduced omental tumor expansion and limited tumor vascular complexity.
The study utilized human omentum samples supplied by the Washington University Gynecology Oncology Tissue Bank, with genomic analysis supported by the McDonnell Genome Institute. Grants from the National Institutes of Health and the National Cancer Institute funded the project, which was completed in partial fulfillment of Mintz's doctoral degree.
