Back

BRCA mutation alters the stromal landscape in normal ovaries

Vaishnav, H. T.; Murray, A.; Piccolo, O. R.; McCloskey, C. W.; Yakubovich, E.; Macdonald, E.; Echaibi, M.; de Ladurantaye, M.; Jung, E.; Fazio, T. J.; Trudel, D.; Mes-Masson, A.-M.; Drapkin, R.; Landry, D. A.; Vanderhyden, B. C.

2025-12-21 molecular biology
10.1101/2025.10.01.679597 bioRxiv
Show abstract

For BRCA mutation (BRCA+) carriers, the risk of ovarian cancer can be as high as 59% compared with 1.4% for the general population. While the impact of BRCA mutations on epithelial cell transformation has been extensively studied, we hypothesize that these mutations cause structural changes that prematurely transform the ovary into a rich metastatic niche that supports the early onset of ovarian cancer. Analysis of collagen content and organization in human ovaries revealed increased coherence associated with fibrosis in premenopausal BRCA+ ovaries relative to those without a BRCA mutation. Brca1 deficiency and haploinsufficiency in murine ovarian fibroblasts triggered the expression of hallmarks of senescence, including Cdkn2a (p16) and acidic {beta}-galactosidase activity. Brca1-deficient fibroblasts also acquired an antigen-presenting myofibroblastic phenotype, characterized by expression of MHC-II molecules, -SMA and extracellular matrix components, suggesting the capacity to modulate immune activity and drive structural changes resembling fibrosis. These results provide insight into the mechanisms contributing to accelerated ovarian aging in BRCA+ carriers. TeaserBRCA mutation promotes fibroblast hyperactivity and senescence that changes the stromal architecture of the ovarian niche.

Matching journals

The top 12 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.