A wealth of evidence has demonstrated that the microenvironment in which a tumorigenic cell evolves is as critical to its evolution as the genetic mutations it accrues. We found that carcinoma-associated fibroblasts (CAFs), and the distinct ECM they deposit, can cause increased dissemination and metastasis, while healthy fibroblasts constrain these traits. A defining molecular characteristic of CAFs is their repression of CD36 and the reprogramming of adjacent cells in the stromal microenvironment that ensues. Using both in vitro and in vivo assays, we demonstrated that CD36 repression is necessary and sufficient to recapitulate the pro-tumorigenic phenotypes observed in desmoplasia. Consistent with a functional role for this coordinated, multi-cellular program in tumorigenesis, we observed that clinical outcomes were strongly associated with low CD36 expression. Modulating CD36 may be a valuable tool in prevention and intervention of carcinogenesis.
***Please note this seminar is on a Friday***
- Speaker: Thea D Tlsty, University of California San Francisco (UCSF) Helen Diller Comprehensive Cancer Center and Department of Pathology, 513 Parnassus Avenue, San Francisco, CA 94143-0511
- Friday 26 April 2019, 13:00-14:00
- Venue: CRUK CI Lecture Theatre.
- Series: Cancer Research UK Cambridge Institute (CRUK CI) Seminars in Cancer; organiser: Kate Davenport.