| First Author | Aydin IT | Year | 2017 |
| Journal | Pigment Cell Melanoma Res | Volume | 30 |
| Issue | 6 | Pages | 571-574 |
| PubMed ID | 28581198 | Mgi Jnum | J:320946 |
| Mgi Id | MGI:6883150 | Doi | 10.1111/pcmr.12603 |
| Citation | Aydin IT, et al. (2017) FBXW7 inactivation in a Braf(V600E) -driven mouse model leads to melanoma development. Pigment Cell Melanoma Res 30(6):571-574 |
| abstractText | Human melanocytic nevi driven by BRAF(V600E) are in a growth-arrested state referred as oncogene-induced senescence. FBXW7 tumor suppressor is mutated in melanomas, but not in benign precursor melanocytic nevi. In order to characterize whether inactivation of FBXW7 in cooperation with BRAF(V600E) (Braf(V637E) in the mouse) is sufficient to bypass from the growth-arrested state, we generated a murine model by conditionally silencing Fbxw7 in an established system, Tyr::CreER; Braf(CA) (or Tyr::CreER; Braf(V600E)). We show that loss of Fbxw7 in the presence of Braf(V600E) mutation is consequential and sufficient to drive tumorigenesis. This model provides further evidence that Fbxw7 is a tumor suppressor in the melanocytic lineage, and can serve as a tool for future pre-clinical studies. |
