Marc A. Vittoria

TL;DR: Together these data suggest that common abnormalities of melanomas linked to tumorigenesis - amplified centrosomes and whole-genome doubling events - can be induced by oncogenic BRAF and other mutations that increase RAS/MAPK pathway activity.

TL;DR: The data reveal several avenues through which tetraploid cells may regain the proliferative capacity necessary to drive tumorigenesis, and a comprehensive, gain-of-function genome-wide screen to identify miRNAs that are sufficient to promote the proliferation of tetraPloid cells.

TL;DR: It is demonstrated that loss of STK25 blunts the ability of cells to activate Hippo signaling and is sufficient to significantly increase levels of active YAP/TAZ to enhance cellular proliferation.

TL;DR: In this article, the Hippo tumor suppressor pathway was shown to be activated in growth-arrested nevus melanocytes in vivo, both from single-cell sequencing of mouse models of nevogenesis and human tissue samples.

TL;DR: It is demonstrated that loss of STK25 promotes YAP/TAZ activation and enhanced cellular proliferation, even under normally growth-suppressive conditions, and that STk25 activates LATS via a previously unobserved mechanism, in which STK 25 directly phosphorylates the LATS activation loop.