Marc A. Vittoria

TL;DR: This paper showed that WGD+ cells are more dependent than WGD-cells on signalling from the spindle-assembly checkpoint, DNA-replication factors and proteasome function and identified KIF18A, which encodes a mitotic kinesin protein, as being specifically required for the viability of whole-genome doubling (WGD+) cells.

TL;DR: It is shown that WGD gives rise to common genetic traits that are accompanied by unique vulnerabilities, and KIF18A, which encodes for a mitotic kinesin, is identified as being specifically required for the viability of WGD+ cells.

TL;DR: It is demonstrated that loss of STK25 promotes YAP/TAZ activation and enhanced cellular proliferation, even under normally growth-suppressive conditions both in vitro and in vivo, and is significantly focally deleted across a wide spectrum of human cancers.

TL;DR: A comprehensive gain-of-function genome-wide screen to identify microRNAs (miRNAs) that are sufficient to promote the proliferation of tetraploid cells reveals several avenues through which tetraPloid cells may regain the proliferative capacity necessary to drive tumorigenesis.

TL;DR: Live-cell imaging protocols to assess cell fate decisions following treatment with the anti-mitotic drug paclitaxel are described and methods to visualize whether mitotically arrested cells die directly from mitosis or slip back into interphase are demonstrated.