Chris Mitchell

TL;DR: The flagship paper of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes Consortium describes the generation of the integrative analyses of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types, the structures for international data sharing and standardized analyses, and the main scientific findings from across the consortium studies.

TL;DR: It is shown that gene breakage commonly inactivates the tumour suppressors RB1, NF1, RAD51B and PTEN in HGSC, and contributes to acquired chemotherapy resistance.

TL;DR: Findings suggest a specific dependency of CC NE1-amplified tumors for AKT activity, and point to a novel combination of dinaciclib and AKT inhibitors that may selectively target patients with CCNE1-AMplified HGSC.

TL;DR: The findings suggest that cyclinE1/CDK2 is an important therapeutic target in HGSC, but that resistance to CDK 2 inhibitors may emerge due to upregulation of CDK2 target protein and through preexisting cellular polyploidy.

TL;DR: After six months of imatinib, computed tomography and positron emission tomography imaging demonstrated a significant size reduction and complete metabolic response to treatment, rendering the tumour resectable.