Evaluating the landscape of gene cooperativity with receptor tyrosine kinases in liver tumorigenesis using transposon-mediated mutagenesis

Hepatocellular carcinoma (HCC) is among the most aggressive cancers, with an increasing incidence, and few therapeutic options[1]. The exceptional investments on -omics studies over the last decade have unveiled not only an impressive list of alterations, but also a high degree of molecular heterogeneity between HCC patients[2,3]. The uniqueness of HCC in its alterations and heterogeneity may explain how treatments effective in other cancers have largely failed when applied to HCC[4]. Such context challenges the interpretation of -omics data, with the necessity to: 1) determine which of these alterations are functionally relevant for tumorigenic properties, 2) distinguish sets of alterations with a tumour-boosting efficiency linked to specific patient subtypes or genetic contexts, and 3) elucidate how different combinatorial alterations can lead to equivalent versus divergent fitness outcomes in cancer cells.

Source: Journal of Hepatology - December 5, 2018 Category: Gastroenterology Authors: Yannan Fan, Sehrish K. Bazai, Fabrice Daian, Maria Arechederra, Sylvie Richelme, Nuri A. Temiz, Annie Yim, Bianca H. Habermann, Rosanna Dono, David A. Largaespada, Flavio Maina Source Type: research