Registered report: RAF inhibitors prime wild-type RAF to activate the MAPK pathway and enhance growth
Abstract
The Reproducibility Project: Cancer Biology seeks to deal with growing concerns about reproducibility in research by performing replications of selected experiments from numerous high-profile papers in the area of cancer biology. The papers, that have been printed between 2010 and 2012, were selected based on citations and Altmetric scores (Errington et al., 2014). This Registered Report describes the suggested replication plan of key experiments from ‘RAF inhibitors prime wild-type RAF to activate the MAPK path and enhance growth’ by Hatzivassiliou and colleagues, printed anyway this year (Hatzivassiliou et al., 2010). Hatzivassiliou and colleagues examined the paradoxical response of RAF-WT tumors to treatment with RAF inhibitors. The important thing experiments being replicated include Figure 1A, where the original authors shown that management of a subset of BRAF(WT) tumor cell lines with RAF small molecule inhibitors led to a rise in cell viability, Figure 2B, which reported that RAF inhibitor activation from the MAPK path was determined by CRAF although not BRAF, and Figure 4A, in which the dimerization of BRAF and CRAF was modulated through the RAF inhibitor PLX4720, although not GDC-0879. The Reproducibility Project: Cancer Biology is really a collaboration GDC-0879 between your Center for Open Science and Science Exchange, and also the outcomes of the replications is going to be printed by eLife.