Corrigendum to 'p53 Reactivation by PRIMA-1Met (APR-246) Sensitises V600E/KBRAF Melanoma to Vemurafenib'[eur J of Cancer 55 (2016) 98-110].

The authors regret that an unintentional mistake occurred when mounting the final figures, It concerns control experiments (Fig. 5B-MM074-ERK, Fig. 5B-AKT, and Fig. 5E-AKT), this mistake does not change or alter the content and conclusions of the paper. Please find here the correct figures.View Large Image Figure ViewerDownload Hi-res image Download (PPT) The authors would like to apologise for any inconvenience caused. p53 Reactivation by PRIMA-1Met (APR-246) sensitises V600E/KBRAF melanoma to vemurafenibEuropean Journal of CancerVol. 55PreviewIntrinsic and acquired resistance of metastatic melanoma to V600E/KBRAF and/or MEK inhibitors, which is often caused by activation of the PI3K/AKT survival pathway, represents a major clinical challenge. Given that p53 is capable of antagonising PI3K/AKT activation we hypothesised that pharmacological restoration of p53 activity may increase the sensitivity of BRAF-mutant melanoma to MAPK-targeted therapy and eventually delay and/or prevent acquisition of drug resistance. To test this possibility we exposed a panel of vemurafenib-sensitive and resistant (innate and acquired) V600E/KBRAF melanomas to a V600E/KBRAF inhibitor (vemurafenib) alone or in combination with a direct p53 activator (PRIMA-1Met/APR-246). Full-Text PDF