{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Rose AAN"],"funding":["Conquer Cancer Foundation (Conquer Cancer Foundation of the American Society of Clinical Oncology)","Canada Foundation for Innovation (Fondation canadienne pour l'innovation)","Gouvernement du Canada | Canadian Institutes of Health Research (Instituts de Recherche en Santé du Canada)"],"pagination":["1323"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12873207"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["17(1)"],"pubmed_abstract":["Class 2 and 3 non-V600E BRAF mutations are oncogenic drivers in many cancer types. Currently, there are no established targeted therapies with proven efficacy for cancers with non-V600E BRAF mutations. We developed the investigator-initiated, Phase II BEAVER clinical trial (NCT03839342) to evaluate the efficacy of BRAF and MEK inhibitors in patients with non-V600E BRAF mutations. The primary outcome was objective response rate (ORR). The best ORR was 14% (3/21), the primary endpoint was not met. By analyzing genomic data from patient tumors, circulating tumor DNA (ctDNA), patient-derived xenograft (PDX) models generated from enrolled patients, and Class 2 & 3 BRAF mutant cell lines, we discovered MAPK-dependent and independent mechanisms of resistance to BRAF/MEK inhibition. These mechanis"],"journal":["Nature communications"],"pubmed_title":["Binimetinib and encorafenib for the treatment of advanced solid tumors with non-V600E BRAF mutations: results from the Phase II BEAVER trial."],"pmcid":["PMC12873207"],"funding_grant_id":["707457","42153","180379","197819"],"pubmed_authors":["Biondini M","Elia AJ","Cescon DW","Cianfarano E","Kamil ZS","King I","Soria-Bretones I","Maxwell J","Spreafico A","Siegel PM","Siu LL","Riaud M","Butler M","Hansen A","Saibil SD","Tobin C","Pugh TJ","Elkholi IE","Law RWY","Rousselle E","Rose AAN","McGuire M","Bedard PL","Wang BX","Zhang T","Shepherd FA","Mukonoweshuro CL","Leighl NB","Razak AA"],"additional_accession":[]},"is_claimable":false,"name":"Binimetinib and encorafenib for the treatment of advanced solid tumors with non-V600E BRAF mutations: results from the Phase II BEAVER trial.","description":"Class 2 and 3 non-V600E BRAF mutations are oncogenic drivers in many cancer types. Currently, there are no established targeted therapies with proven efficacy for cancers with non-V600E BRAF mutations. We developed the investigator-initiated, Phase II BEAVER clinical trial (NCT03839342) to evaluate the efficacy of BRAF and MEK inhibitors in patients with non-V600E BRAF mutations. The primary outcome was objective response rate (ORR). The best ORR was 14% (3/21), the primary endpoint was not met. By analyzing genomic data from patient tumors, circulating tumor DNA (ctDNA), patient-derived xenograft (PDX) models generated from enrolled patients, and Class 2 & 3 BRAF mutant cell lines, we discovered MAPK-dependent and independent mechanisms of resistance to BRAF/MEK inhibition. These mechanis","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Jan","modification":"2026-07-15T13:52:28.975Z","creation":"2026-07-05T03:11:42.462Z"},"accession":"S-EPMC12873207","cross_references":{"pubmed":["41484121"],"doi":["10.1038/s41467-025-68076-7"]}}