{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["McFall T"],"funding":["National Cancer Institute","NCI NIH HHS"],"pagination":["179"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7643456"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["18(1)"],"pubmed_abstract":["Phase three clinical trial evidence suggests that colorectal cancers with the KRAS G13D mutation may benefit from EGFR inhibitors, like cetuximab, in contrast to the other most common KRAS mutations. A mechanism to explain why this mutation behaves differently from other KRAS mutations had long been lacking. Two recent studies have reproduced KRAS G13D specific sensitivity to cetuximab in cellular models, and both have implicated the tumor suppressor NF1 as a critical variable in determining sensitivity and resistance. One study proposes a mechanism that focuses on the inhibition of active, GTP-bound wild-type RAS, which is proposed to occur to a greater extent in KRAS G13D tumors due to the inability of KRAS G13D to bind NF1 well. The other study suggests NF1 can convert GTP-bound KRAS G1"],"journal":["Cell communication and signaling : CCS"],"pubmed_title":["Discernment between candidate mechanisms for KRAS G13D colorectal cancer sensitivity to EGFR inhibitors."],"pmcid":["PMC7643456"],"funding_grant_id":["P30CA014195","R01CA223495","T32CA009370","K22CA216318","T32 CA009370","L30 CA162395","P30 CA014195","K22 CA216318","R01 CA223495"],"pubmed_authors":["Schomburg NK","McFall T","Stites EC","Rossman KL"],"additional_accession":[]},"is_claimable":false,"name":"Discernment between candidate mechanisms for KRAS G13D colorectal cancer sensitivity to EGFR inhibitors.","description":"Phase three clinical trial evidence suggests that colorectal cancers with the KRAS G13D mutation may benefit from EGFR inhibitors, like cetuximab, in contrast to the other most common KRAS mutations. A mechanism to explain why this mutation behaves differently from other KRAS mutations had long been lacking. Two recent studies have reproduced KRAS G13D specific sensitivity to cetuximab in cellular models, and both have implicated the tumor suppressor NF1 as a critical variable in determining sensitivity and resistance. One study proposes a mechanism that focuses on the inhibition of active, GTP-bound wild-type RAS, which is proposed to occur to a greater extent in KRAS G13D tumors due to the inability of KRAS G13D to bind NF1 well. The other study suggests NF1 can convert GTP-bound KRAS G1","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Nov","modification":"2026-07-09T10:35:46.804Z","creation":"2026-07-09T10:26:11.99Z"},"accession":"S-EPMC7643456","cross_references":{"pubmed":["33153459"],"doi":["10.1186/s12964-020-00645-3"]}}