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|Protein Effect||loss of function - predicted|
|Gene Variant Descriptions||NRAS G13R is a hotspot mutation that lies within a GTP-binding region of the Nras protein (UniProt.org). G13R has not been characterized, but can be predicted to confer a loss of function on Nras protein based on the effects of HRAS G13R, which results in increased GTP-bound Hras, constitutive activation of Mapk and Akt signaling, and increased cell proliferation in culture (PMID: 22683711).|
|Associated Drug Resistance|
|Transcript||gDNA||cDNA||Protein||Source Database||Genome Build|
|Molecular Profile||Indication/Tumor Type||Response Type||Therapy Name||Approval Status||Evidence Type||Efficacy Evidence||References|
|BRAF G596V NRAS G13R||colorectal cancer||sensitive||Cetuximab + LSN3074753||Preclinical - Pdx||Actionable||In a preclinical study, LSN3074753 and Erbitux (cetuximab) worked synergistically, resulting in tumor regression in a patient-derived xenograft model of colorectal cancer harboring BRAF G596V and NRAS G13R (PMID: 28611205).||28611205|
|BRAF V600E NRAS G13R||colorectal cancer||predicted - resistant||Alpelisib + Cetuximab + Encorafenib||Case Reports/Case Series||Actionable||In a clinical case study, a patient with BRAF V600E colorectal cancer developed progressive disease after a partial response lasting 24 weeks to Alpelisib (BYL719), Erbitux (cetuximab), and Braftovi (encorafenib) combination treatment, NRAS G13R was identified as an acquired mutation in liver metastasis at the time of progression (PMID: 28951457).||28951457|
|BRAF V600E NRAS G13R||colorectal cancer||predicted - sensitive||BGB659 + Cetuximab||Preclinical - Pdx||Actionable||In a preclinical study, BGB659 and Erbitux (cetuximab) combination treatment resulted in sustained inhibition of Mek and Erk phosphorylation, lead to tumor regression in patient-derived xenograft models of colorectal cancer harboring BRAF V600E and NRAS G13R (PMID: 28951457).||28951457|