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|Protein Effect||loss of function|
|Gene Variant Descriptions||HRAS G13R is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). G13R confers a loss of function on Hras protein as indicated by activation of Mapk and Pi3k signaling, 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|
|HRAS G13R||head and neck squamous cell carcinoma||predicted - sensitive||Tipifarnib||Preclinical - Pdx||Actionable||In a preclinical study, a head and neck squamous cell carcinoma patient-derived xenograft (PDX) model harboring HRAS G13R was sensitive to treatment with Zarnestra (tipifarnib), demonstrating inhibition of tumor growth, decreased cell proliferation, and reduced Erk activity (PMID: 32727882).||32727882|
|HRAS G13R||renal pelvis transitional cell carcinoma||predicted - sensitive||Tipifarnib||Case Reports/Case Series||Actionable||In a Phase II trial, Zarnestra (tipifarnib) demonstrated manageable toxicity profile, resulted in an objective response rate of 33.3% (5/15) in patients with transitional cell carcinoma harboring HRAS mutations, a patient with renal pelvis transitional cell carcinoma harboring HRAS G13R achieved a partial response (PMID: 32636318; NCT02535650).||32636318|
|HRAS G13R||thyroid gland cancer||sensitive||MK2206||Preclinical - Cell culture||Actionable||In a preclinical study, MK2206 inhibited AKT activation, proliferation, and growth of thyroid cancer cell lines with PI3K/AKT pathway alterations in culture, including an anaplastic thyroid cancer cell line harboring HRAS G13R (PMID: 21289267).||21289267|