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HRAS mutation

Deterministic view of the source YAML entity. Clinical authority remains with the cited source IDs and reviewer sign-off state.

IDBIO-HRAS
TypeBiomarker
Aliases
HRAS G12HRAS G13HRAS Q61Мутація HRAS
Statusreviewed 2026-04-27 | pending_clinical_signoff
DiseasesNone declared
SourcesSRC-NCCN-BLADDER-2025 SRC-ONCOKB

Biomarker Facts

Biomarker typegene_mutation
Mutation details{"functional_impact": "Constitutive GTP-bound HRAS → MAPK / PI3K signaling", "gene": "HRAS", "gene_hugo_id": "HGNC:5173", "hotspots": ["G12X (exon 2 — codon 12; G12V / G12D / G12S most common)", "G13X (exon 2 — codon 13)", "Q61X (exon 3 — codon 61; Q61R / Q61K most common in HNSCC)"], "variant_type": "activating missense"}
Measurement
MethodDNA-NGS (preferred) OR ctDNA NGS OR allele-specific PCR (codon 12 / 13 / 61)
Unitscategorical; variant + VAF reported
Sensitivity requirementStandard NGS; tipifarnib enrolment uses VAF threshold ≥20% in some trials
Related biomarkersBIO-KRAS-G12C BIO-RAS-MUTATION

Notes

HNSCC: ~5–8% (KURRENT-HN — tipifarnib + alpelisib activity in HRAS-mutant + PIK3CA-mut/amp subset). Thyroid (PDTC / ATC subset): ~5%. Urothelial / bladder: ~5%. Salivary duct carcinoma: ~10–15%. Tipifarnib (farnesyl-transferase inhibitor) is the only HRAS-targeted agent with positive single-arm signal — KO-TIP-001 (Ho et al, JCO 2021) in R/M HRAS-mutant HNSCC achieved ORR ~55% in VAF-≥20% subset → FDA breakthrough designation; phase 3 AIM-HN ongoing. HRAS depends on farnesylation for membrane localization (KRAS / NRAS use geranylgeranyl alternative pathway → tipifarnib less active vs KRAS / NRAS).

Used By

Diseases

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