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PDGFRA mutation

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

IDBIO-PDGFRA
TypeBiomarker
Aliases
PDGFR-α mutationPDGFRA D842VМутація PDGFRA
Statusreviewed 2026-04-27 | pending_clinical_signoff
DiseasesNone declared
SourcesSRC-NCCN-MELANOMA-2025 SRC-ONCOKB

Biomarker Facts

Biomarker typegene_mutation
Mutation details{"functional_impact": "Constitutive PDGFRA tyrosine kinase activation", "gene": "PDGFRA", "gene_hugo_id": "HGNC:8803", "hotspots": ["D842V (exon 18 — activation loop; ~70% of PDGFRA-mutant GIST; imatinib-RESISTANT, avapritinib-sensitive)", "exon 18 non-D842V (deletions — imatinib-sensitive)", "exon 12 (juxtamembrane — imatinib-sensitive; rare)", "exon 14 (kinase domain — rare)"], "variant_type": "missense / deletion"}
Measurement
MethodDNA-NGS (preferred — covers exons 12 / 14 / 18) OR Sanger directed at exons 12 + 18
Unitscategorical; variant + exon reported
Sensitivity requirementStandard NGS
Related biomarkersBIO-KIT

Notes

~10% of GIST overall; ~80% of stomach (vs small-bowel) GIST. D842V (the dominant variant) is imatinib-RESISTANT and historically the worst-prognosis GIST subtype. Avapritinib (NAVIGATOR / VOYAGER) changed the paradigm — FDA-approved for unresectable / metastatic PDGFRA-D842V-mutant GIST 1L; ORR ~88% historical control vs ~0% on imatinib. Non-D842V exon-18 mutations and exon 12 mutations remain imatinib-sensitive. Eosinophilic disorders (myeloid neoplasms with PDGFRA fusion to FIP1L1 etc.) are a separate entity and use imatinib 100 mg / day.

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