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MYD88 L265P mutation

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

IDBIO-MYD88-L265P
TypeBiomarker
Aliases
MYD88 L265PМутація MYD88 L265P
Statusreviewed 2026-04-25 | pending_clinical_signoff
DiseasesNone declared
SourcesSRC-NCCN-BCELL-2025

Biomarker Facts

Biomarker typegene_mutation
Mutation details{"functional_impact": "activating (constitutive NF-κB signaling)", "gene": "MYD88", "hgvs_protein": "p.L265P", "variant_type": "missense"}
Measurement
MethodPCR / ASO / NGS on bone marrow or peripheral blood
Unitscategorical (positive | negative)
Actionability lookup{"gene": "MYD88", "variant": "L265P"}
Related biomarkersBIO-CXCR4-WHIM

Notes

Cross-disease relevance — activating mutation in TLR/NF-κB pathway: - **Waldenström / LPL** (defining ~95%): predicts BTKi response — MYD88-mut patients respond well to zanubrutinib/ibrutinib monotherapy; MYD88-WT (rare) does NOT respond well, chemoimmuno (DRC, BR) preferred. CXCR4-WHIM co-mutation modulates depth of BTKi response. - **Primary CNS Lymphoma (PCNSL)** (~70-90%): defining-like marker; drives BTKi activity in r/r PCNSL (ibrutinib monotherapy emerging). - **DLBCL ABC subtype** (~30%): predicts ibrutinib activity (PHOENIX trial subset signal) — investigational, not yet driving 1L choice. - **Cutaneous DLBCL of leg type** (~70%): MYD88-mut frequent. Direct algorithm impact in WM 1L. Future: PCNSL workstream + DLBCL ABC 2L+ ibrutinib pathway.

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