OpenOnco
UA EN

Onco Wiki / Biomarker

MAP2K1 activating mutation (MEK1)

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

IDBIO-MAP2K1
TypeBiomarker
Aliases
MAP2K1 / MEK1 mutationАктивуюча мутація MAP2K1 (MEK1)
Statusreviewed 2026-05-04 | pending_clinical_signoff
DiseasesNone declared
SourcesSRC-EANO-LGG-2024 SRC-NCCN-CNS-2025

Biomarker Facts

Biomarker typegene_mutation
Mutation details{"exon": "2, 3 (kinase domain)", "functional_impact": "activating", "gene": "MAP2K1", "variant_type": "missense activating"}
Measurement
MethodTumor NGS panel; key variants: K57E (~30% of HCL-V), Q56P, E203K, F53L, D67N
Actionability lookup{"gene": "MAP2K1", "variant": "activating_mutation"}
Related biomarkersBIO-BRAF-V600E

Notes

MAP2K1 (MEK1) is a dual-specificity kinase directly downstream of BRAF and upstream of ERK1/2. Activating mutations constitute an alternative mechanism of MAPK pathway activation in tumors that lack BRAF mutations. Key clinical contexts: (1) Hairy cell leukemia variant (HCL-V): MAP2K1 K57E present in ~40–50% of HCL-V cases (which are BRAF V600E-negative by definition). Cobimetinib (MEK inhibitor) shows activity in MAP2K1-mutant HCL-V in small series; no FDA approval but NCCN 2B evidence. (2) Low-grade glioma (LGG): MAP2K1 mutations are one of the MAPK pathway alterations (~5–10% of BRAF-fusion-negative LGGs). Trametinib (MEK inhibitor) shows activity in pediatric LGG with MAPK pathway alterations per FIREFLY-1 trial (binimetinib/trametinib). (3) Melanoma: MAP2K1 mutations occur in ~5–8% as secondary resistance to BRAF inhibitors; MEK inhibitors still active but combination needed. (4) Histiocytic disorders (ECD, LCH): MAP2K1 mutations as alternative to BRAF V600E. Do not confuse MEK inhibitors approved for BRAF V600E indications — those approvals are as adjuncts to BRAF inhibitors (vemurafenib + cobimetinib; dabrafenib + trametinib) and are not driven by MAP2K1 mutation status.

Used By

Actionability