Familial meningioma: genes and variants

Familial meningioma is linked to 4 analyzed proteins (SMARCE1, PTEN, NF2 and SUFU). 7 DNA variants are known to cause it; 461 more are uncertain, and 0 of those already look disease-causing on computable evidence.

Last updated 2026-09-30. Research information, not medical advice.

Genes linked to Familial meningioma

Weakly linked (only a few uncertain records): RARA and BMPR1A.

Known disease-causing variants in Familial meningioma

VariantPositionProtein partClinical label
SMARCE1 R105Q105HMG boxDisease-causing (★★★★)
PTEN Y68H68Phosphatase tensin-typeDisease-causing (★★)
PTEN I135K135Phosphatase tensin-typeDisease-causing (★★)
SMARCE1 Y73C73HMG boxDisease-causing (★)
SMARCE1 G101S101HMG boxDisease-causing (★)
PTEN V255G255C2 tensin-typeDisease-causing (★)
SMARCE1 Y126D126HMG boxDisease-causing (★)

Same protein, different disease

Diseases related to Familial meningioma

Frequently asked questions

Which genes are linked to Familial meningioma?

In CATVariant, Familial meningioma is linked to 4 analyzed proteins: SMARCE1 (SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily E member 1), PTEN (Phosphatidylinositol 3,4,5-trisphosphate 3-phosphatase and dual-specificity protein phosphatase PTEN), NF2 (Merlin) and SUFU (Suppressor of fused homolog).

How many genetic variants are linked to Familial meningioma?

496 variants: 7 are classified as disease-causing (pathogenic or likely pathogenic) in ClinVar and 461 are of uncertain significance or have conflicting reports.

Which uncertain variants in Familial meningioma look disease-causing?

None of the uncertain variants currently reaches the likely-pathogenic range on computable evidence alone.

About this data

Variant–disease links come from ClinVar, Open Targets and UniProt, pooled from the latest public CATVariant analysis of each human protein. Evidence scores use the ACMG/AMP Bayesian points scale with computable criteria only (position among known disease variants, rarity in gnomAD, calibrated predictors, deep mutational scanning); there is no family or patient data, so they prioritise variants for expert review and never classify them.

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