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Cerebral vascular malformations v3.28 FOXM1 Achchuthan Shanmugasundram Classified gene: FOXM1 as Amber List (moderate evidence)
Cerebral vascular malformations v3.28 FOXM1 Achchuthan Shanmugasundram Added comment: Comment on list classification: As reviewed by Alexandra Njegic, PMID:38969938 reported a 60-year-old father and 31-year-old daughter with unilateral Moyamoya Disease and with c.1205 C > A variant in FOXM1 gene (p.(Ala402Glu). There is also functional evidence available for the identified variant from the publication.

This gene should be rated amber with current evidence.
Cerebral vascular malformations v3.28 FOXM1 Achchuthan Shanmugasundram Gene: foxm1 has been classified as Amber List (Moderate Evidence).
Cerebral vascular malformations v3.27 FOXM1 Achchuthan Shanmugasundram Phenotypes for gene: FOXM1 were changed from Moyamoya Disease (Unilateral) to Moyamoya disease, MONDO:0016820
Cerebral vascular malformations v3.26 FOXM1 Achchuthan Shanmugasundram edited their review of gene: FOXM1: Changed mode of inheritance: MONOALLELIC, autosomal or pseudoautosomal, imprinted status unknown
Cerebral vascular malformations v3.26 FOXM1 Achchuthan Shanmugasundram reviewed gene: FOXM1: Rating: AMBER; Mode of pathogenicity: None; Publications: 38969938; Phenotypes: Moyamoya disease, MONDO:0016820; Mode of inheritance: MONOALLELIC, autosomal or pseudoautosomal, NOT imprinted
Cerebral vascular malformations v3.18 FOXM1 Alexandra Njegic gene: FOXM1 was added
gene: FOXM1 was added to Cerebral vascular malformations. Sources: Literature
Mode of inheritance for gene: FOXM1 was set to MONOALLELIC, autosomal or pseudoautosomal, imprinted status unknown
Publications for gene: FOXM1 were set to 38969938
Phenotypes for gene: FOXM1 were set to Moyamoya Disease (Unilateral)
Penetrance for gene: FOXM1 were set to unknown
Review for gene: FOXM1 was set to AMBER
Added comment: 38969938: 1 family, affected father and daughter. In vitro studies with hCMEC/D3 cells overexpressing the variant showed reduced migration and tube formation and increased apoptosis proposed to be due to reduced BCL2 transcription.
Sources: Literature