Supratentorial ependymoma

Summary

Supratentorial ependymoma (MONDO:0850340) is a disease. A subtype of anaplastic ependymoma — broader associated-gene and molecular evidence is on the parent page (see Disease family below).

Clinical features

No curated clinical features (Orphanet) for this disease.

Identifiers

Disease identifiers

Field	Value
Canonical name	supratentorial ependymoma
Mondo ID	MONDO:0850340
DOID	DOID:0080890
NCIT	C186343
UMLS	C5670470
MedGen	1811811
GARD	0026606
Is cancer (heuristic)	no

Disease family

This is a subtype of anaplastic ependymoma. Genetic, therapeutic, and trial evidence is largely curated at the broader-term level — see the parent page for the associated-gene cohort and molecular evidence.

Classification path: human disease › disease by etiologic mechanism › cancer or benign tumor › neoplastic disease or syndrome › neoplasm › nervous system neoplasm › neuroepithelial neoplasm › glioma › ependymal tumor › anaplastic ependymoma › supratentorial ependymoma

Related subtypes (2): adult anaplastic ependymoma, posterior fossa ependymoma

Subtypes (3): YAP1-MAMLD1 fusion-positive supratentorial ependymoma, supratentorial ependymoma, ZFTA fusion–positive, supratentorial ependymoma, YAP1 fusion–positive

Genetics & variants

GWAS landscape

No GWAS associations recorded — common-variant (GWAS) studies don’t cover this disease (typical for Mendelian / rare diseases). See the curated gene cohort and Mendelian overlap below.

Variant details and genetic-evidence tiers

No tiered GWAS variants or ClinVar records for this disease.

Genes & proteins

No associated-gene cohort resolved for this disease. Atlas builds the molecular and therapeutic sections — associated genes, protein families, druggability, pathways, interactions, and drug associations — by aggregating over a disease’s associated genes (resolved via GWAS / GenCC / ClinVar / CIViC), and none resolved here. This is expected for antibody-mediated, autoimmune, or otherwise non-gene-defined conditions; the curated evidence for this disease is its clinical features, GWAS susceptibility, and clinical trials (above).

Function

No pathway enrichment — requires an associated-gene cohort.

Therapeutics

No druggable-target or therapeutic data for this disease’s cohort.

Clinical trials & evidence

Clinical trials

Clinical trials: 0.