Subserous uterine fibroid

Summary

Subserous uterine fibroid (MONDO:0001745) is a disease. A subtype of uterine corpus leiomyoma — 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	subserous uterine fibroid
Mondo ID	MONDO:0001745
DOID	DOID:13560
SNOMED CT	95280005
UMLS	C0153995
MedGen	509503
GARD	0023001
Is cancer (heuristic)	no

Also known as: subserous leiomyoma of uterus

Disease family

This is a subtype of uterine corpus leiomyoma. 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: disease › human disease › disease by body system or component › musculoskeletal system disorder › musculoskeletal system benign neoplasm › benign muscle neoplasm › benign smooth muscle neoplasm › leiomyoma › uterine corpus leiomyoma › subserous uterine fibroid

Related subtypes (10): submucous uterine fibroid, uterine corpus epithelioid leiomyoma, uterine corpus dissecting leiomyoma, uterus interstitial leiomyoma, uterine corpus myxoid leiomyoma, uterine corpus lipoleiomyoma, uterine corpus bizarre leiomyoma, uterine corpus diffuse leiomyomatosis, uterine corpus apoplectic leiomyoma, uterine corpus cellular leiomyoma

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.