Intravascular papillary endothelial hyperplasia

Summary

Intravascular papillary endothelial hyperplasia (MONDO:0043349) is a disease. A subtype of angiomatosis — 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	intravascular papillary endothelial hyperplasia
Mondo ID	MONDO:0043349
Orphanet	673525
ICD-11	1397961760
NCIT	C4391
SNOMED CT	238770007
UMLS	C0343083
MedGen	91005
GARD	0027060
Is cancer (heuristic)	no

Also known as: intravascular papillary endothelial hyperplasia · Masson lesion · Masson pseudotumor · Masson’s pseudoangiosarcoma · Masson’s pseudosarcoma · Masson’s pseudotumor · Masson’s tumor · Masson’s tumour · Masson’s vegetant hemangioma · Masson’s vegetant intravascular hemangio-endothelioma · papillary endothelial hyperplasia

Disease family

This is a subtype of angiomatosis. 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 etiologic mechanism › cancer or benign tumor › neoplastic disease or syndrome › neoplasm › benign neoplasm › cardiovascular organ benign neoplasm › benign blood vessel neoplasm › angiomatosis › intravascular papillary endothelial hyperplasia

Related subtypes (1): bacillary angiomatosis

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.