Variant Synonymizer: Platform to identify mutations defined in different ways is available now!

VarSy

Over 2,000 gene–disease validation summaries are now available—no login required!

Browse Summaries

TC2N – von Willebrand Disease

The current evidence for the association between TC2N (HGNC:19859) and von Willebrand disease (MONDO_0024574) is limited. In multi‐patient studies, TC2N was included in a resequencing panel of eight genes evaluated in 104 Swedish von Willebrand disease patients (PMID:33145474). Although common variants across the panel were examined, TC2N did not display a statistically significant enrichment of rare or low-frequency variants relative to control populations, and there were no noted reports of family segregation or additional affected relatives carrying TC2N variants (PMID:25832887).

Functional studies and mechanistic assessments in these reports did not separately interrogate the role of TC2N, providing no direct experimental evidence to support a pathogenic mechanism. Consequently, while TC2N remains of interest as a potential modifier within the context of von Willebrand factor level variation, its contribution to disease etiology is not definitively established. The limited genetic and experimental evidence currently restricts its clinical utility, though further studies may clarify its role.

References

  • TH open: companion journal to thrombosis and haemostasis • 2020 • Common and Rare Variants in Genes Associated with von Willebrand Factor Level Variation: No Accumulation of Rare Variants in Swedish von Willebrand Disease Patients. PMID:33145474
  • Journal of thrombosis and haemostasis • 2015 • CLEC4M and STXBP5 gene variations contribute to von Willebrand factor level variation in von Willebrand disease. PMID:25832887

Evidence Based Scoring (AI generated)

Gene–Disease Association

Limited

Limited evidence from multi‑patient studies without significant variant enrichment or familial segregation specific to TC2N (PMID:33145474, PMID:25832887).

Genetic Evidence

Limited

TC2N was analyzed alongside other genes in large cohorts, yet no significant accumulation of pathogenic variants was observed in cases compared to controls.

Functional Evidence

Limited

No direct functional or mechanistic studies were performed for TC2N, limiting experimental support for its role in disease pathogenesis.