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The association between FCGRT and uterine corpus leiomyoma is currently supported by limited clinical evidence. In a multi‐gene family study of familial cancers, FCGRT (HGNC:3621) was identified among several candidate genes in patients presenting with uterine corpus leiomyoma (MONDO_0007886) along with other neoplasms, such as colon, breast, and prostate cancers (PMID:27900359). However, no FCGRT‑specific pathogenic variant was reported, and segregation analysis in affected families remains uninformative, with no additional affected relatives clearly segregating a FCGRT variant. These factors constrain the strength of the gene‑disease association.
Functional assays provide moderate support for FCGRT’s biological role. Multiple in vitro studies have confirmed that FCGRT, which encodes the neonatal Fc receptor, has a robust role in binding immunoglobulin G and regulating its homeostasis (PMID:8700168), yet these investigations have not directly demonstrated a link between FCGRT dysfunction and the development of uterine corpus leiomyoma. In summary, while the molecular function of FCGRT is well established, its contribution to uterine corpus leiomyoma pathogenesis remains to be clearly elucidated. Key take‑home: Current evidence, while informative on molecular function, mandates further focused studies to establish a causal role in uterine corpus leiomyoma.
Gene–Disease AssociationLimitedThe association is supported by limited evidence from multi‐gene analyses in familial cancer cases showing co‐occurrence with uterine corpus leiomyoma (PMID:27900359). The absence of FCGRT‐specific variants and clear segregation data restricts a stronger clinical assertion. Genetic EvidenceLimitedNo FCGRT‐specific pathogenic variants were identified. Genetic evidence is restricted to incidental findings within regions of homozygosity without independent replication (PMID:27900359). Functional EvidenceModerateRobust in vitro studies confirm FCGRT’s role in IgG binding and homeostasis (PMID:8700168); however, these assays do not directly link altered receptor function to the pathogenesis of uterine corpus leiomyoma. |