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Article

Activating mutations in FGFR3 and HRAS reveal a shared genetic origin for congenital disorders and testicular tumors.

Nature genetics - 1 Nov 2009

Goriely Anne, Hansen Ruth M S, Taylor Indira B, Olesen Inge A, Jacobsen Grete Krag, McGowan Simon J, Pfeifer Susanne P, McVean Gilean A T, Rajpert-De Meyts Ewa, Wilkie Andrew O M

Abstract excerpt

Genes mutated in congenital malformation syndromes are frequently implicated in oncogenesis, but the causative germline and somatic mutations occur in separate cells at different times of an organism's life. Here we unify these processes to a single cellular event for mutations arising in male germ cells that show a paternal age effect. Screening of 30 spermatocytic seminomas for oncogenic mutations in 17 genes...

Read the complete abstract on PubMed

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Share to Age Distribution
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Aged, 80 and over

Share to Base Sequence

Share to Genes, ras

Share to Receptor, Fibroblast Growth Factor, Type 3

Share to Spermatozoa

Share to Testicular Neoplasms

Source

Open in PubMed Open full text

Identifiers

PMID: 19855393
DOI: 10.1038/ng.470
PMCID: PMC2817493

Genes

FGFR3
HRAS

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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