Report of a bi-allelic truncating germline mutation in TP53

Fam Cancer. 2019 Jan;18(1):101-104. doi: 10.1007/s10689-018-0087-1.

Abstract

The TP53 gene is fundamental to genomic integrity, cell cycle regulation, and apoptosis; it is the most commonly mutated gene in human cancer. Heterozygous germline mutations cause the autosomal dominant cancer predisposition syndrome, Li-Fraumeni Syndrome. Homozygous germline TP53 mutations in humans are rare. We report an infant from a consanguineous family who presented with synchronous malignancies. Remarkably, he carries a homozygous germline TP53 mutation (NM_000546.4:c.52delA), predicted to cause protein truncation. The family history is consistent with Li-Fraumeni syndrome.

Keywords: Homozygous germline; Li-Fraumeni syndrome; Pediatric oncology; TP53.

Publication types

  • Case Reports
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Carcinoma / diagnostic imaging
  • Carcinoma / genetics*
  • Choroid Plexus Neoplasms / diagnostic imaging
  • Choroid Plexus Neoplasms / genetics*
  • Consanguinity
  • Germ-Line Mutation
  • Homozygote
  • Humans
  • Infant
  • Li-Fraumeni Syndrome / genetics*
  • Magnetic Resonance Imaging
  • Male
  • Neoplasms, Multiple Primary / diagnostic imaging
  • Neoplasms, Multiple Primary / genetics*
  • Orbital Neoplasms / diagnostic imaging
  • Orbital Neoplasms / genetics*
  • Pedigree
  • Rhabdomyosarcoma, Embryonal / diagnostic imaging
  • Rhabdomyosarcoma, Embryonal / genetics*
  • Tumor Suppressor Protein p53 / genetics*

Substances

  • TP53 protein, human
  • Tumor Suppressor Protein p53

Supplementary concepts

  • Choroid Plexus Carcinoma

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