Extensive somatic microsatellite mutations in normal human tissue

Cancer Res. 2001 Jun 1;61(11):4541-4.

Abstract

Microsatellite (MS) instability occurs in tumors with DNA mismatch repair (MMR) deficiencies but is typically absent in adjacent normal tissue. However, MS mutations have been observed in normal tissues from rare individuals with congenital MMR deficiencies. Autopsy tissues from a 4-year-old with congenital MMR deficiency (MLH1-/-) were examined for MS mutations. Insertions and deletions were observed in CA-repeat MS loci. Approximately 0.26 to 1.4 mutations per MS locus per cell were estimated to be present in normal heart, lymph node, kidney, and bladder epithelium. These findings illustrate that phenotypically normal MMR-deficient cells commonly accumulate MS mutations. Loss of MMR and the accumulation of some MS mutations may occur early in MMR-deficient tumor progression, even before a gatekeeper mutation.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adaptor Proteins, Signal Transducing
  • Base Pair Mismatch*
  • Brain Neoplasms / genetics
  • Carrier Proteins
  • Child, Preschool
  • DNA / genetics
  • DNA / isolation & purification
  • DNA Repair / genetics*
  • Female
  • Glioma / genetics
  • Humans
  • Microsatellite Repeats / genetics*
  • MutL Protein Homolog 1
  • Mutation
  • Neoplasm Proteins / genetics
  • Nuclear Proteins

Substances

  • Adaptor Proteins, Signal Transducing
  • Carrier Proteins
  • MLH1 protein, human
  • Neoplasm Proteins
  • Nuclear Proteins
  • DNA
  • MutL Protein Homolog 1