High frequency in vivo loss of heterozygosity is primarily a consequence of mitotic recombination

Pawan K. Gupta, Amrik Sahota, Simeon A. Boyadjiev, Steven Bye, Changshun Shao, J. Patrick O'Neill, Timothy C. Hunter, Richard J. Albertini, Peter J. Stambrook, Jay A. Tischfieid

Research output: Contribution to journalArticlepeer-review

Abstract

We have used the adenine phosphoribosyltransferase gene (APRT; 16q24) to investigate the mechanisms of loss of heterozygosity (LOH) in normal human somatic cells in vivo. APRT-deficient (APRT(-/-), APRT(-/0) T lymphocytes from the peripheral blood of four obligate APRT heterozygotes (APRT(+/-) with characterized germ-line mutations were selected in medium containing 100 μM 2,6-diaminopurine. A total of 80 2,6-diaminopurine-resistant T-cell clones from 2 of the heterozygotes were analyzed for this study. The presence or absence of LOH of proximal linked microsatellite repeat markers was used to divide the clones into two groups: (a) those in which LOH was likely due to localized changes in APRT (e.g., point mutations); and (b) those with LOH at additional loci. A total of 61 clones (76%) exhibited LOH of linked microsatellite repeat markers at different locations of 16q, which extended from the smallest measured region (

Original languageEnglish (US)
Pages (from-to)1188-1193
Number of pages6
JournalCancer Research
Volume57
Issue number6
StatePublished - 1997
Externally publishedYes

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

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