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 language | English (US) |
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Pages (from-to) | 1188-1193 |
Number of pages | 6 |
Journal | Cancer Research |
Volume | 57 |
Issue number | 6 |
State | Published - 1997 |
Externally published | Yes |
ASJC Scopus subject areas
- Cancer Research
- Oncology