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

@article{Gupta1997HighFI,
  title={High frequency in vivo loss of heterozygosity is primarily a consequence of mitotic recombination.},
  author={Puspendra Kumar Gupta and Amrik Sahota and Simeon A. Boyadjiev and Stephen J. Bye and Chunbo Shao and John Patrick O'Neill and Timothy C. Hunter and Richard J. Albertini and Peter J. Stambrook and Jay A. Tischfield},
  journal={Cancer research},
  year={1997},
  volume={57 6},
  pages={1188-93}
}
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 microM 2,6-diaminopurine. A total of 80 2,6-diaminopurine-resistant T-cell clones from 2 of the heterozygotes were analyzed for… CONTINUE READING