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 journalArticle

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

Fingerprint

Loss of Heterozygosity
Genetic Recombination
Microsatellite Repeats
Clone Cells
Heterozygote
Adenine Phosphoribosyltransferase
T-Lymphocytes
Germ-Line Mutation
Point Mutation
Genes
2,6-diaminopurine

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

Gupta, P. K., Sahota, A., Boyadjiev, S. A., Bye, S., Shao, C., Patrick O'Neill, J., ... Tischfieid, J. A. (1997). High frequency in vivo loss of heterozygosity is primarily a consequence of mitotic recombination. Cancer Research, 57(6), 1188-1193.

High frequency in vivo loss of heterozygosity is primarily a consequence of mitotic recombination. / Gupta, Pawan K.; Sahota, Amrik; Boyadjiev, Simeon A.; Bye, Steven; Shao, Changshun; Patrick O'Neill, J.; Hunter, Timothy C.; Albertini, Richard J.; Stambrook, Peter J.; Tischfieid, Jay A.

In: Cancer Research, Vol. 57, No. 6, 1997, p. 1188-1193.

Research output: Contribution to journalArticle

Gupta, PK, Sahota, A, Boyadjiev, SA, Bye, S, Shao, C, Patrick O'Neill, J, Hunter, TC, Albertini, RJ, Stambrook, PJ & Tischfieid, JA 1997, 'High frequency in vivo loss of heterozygosity is primarily a consequence of mitotic recombination', Cancer Research, vol. 57, no. 6, pp. 1188-1193.
Gupta PK, Sahota A, Boyadjiev SA, Bye S, Shao C, Patrick O'Neill J et al. High frequency in vivo loss of heterozygosity is primarily a consequence of mitotic recombination. Cancer Research. 1997;57(6):1188-1193.
Gupta, Pawan K. ; Sahota, Amrik ; Boyadjiev, Simeon A. ; Bye, Steven ; Shao, Changshun ; Patrick O'Neill, J. ; Hunter, Timothy C. ; Albertini, Richard J. ; Stambrook, Peter J. ; Tischfieid, Jay A. / High frequency in vivo loss of heterozygosity is primarily a consequence of mitotic recombination. In: Cancer Research. 1997 ; Vol. 57, No. 6. pp. 1188-1193.
@article{f7e2de6bc2e1403faabff69e4faaf61d,
title = "High frequency in vivo loss of heterozygosity is primarily a consequence of mitotic recombination",
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 (",
author = "Gupta, {Pawan K.} and Amrik Sahota and Boyadjiev, {Simeon A.} and Steven Bye and Changshun Shao and {Patrick O'Neill}, J. and Hunter, {Timothy C.} and Albertini, {Richard J.} and Stambrook, {Peter J.} and Tischfieid, {Jay A.}",
year = "1997",
language = "English (US)",
volume = "57",
pages = "1188--1193",
journal = "Journal of Cancer Research",
issn = "0099-7013",
publisher = "American Association for Cancer Research Inc.",
number = "6",

}

TY - JOUR

T1 - High frequency in vivo loss of heterozygosity is primarily a consequence of mitotic recombination

AU - Gupta, Pawan K.

AU - Sahota, Amrik

AU - Boyadjiev, Simeon A.

AU - Bye, Steven

AU - Shao, Changshun

AU - Patrick O'Neill, J.

AU - Hunter, Timothy C.

AU - Albertini, Richard J.

AU - Stambrook, Peter J.

AU - Tischfieid, Jay A.

PY - 1997

Y1 - 1997

N2 - 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 (

AB - 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 (

UR - http://www.scopus.com/inward/record.url?scp=0030890994&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030890994&partnerID=8YFLogxK

M3 - Article

C2 - 9067291

AN - SCOPUS:0030890994

VL - 57

SP - 1188

EP - 1193

JO - Journal of Cancer Research

JF - Journal of Cancer Research

SN - 0099-7013

IS - 6

ER -