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

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

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114 Scopus citations

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)
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

Cite this

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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 = "Cancer Research",

issn = "0008-5472",

publisher = "American Association for Cancer Research Inc.",

number = "6",

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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 (

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M3 - Article

C2 - 9067291

AN - SCOPUS:0030890994

SN - 0008-5472

VL - 57

SP - 1188

EP - 1193

JO - Cancer Research

JF - Cancer Research

IS - 6

ER -

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

Abstract

ASJC Scopus subject areas

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