Gastrointestinal hyperplasia with altered expression of DNA polymerase beta.

<h4>Background</h4>Altered expression of DNA polymerase beta (Pol beta) has been documented in a large percentage of human tumors. However, tumor prevalence or predisposition resulting from Pol beta over-expression has not yet been evaluated in a mouse model.<h4>Methodology/princip...

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Autores principales: Katsuhiko Yoshizawa, Elena Jelezcova, Ashley R Brown, Julie F Foley, Abraham Nyska, Xiangli Cui, Lorne J Hofseth, Robert M Maronpot, Samuel H Wilson, Antonia R Sepulveda, Robert W Sobol
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Publicado: Public Library of Science (PLoS) 2009
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spelling oai:doaj.org-article:b65921f2bf664cfdb0ae6713d59bfa0a2021-12-02T20:12:07ZGastrointestinal hyperplasia with altered expression of DNA polymerase beta.1932-620310.1371/journal.pone.0006493https://doaj.org/article/b65921f2bf664cfdb0ae6713d59bfa0a2009-08-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/19654874/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>Altered expression of DNA polymerase beta (Pol beta) has been documented in a large percentage of human tumors. However, tumor prevalence or predisposition resulting from Pol beta over-expression has not yet been evaluated in a mouse model.<h4>Methodology/principal findings</h4>We have recently developed a novel transgenic mouse model that over-expresses Pol beta. These mice present with an elevated incidence of spontaneous histologic lesions, including cataracts, hyperplasia of Brunner's gland and mucosal hyperplasia in the duodenum. In addition, osteogenic tumors in mice tails, such as osteoma and osteosarcoma were detected. This is the first report of elevated tumor incidence in a mouse model of Pol beta over-expression. These findings prompted an evaluation of human gastrointestinal tumors with regard to Pol beta expression. We observed elevated expression of Pol beta in stomach adenomas and thyroid follicular carcinomas, but reduced Pol beta expression in esophageal adenocarcinomas and squamous carcinomas.<h4>Conclusions/significance</h4>These data support the hypothesis that balanced and proficient base excision repair protein expression and base excision repair capacity is required for genome stability and protection from hyperplasia and tumor formation.Katsuhiko YoshizawaElena JelezcovaAshley R BrownJulie F FoleyAbraham NyskaXiangli CuiLorne J HofsethRobert M MaronpotSamuel H WilsonAntonia R SepulvedaRobert W SobolPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 4, Iss 8, p e6493 (2009)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Katsuhiko Yoshizawa
Elena Jelezcova
Ashley R Brown
Julie F Foley
Abraham Nyska
Xiangli Cui
Lorne J Hofseth
Robert M Maronpot
Samuel H Wilson
Antonia R Sepulveda
Robert W Sobol
Gastrointestinal hyperplasia with altered expression of DNA polymerase beta.
description <h4>Background</h4>Altered expression of DNA polymerase beta (Pol beta) has been documented in a large percentage of human tumors. However, tumor prevalence or predisposition resulting from Pol beta over-expression has not yet been evaluated in a mouse model.<h4>Methodology/principal findings</h4>We have recently developed a novel transgenic mouse model that over-expresses Pol beta. These mice present with an elevated incidence of spontaneous histologic lesions, including cataracts, hyperplasia of Brunner's gland and mucosal hyperplasia in the duodenum. In addition, osteogenic tumors in mice tails, such as osteoma and osteosarcoma were detected. This is the first report of elevated tumor incidence in a mouse model of Pol beta over-expression. These findings prompted an evaluation of human gastrointestinal tumors with regard to Pol beta expression. We observed elevated expression of Pol beta in stomach adenomas and thyroid follicular carcinomas, but reduced Pol beta expression in esophageal adenocarcinomas and squamous carcinomas.<h4>Conclusions/significance</h4>These data support the hypothesis that balanced and proficient base excision repair protein expression and base excision repair capacity is required for genome stability and protection from hyperplasia and tumor formation.
format article
author Katsuhiko Yoshizawa
Elena Jelezcova
Ashley R Brown
Julie F Foley
Abraham Nyska
Xiangli Cui
Lorne J Hofseth
Robert M Maronpot
Samuel H Wilson
Antonia R Sepulveda
Robert W Sobol
author_facet Katsuhiko Yoshizawa
Elena Jelezcova
Ashley R Brown
Julie F Foley
Abraham Nyska
Xiangli Cui
Lorne J Hofseth
Robert M Maronpot
Samuel H Wilson
Antonia R Sepulveda
Robert W Sobol
author_sort Katsuhiko Yoshizawa
title Gastrointestinal hyperplasia with altered expression of DNA polymerase beta.
title_short Gastrointestinal hyperplasia with altered expression of DNA polymerase beta.
title_full Gastrointestinal hyperplasia with altered expression of DNA polymerase beta.
title_fullStr Gastrointestinal hyperplasia with altered expression of DNA polymerase beta.
title_full_unstemmed Gastrointestinal hyperplasia with altered expression of DNA polymerase beta.
title_sort gastrointestinal hyperplasia with altered expression of dna polymerase beta.
publisher Public Library of Science (PLoS)
publishDate 2009
url https://doaj.org/article/b65921f2bf664cfdb0ae6713d59bfa0a
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