Impaired expression of NER gene network in sporadic solid tumors

Detalhes bibliográficos
Autor(a) principal: Castro, Mauro Antônio Alves
Data de Publicação: 2007
Outros Autores: Mombach, Jose Carlos Merino, Almeida, Rita Maria Cunha de, Moreira, Jose Claudio Fonseca
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UFRGS
Texto Completo: http://hdl.handle.net/10183/21537
Resumo: Nucleotide repair genes are not generally altered in sporadic solid tumors. However, point mutations are found scattered throughout the genome of cancer cells indicating that the repair pathways are dysfunctional. To address this point, in this work we focus on the expression pathways rather than in the DNA structure of repair genes related to either genome stability or essential metabolic functions. We present here a novel statistical analysis comparing ten gene expression pathways in human normal and cancer cells using serial analysis of gene expression (SAGE) data. We find that in cancer cells nucleotide-excision repair (NER) and apoptosis are the most impaired pathways and have a highly altered diversity of gene expression profile when compared to normal cells. We propose that genome point mutations in sporadic tumors can be explained by a structurally conserved NER with a functional disorder generated from its entanglement with the apoptosis gene network.
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spelling Castro, Mauro Antônio AlvesMombach, Jose Carlos MerinoAlmeida, Rita Maria Cunha deMoreira, Jose Claudio Fonseca2010-05-05T04:15:44Z20070305-1048http://hdl.handle.net/10183/21537000603211Nucleotide repair genes are not generally altered in sporadic solid tumors. However, point mutations are found scattered throughout the genome of cancer cells indicating that the repair pathways are dysfunctional. To address this point, in this work we focus on the expression pathways rather than in the DNA structure of repair genes related to either genome stability or essential metabolic functions. We present here a novel statistical analysis comparing ten gene expression pathways in human normal and cancer cells using serial analysis of gene expression (SAGE) data. We find that in cancer cells nucleotide-excision repair (NER) and apoptosis are the most impaired pathways and have a highly altered diversity of gene expression profile when compared to normal cells. We propose that genome point mutations in sporadic tumors can be explained by a structurally conserved NER with a functional disorder generated from its entanglement with the apoptosis gene network.application/pdfengNucleic acids research. Oxford. Vol. 35, no. 6 (Mar. 2007), p. 1859-1867TumoresReparação do DNANucleotídeosGenéticaImpaired expression of NER gene network in sporadic solid tumorsEstrangeiroinfo:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UFRGSinstname:Universidade Federal do Rio Grande do Sul (UFRGS)instacron:UFRGSORIGINAL000603211.pdf000603211.pdfTexto completo (inglês)application/pdf205201http://www.lume.ufrgs.br/bitstream/10183/21537/1/000603211.pdf73caf55922710d964f6aae661a78b7c7MD51TEXT000603211.pdf.txt000603211.pdf.txtExtracted Texttext/plain40860http://www.lume.ufrgs.br/bitstream/10183/21537/2/000603211.pdf.txt83d39705f87c2312b113724340b6a613MD52THUMBNAIL000603211.pdf.jpg000603211.pdf.jpgGenerated Thumbnailimage/jpeg2175http://www.lume.ufrgs.br/bitstream/10183/21537/3/000603211.pdf.jpg82f7e91826422c26c2fc74de3e175dc7MD5310183/215372024-03-29 06:17:08.166985oai:www.lume.ufrgs.br:10183/21537Repositório de PublicaçõesPUBhttps://lume.ufrgs.br/oai/requestopendoar:2024-03-29T09:17:08Repositório Institucional da UFRGS - Universidade Federal do Rio Grande do Sul (UFRGS)false
dc.title.pt_BR.fl_str_mv Impaired expression of NER gene network in sporadic solid tumors
title Impaired expression of NER gene network in sporadic solid tumors
spellingShingle Impaired expression of NER gene network in sporadic solid tumors
Castro, Mauro Antônio Alves
Tumores
Reparação do DNA
Nucleotídeos
Genética
title_short Impaired expression of NER gene network in sporadic solid tumors
title_full Impaired expression of NER gene network in sporadic solid tumors
title_fullStr Impaired expression of NER gene network in sporadic solid tumors
title_full_unstemmed Impaired expression of NER gene network in sporadic solid tumors
title_sort Impaired expression of NER gene network in sporadic solid tumors
author Castro, Mauro Antônio Alves
author_facet Castro, Mauro Antônio Alves
Mombach, Jose Carlos Merino
Almeida, Rita Maria Cunha de
Moreira, Jose Claudio Fonseca
author_role author
author2 Mombach, Jose Carlos Merino
Almeida, Rita Maria Cunha de
Moreira, Jose Claudio Fonseca
author2_role author
author
author
dc.contributor.author.fl_str_mv Castro, Mauro Antônio Alves
Mombach, Jose Carlos Merino
Almeida, Rita Maria Cunha de
Moreira, Jose Claudio Fonseca
dc.subject.por.fl_str_mv Tumores
Reparação do DNA
Nucleotídeos
Genética
topic Tumores
Reparação do DNA
Nucleotídeos
Genética
description Nucleotide repair genes are not generally altered in sporadic solid tumors. However, point mutations are found scattered throughout the genome of cancer cells indicating that the repair pathways are dysfunctional. To address this point, in this work we focus on the expression pathways rather than in the DNA structure of repair genes related to either genome stability or essential metabolic functions. We present here a novel statistical analysis comparing ten gene expression pathways in human normal and cancer cells using serial analysis of gene expression (SAGE) data. We find that in cancer cells nucleotide-excision repair (NER) and apoptosis are the most impaired pathways and have a highly altered diversity of gene expression profile when compared to normal cells. We propose that genome point mutations in sporadic tumors can be explained by a structurally conserved NER with a functional disorder generated from its entanglement with the apoptosis gene network.
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dc.relation.ispartof.pt_BR.fl_str_mv Nucleic acids research. Oxford. Vol. 35, no. 6 (Mar. 2007), p. 1859-1867
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