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dc.contributor.CRUESPUNIVERSIDADE DE ESTADUAL DE CAMPINASpt_BR
dc.typeArtigo de periódicopt_BR
dc.titleCell Death Evaluation In Benzo[a]pyrene-transformed Human Breast Epithelial Cells After Microcell-mediated Transfer Of Chromosomes 11 And 17.pt_BR
dc.contributor.authorMello, Maria Luiza Spt_BR
dc.contributor.authorBarbisan, Luis Fernandopt_BR
dc.contributor.authorLareef, Mohamed Hpt_BR
dc.contributor.authorRusso, Josept_BR
dc.contributor.authorVidal, Benedicto de Campospt_BR
unicamp.authorMaria Luiza S Mello, Department of Cell Biology, Institute of Biology, UNICAMP, 13084-971 Campinas (SP), Brazil. mlsmello@unicamp.brpt_BR
unicamp.author.externalLuis Fernando Barbisan,pt
unicamp.author.externalMohamed H Lareef,pt
unicamp.author.externalJose Russo,pt
unicamp.author.externalBenedicto de Campos Vidal,pt
dc.subjectApoptosispt_BR
dc.subjectBenzo(a)pyrenept_BR
dc.subjectBreastpt_BR
dc.subjectCell Line, Transformedpt_BR
dc.subjectChromosomes, Human, Pair 11pt_BR
dc.subjectChromosomes, Human, Pair 17pt_BR
dc.subjectEpithelial Cellspt_BR
dc.subjectHumanspt_BR
dc.description.abstractThe incidence of apoptosis and nuclear instability, including the incidence of catastrophic death, were investigated in benzo[a]pyrene (BP)-transformed human breast epithelial cells (BP1-E cell line) after microcell-mediated transfer of chromosomes 11 and 17. Since the introduction of normal chromosomes 11 and 17 into tumorigenic human breast BP1-E cells reverts some of these cells' characteristics (especially those affected by microsatellite instabilities and loss of heterozygosity) to those of parental non-transformed MCF-10F cells, it was expected that the cell death rates would also be affected by this treatment. The transfer of the mentioned chromosomes, especially chromosome 17, to tumorigenic BP1-E cells increased the apoptotic ratios and decreased the nuclear instability ratios, thus showing that the microsatellite instability and loss of heterozygosity induced by BP in these chromosomes of MCF-10F cells affect the control of cell death mechanisms.en
dc.relation.ispartofMutation Researchpt_BR
dc.relation.ispartofabbreviationMutat. Res.pt_BR
dc.date.issued2004-Febpt_BR
dc.identifier.citationMutation Research. v. 546, n. 1-2, p. 39-43, 2004-Feb.pt_BR
dc.language.isoengpt_BR
dc.description.volume546pt_BR
dc.description.firstpage39-43pt_BR
dc.rightsfechadopt_BR
dc.sourcePubMedpt_BR
dc.identifier.issn0027-5107pt_BR
dc.identifier.urlhttp://www.ncbi.nlm.nih.gov/pubmed/14757191pt_BR
dc.date.available2015-11-27T12:58:25Z-
dc.date.accessioned2015-11-27T12:58:25Z-
dc.description.provenanceMade available in DSpace on 2015-11-27T12:58:25Z (GMT). No. of bitstreams: 1 pmed_14757191.pdf: 105426 bytes, checksum: 8ec406ea9ad818eb632e651f0876f305 (MD5) Previous issue date: 2004en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/195932-
dc.identifier.idPubmed14757191pt_BR
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