Chromosomal imbalances in successive moments of human bladder urothelial carcinoma

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dc.contributor.authorNascimento e Pontes, Merielen Garcia [UNESP]
dc.contributor.authorda Silveira, Sara Martorelli
dc.contributor.authorde Souza Trindade Filho, José Carlos
dc.contributor.authorRogatto, Silvia Regina [UNESP]
dc.contributor.authorCamargo, João Lauro Viana de [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionAC Camargo Cancer Treatment and Research Center
dc.date.accessioned2014-05-27T11:30:05Z
dc.date.available2014-05-27T11:30:05Z
dc.date.issued2013-08-01
dc.description.abstractObjective: To understand developmental characteristics of urinary bladder carcinomas (UBC) by evaluating genomic alterations and p53 protein expression in primary tumors, their recurrences, and in the morphologically normal urothelium of UBC patients. Methods: Tumors and their respective recurrences, six low-grade and five high-grade cases, provided 19 samples that were submitted to laser microdissection capture followed by high resolution comparative genomic hybridization (HR-CGH). HR-CGH profiles went through two different analyses-all tumors combined or classified according to their respective histologic grades. In a supplementary analysis, 124 primary urothelial tumors, their recurrences, and normal urothelium biopsied during the period between tumor surgical resection and recurrence, were submitted to immunohistochemical analyses of the p53 protein. During the follow-up of at least 21 patients, urinary bladder washes citologically negative for neoplastic cells were submitted to fluorescence in situ hybridization (FISH) to detect copy number alterations in centromeres 7, 17, and 9p21 region. Results and Conclusions: HR-CGH indicated high frequencies (80%) of gains in 11p12 and losses in 16p12, in line with suggestions that these chromosome regions contain genes critical for urinary bladder carcinogenesis. Within a same patient, tumors and their respective recurrences showed common genomic losses and gains, which implies that the genomic profile acquired by primary tumors was relatively stable. There were exclusive genomic alterations in low and in high grade tumors. Genes mapped in these regions should be investigated on their involvement in the urinary bladder carcinogenesis. Successive tumors from same patient did not present similar levels of protein p53 expression; however, when cases were grouped according to tumor histologic grades, p53 expression was directly proportional to tumor grades. Biopsies taken during the follow-up of patients with history of previously resected UBC revealed that 5/15 patients with no histologic alterations had more than 25% of urothelial cells expressing the p53 protein, suggesting that the apparently normal urothelium was genomically unstable. No numerical alterations of the chromosomes 7, 17, and 9p21 region were found by FISH during the periods free-of-neoplasia. Our data are informative for further studies to better understand urinary bladder urothelial carcinogenesis. © 2013 Elsevier Inc.en
dc.description.affiliationCenter for Evaluation of Environmental Impact of Human Health (TOXICAM) Department of Pathology Botucatu Medical School, UNESP-São Paulo State University, Botucatu, SP
dc.description.affiliationDepartment of Urology Botucatu Medical School UNESP-São Paulo State University, Botucatu, SP
dc.description.affiliationAC Camargo Cancer Treatment and Research Center, São Paulo
dc.description.affiliationUnespCenter for Evaluation of Environmental Impact of Human Health (TOXICAM) Department of Pathology Botucatu Medical School, UNESP-São Paulo State University, Botucatu, SP
dc.description.affiliationUnespDepartment of Urology Botucatu Medical School UNESP-São Paulo State University, Botucatu, SP
dc.format.extent827-835
dc.identifierhttp://dx.doi.org/10.1016/j.urolonc.2011.05.015
dc.identifier.citationUrologic Oncology: Seminars and Original Investigations, v. 31, n. 6, p. 827-835, 2013.
dc.identifier.doi10.1016/j.urolonc.2011.05.015
dc.identifier.issn1078-1439
dc.identifier.issn1873-2496
dc.identifier.lattes2259986546265579
dc.identifier.scopus2-s2.0-84880699810
dc.identifier.urihttp://hdl.handle.net/11449/76143
dc.identifier.wosWOS:000322681800015
dc.language.isoeng
dc.relation.ispartofUrologic Oncology: Seminars and Original Investigations
dc.relation.ispartofjcr3.397
dc.relation.ispartofsjr1,202
dc.rights.accessRightsAcesso restrito
dc.sourceScopus
dc.subjectprotein p53
dc.subjectaged
dc.subjectbladder carcinogenesis
dc.subjectbladder carcinoma
dc.subjectcancer grading
dc.subjectcancer patient
dc.subjectcancer recurrence
dc.subjectchromosome
dc.subjectchromosome 17
dc.subjectchromosome 9p
dc.subjectchromosome imbalance
dc.subjectchromosomes and chromosomal phenomena
dc.subjectclinical article
dc.subjectcomparative genomic hybridization
dc.subjectcontrolled study
dc.subjectfemale
dc.subjectfluorescence in situ hybridization
dc.subjectfollow up
dc.subjectgene dosage
dc.subjecthistopathology
dc.subjecthuman
dc.subjectimmunohistochemistry
dc.subjectlaser microdissection
dc.subjectmale
dc.subjectprimary tumor
dc.subjectpriority journal
dc.subjectprotein expression
dc.subjecturogenital tract tumor
dc.titleChromosomal imbalances in successive moments of human bladder urothelial carcinomaen
dc.typeArtigo
dcterms.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
unesp.author.lattes2259986546265579
unesp.author.orcid0000-0003-3833-4172[5]
unesp.author.orcid0000-0002-8021-5006[1]
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Medicina, Botucatupt

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