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dc.contributor.authorVolkweis, Bernardo Silveirapt_BR
dc.contributor.authorGurski, Richard Ricachenevskypt_BR
dc.date.accessioned2013-11-13T01:46:36Zpt_BR
dc.date.issued2008pt_BR
dc.identifier.issn0100-6991pt_BR
dc.identifier.urihttp://hdl.handle.net/10183/80296pt_BR
dc.description.abstractThe Barrett’s esophagus (BE) is defined as endoscopically visible columnar mucosa at the distal esophagus, of any extension, proved to harbor intestinal metaplasia on biopsy, highlighted by the presence of goblet cells. BE denotes long-standing gastroesophageal reflux disease (GERD) and is an important risk factor for the development of esophageal adenocarcinoma (EAC). Therefore, these patients must be on follow-up, in order to diagnose cancer early. BE patients have frequent alterations in esophageal physiologyc studies. Alkaline duodenogastroesophageal reflux seems to have important role. The development BE occurs in steps, initially with formation of cardiac type mucosa subsequent intestinalization. Futher progression can follow a sequence, from low grade dysplasia, to high grade dysplasia and esophageal adenocarcinoma. Current follow-up is based on the presence of dysplasia. It has limitations, grouping patients heterogeneously. Different steps of carcinogenesis have been studied looking for an ideal prognostic marker. Uncontrolled proliferative activity, apoptosis inhibition, angiogenesis, tissue invasion and metastases formation are all implicated in cancer origin. Some cycle cell molecules have been studied in BE, such as retinoblastoma protein, ciclins, kinase dependent ciclins and cell cycle inhibitors. The P53 protein is one of the most investigated in the metaplasia-adenocarcinoma progression. Growth Factors, apoptotic proteins, telomers and DNA ploidy have also been searched. Increased proliferative activity has been implicated in Barrett’s carcinogenesis and the Ki-67 antigen, through imunohistochemical analysis, has become the the method of choice. Present in the nucleus, it is found in proliferative cells only. Some studies suport association between Ki-67 activity and the metaplasia-dysplasia-adenocarcinoma sequence.The results, however, are inconclusive and research should follow this way.en
dc.format.mimetypeapplication/pdf
dc.language.isoporpt_BR
dc.relation.ispartofRevista do Colégio Brasileiro de Cirurgiões. Rio de Janeiro. Vol. 35, n. 2 (mar. 2008), p. 114-123pt_BR
dc.rightsOpen Accessen
dc.subjectEsôfago de Barrettpt_BR
dc.subjectBarrett esophagusen
dc.subjectAdenocarcinomapt_BR
dc.subjectEsophageal neoplasmsen
dc.subjectKi-67 antigenen
dc.subjectNeoplasias esofágicaspt_BR
dc.subjectTumor markers, biologicalen
dc.subjectAntígeno Ki-67pt_BR
dc.subjectBiomarcadores tumoraispt_BR
dc.subjectMetaplasiapt_BR
dc.titleEsôfago de Barrett : aspectos fisiopatológicos e moleculares da seqüência metaplasia-displasia-adenocarcinoma - artigo de revisãopt_BR
dc.title.alternativeBarrett's esophagus : physiopathological and molecular aspects of metaplasia-dysplasia-adenocarcinoma sequence - review articleen
dc.typeArtigo de periódicopt_BR
dc.identifier.nrb000721372pt_BR
dc.type.originNacionalpt_BR


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