Tp53 Abnormalities Are Frequent and Early Events in the Sequential Pathogenesis of Gallbladder Carcinoma

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dc.catalogadoryvc
dc.contributor.authorMoreno, M.
dc.contributor.authorPimentel González, Eduardo Fernando
dc.contributor.authorGazdar, Adi F.
dc.contributor.authorWistuba Oyarzun, Ignacio
dc.contributor.authorMiquel Poblete Juan Francisco
dc.date.accessioned2024-08-08T21:42:34Z
dc.date.available2024-08-08T21:42:34Z
dc.date.issued2005
dc.description.abstractBackground: Gallbladder carcinoma (GBC) is a frequent neoplasm in Hispanic and native American populations. GBC is preceded by gallstones, chronic cholecystitis and dysplastic changes of the gallbladder epithelium. The knowledge of the molecular events involved in its pathogenesis is scarce. Aims: We investigated the role of TP53 inactivation in the sequential pathogenesis of GBC. Methods: Invasive tumor-, dysplastic- and histologically normal GB ep ithelial-cells were obtained from archival formalin fixed tissues from GBC and GB from gallstone pa tients without GBC. Normal GB epithelia from 5 non-gallstone specimens were also studied. DNA extracted was examined for loss of heterozygosity (LOH) using 2 microsatellite markers and for TP53 mutations at exons 5 to 8. Results: GBCs demonstrated a high frequency of LOH (81%) and mutation (67%), and both abnormalities indicating gene inactivation were detected in 52%. Similar frequency of TP53 Abnormalities are frequent and early events in the sequential pathogenesis of gallbladder carcinomaivation (38%) were detected in their accompanying normal and dysplastic epithelia. Noteworthy, one third of normal and dysplastic epithelia obtained from GBs of gallstone patients without GBC demonstrated either TP53 allele loss or mutation, but gene inactivation was less frequent (11%). Most mutations affected exons 5 and 7, and they were more frequently missense point mutations. The same TP53 mutation was de tected in only a subset (27%) of comparisons between non-malignant epithelia adjacent to GBCs, indicating that TP53 mutation occurs independently at several epithelial foci. Conclusions: These findings indicate that TP53 abnormalities are early and frequent events in the pathogenesis of GBC, starting from chronic cholecystitis.
dc.description.funderFondecyt
dc.fechaingreso.objetodigital2024-08-08
dc.format.extent8 páginas
dc.fuente.origenHistorial Académico
dc.identifier.citationMoreno, M. et al. Tp53 Abnormalities Are Frequent and Early Events in the Sequential Pathogenesis of Gallbladder Carcinoma. Annals Of Hepatology. 2005;4(3):192-199.
dc.identifier.issn1665-2681
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/87380
dc.information.autorucEscuela de Medicina; Pimentel González, Eduardo Fernando; S/I; 205651
dc.information.autorucS/I;Wistuba Oyarzun, Ignacio; S/I; 100278
dc.information.autorucEscuela de Medicina;Miquel Poblete, Juan Francisco;0000-0002-0526-4377; 72216
dc.issue.numero3
dc.language.isoen
dc.nota.accesocontenido completo
dc.pagina.final199
dc.pagina.inicio192
dc.revistaAnnals of Hepatology
dc.rightsacceso abierto
dc.rights.licenseCC BY-NC-ND Atribución NoComercial-SinDerivados Internacional 4.0
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/deed.es
dc.subjectMutations
dc.subjectLoss of heterozygosity
dc.subjectMicrodissection
dc.subjectPreneoplastic lesions
dc.subjectGallbladder
dc.subject.ddc610
dc.subject.deweyMedicina y saludes_ES
dc.titleTp53 Abnormalities Are Frequent and Early Events in the Sequential Pathogenesis of Gallbladder Carcinoma
dc.typeartículo
dc.volumen4
sipa.codpersvinculados83108
sipa.codpersvinculados205651
sipa.codpersvinculados100278
sipa.codpersvinculados72216
sipa.trazabilidadHistorial Académico;09-07-2021
sipa.trazabilidadORCID;2024-08-05
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