Loss of the CBX7 protein expression correlates with a more aggressive phenotype in pancreatic cancer. (Articolo in rivista)

Type
Label
  • Loss of the CBX7 protein expression correlates with a more aggressive phenotype in pancreatic cancer. (Articolo in rivista) (literal)
Anno
  • 2010-01-01T00:00:00+01:00 (literal)
Alternative label
  • Karamitopoulou E; Pallante P; Zlobec I; Tornillo L; Carafa V; Schaffner T;Borner M; Diamantis I; Esposito F; Brunner T; Zimmermann A; Federico A; Terracciano L; Fusco A. (2010)
    Loss of the CBX7 protein expression correlates with a more aggressive phenotype in pancreatic cancer.
    in European journal of cancer (1990)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Karamitopoulou E; Pallante P; Zlobec I; Tornillo L; Carafa V; Schaffner T;Borner M; Diamantis I; Esposito F; Brunner T; Zimmermann A; Federico A; Terracciano L; Fusco A. (literal)
Pagina inizio
  • 1438 (literal)
Pagina fine
  • 1444 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 46 (literal)
Rivista
Note
  • ISI Web of Science (WOS) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • Second Department of Pathology, University of Athens, Attikon University Hospital, Haidari, Athens, Greece NOGEC (Naples Oncogenomic Center)-CEINGE, Biotecnologie Avanzate-Napoli, and SEMM - European School of Molecular Medicine Naples Site, via Comunale Margherita 482, 80145 Naples, Italy Institute of Pathology, University of Basel, Scho¨nbeinstrasse 40, 4031 Basel, Switzerland Institute of Pathology, University of Bern, Switzerland Institute of Medical Oncology, Insel University Hospital, Bern, Switzerland Second Department of Internal Medicine Propaideutic University of Athens, Attikon University Hospital, Haidari, Athens, Greece Istituto di Endocrinologia ed Oncologia Sperimentale del CNR c/o Dipartimento di Biologia e Patologia Cellulare e Molecolare Istituto di Endocrinologia ed Oncologia Sperimentale del CNR, Facolta` di Medicina e Chirurgia di Napoli, Universita` degli Studi di Napoli 'Federico II', via Pansini 5, 80131 Naples, Italy (literal)
Titolo
  • Loss of the CBX7 protein expression correlates with a more aggressive phenotype in pancreatic cancer. (literal)
Abstract
  • Polycomb group (PcG) proteins function as multiprotein complexes and are part of a gene regulatory mechanism that determines cell fate during normal and pathogenic development. Several studies have implicated the deregulation of different PcG proteins in neoplastic progression. Pancreatic ductal adenocarcinoma is an aggressive neoplasm that follows a multistep model of progression through precursor lesions called pancreatic intraepithelial neoplasia (PanIN). Aim of this study was to investigate the role of PcG protein CBX7 in pancreatic carcinogenesis and to evaluate its possible diagnostic and prognostic significance. We analysed by immunohistochemistry the expression of CBX7 in 210 ductal pancreatic adenocarcinomas from resection specimens, combined on a tissue microarray (TMA) including additional 40 PanIN cases and 40 normal controls. The results were evaluated by using receiver operating characteristic (ROC) curve analysis for the selection of cut-off scores and correlated to the clinicopathological parameters of the tumours and the outcome of the patients. Expression of E-cadherin, a protein positively regulated by CBX7, was also assessed. A significantly differential, and progressively decreasing CBX7 protein expression was found between normal pancreatic tissue, PanINs and invasive ductal adenocarcinoma. Loss of CBX7 expression was associated with increasing malignancy grade in pancreatic adenocarcinoma, whereas the maintenance of CBX7 expression showed a trend toward a longer survival. Moreover, loss of E-cadherin expression was associated with loss of CBX7 and with a trend towards worse patient survival. These results suggest that CBX7 plays a role in pancreatic carcinogenesis and that its loss of expression correlates to a more aggressive phenotype. Copyright (c) 2010 Elsevier Ltd. All rights reserved. (literal)
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