Please use this identifier to cite or link to this item: http://hdl.handle.net/20.500.12779/5634
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dc.contributor.authorChifenti, Ben_us
dc.contributor.authorMorelli, Men_us
dc.contributor.authorZavaglia, Men_us
dc.contributor.authorCoviello, Daen_us
dc.contributor.authorGuerneri, Sen_us
dc.contributor.authorSantucci, Annalisaen_us
dc.contributor.authorPaffetti, Alessandroen_us
dc.contributor.authorMasetti, Men_us
dc.contributor.authorLocci, Mten_us
dc.contributor.authorBertacca, Gen_us
dc.contributor.authorCapodanno, Aen_us
dc.contributor.authorCollecchi, Pen_us
dc.contributor.authorCampani, Den_us
dc.contributor.authorMosca, Fen_us
dc.contributor.authorBevilacqua, Gen_us
dc.contributor.authorCavazzana, Aoen_us
dc.date.accessioned2021-03-30T15:54:00Z-
dc.date.available2021-03-30T15:54:00Z-
dc.date.issued2009-
dc.identifier.issn0885-3177en_US
dc.identifier.urihttp://hdl.handle.net/20.500.12779/5634-
dc.description24577en_US
dc.description.abstractOBJECTIVES: Pancreatic cancer still remains a challenge for its biological complexity and lack of effective therapeutic strategies. Establishing new pancreatic cancer cell lines is therefore of paramount importance to clarify its biology. METHODS: We established and characterized 4 new pancreatic cancer cell lines (PP78, PP109, PP117, and PP161) according to their genetic (K-Ras, TP53, CDKN2A, and MADH4; DNA fingerprinting; karyotype), cytostructural (cytokeratins 7, 8, 18, and 19 vimentin, and ezrin), and functional profiles (doubling time; migration assay). RESULTS: K-Ras, TP53, and CDKN2A gene alterations were detected in all 4 of them. Each cell line had a unique DNA profile revealed by DNA fingerprinting. A complex karyotype with numerous structural and numeric chromosomal abnormalities was present in each cell line. All 4 cell lines showed positivity for cytokeratins 7, 8, and 18. All but PP78 expressed cytokeratin 19, whereas vimentin was expressed only in PP117 and PP78 cells. A different ezrin cellular distribution was noticed in PP78 and PP117, being mostly located at membrane ruffles. This peculiar distribution was associated with the strongest migratory capability. CONCLUSIONS: Our results seem to confirm the pancreatic ductal adenocarcinoma heterogeneity; in fact, the same genetic abnormalities (K-Ras, TP53, and CDKN2A) may have different effects on tumor biology depending on cellular differentiation.en_US
dc.language.isoenen_US
dc.relationNoneen_US
dc.relation.ispartofPANCREASen_US
dc.titleEstablishment and Characterization of 4 New Human Pancreatic Cancer Cell Lines: Evidences of Different Tumor Phenotypesen_US
dc.typeArticleen_US
dc.identifier.doi10.1097/MPA.0b013e31818c746aen_US
dc.identifier.pmid19002021en_US
dc.identifier.scopus2-s2.0-65349175891en_US
dc.identifier.isiWOS:000263905700014en_US
dc.identifier.urlhttp://journals.lww.com/pancreasjournal/pages/articleviewer.aspx?year=2009&issue=03000&article=00014&type=abstract; http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0885-3177&volume=38&issue=2&spage=184en_US
dc.relation.volume38(2)en_US
dc.description.firstpage184en_US
dc.description.lastpage196en_US
dc.description.thirdmissionNot applicableen_US
item.cerifentitytypePublications-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.openairetypeArticle-
item.fulltextNo Fulltext-
crisitem.author.orcid0000-0001-6976-9086-
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