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Bronchial-pulmonary adenocarcinoma subtyping relates with different molecular pathways

dc.contributor.authorSousa, V
dc.contributor.authorBastos, B
dc.contributor.authorSilva, M
dc.contributor.authorAlarcão, AM
dc.contributor.authorCarvalho, L
dc.date.accessioned2017-08-25T10:38:37Z
dc.date.available2017-08-25T10:38:37Z
dc.date.issued2015
dc.description.abstractLung cancer is one of the most common cancers in the world with a high mortality rate. We analyzed 45 surgical samples of the adenocarcinoma, 13 with lymph node metastasis. APC, BCL2, chromogranin A, CK 5/6/18 (LP34), CK20, CK7, cyclin D1, EGFR, ERCC1, HER2, Ki67, LRP, MRP, P53, RB and TTF1 expressions were evaluated by immunohistochemistry (IHC). Higher Ki67, APC, ERCC1 expressions and lower TTF1 expression were identified in advanced stages (IIA and IIIA) of adenocarcinomas, which reflect a more aggressive, less differentiated, possibly a non-TRU adenocarcinoma. Acinar, micropapillary and BA/lepidic adenocarcinoma patterns were the most similar patterns and papillary was the most different pattern followed by solid pattern, according to expression of these markers. Different adenocarcinoma patterns are engaged with different molecular pathways for carcinogenesis, based on the differences of expression. Acinar, BA/lepidic and micropapillary showed higher TTF1 expression (type TRU), and papillary and solid patterns revealed less TTF1 expression, exhibiting a non-TRU/bronchial phenotype. Solid pattern revealed lower HER2 and higher EGFR and ERCC1 (this compared to papillary) expression; papillary higher HER2 and lower ERCC1 expressions; micropapillary higher RB expression; and acinar lower ERCC1 and higher EGFR expressions. Ciclin D1 seems to have more importance in acinar and BA/lepidic patterns than in micropapillary. ERCC1 protein expression in micropapillary, solid and BA/lepidic patterns may indicate DNA repair activation. Inhibition of apoptosis could be explained by BCL2 overexpression, present in all adenocarcinoma patterns. MRP-1 and LRP were overexpressed in all patterns, which may have implications for drug resistance. Further studies are needed to interpret these data regarding to therapy response in advanced staged bronchial-pulmonary carcinomas.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationRev Port Pneumol (2006). 2015 Sep-Oct;21(5):259-70.pt_PT
dc.identifier.doi10.1016/j.rppnen.2014.05.006pt_PT
dc.identifier.urihttp://hdl.handle.net/10400.4/2066
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.subjectAdenocarcinomapt_PT
dc.subjectNeoplasias do Pulmãopt_PT
dc.subjectNeoplasias dos Brônquiospt_PT
dc.titleBronchial-pulmonary adenocarcinoma subtyping relates with different molecular pathwayspt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.endPage270pt_PT
oaire.citation.issue5pt_PT
oaire.citation.startPage259-70pt_PT
oaire.citation.volume21pt_PT
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT

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