Literature DB >> 21400525

Prognostic implications of miR-16 expression levels in resected non-small-cell lung cancer.

Alfons Navarro1, Tania Diaz, Elena Gallardo, Nuria Viñolas, Ramon M Marrades, Bernat Gel, Marc Campayo, Angels Quera, Eva Bandres, Jesus Garcia-Foncillas, Jose Ramirez, Mariano Monzo.   

Abstract

BACKGROUND: MicroRNAs are novel regulators of gene expression that are linked to the main oncogene networks, including the p53 pathway. p53 regulates the maturation process of miR-16 and miR-143. We analyzed the role as prognostic markers of miR-16 and miR-143 in 70 non-small-cell lung cancer (NSCLC) patients.
METHODS: MicroRNAs were analyzed by TaqMan MicroRNA assays. Disease-free survival (DFS) and overall survival (OS) were examined using Kaplan-Meier curves with log-rank tests and the Cox proportional hazard model.
RESULTS: When patients were classified in three groups according to their miR-16 expression levels, those with normal levels had the best outcome while those with high levels had the worst. DFS was 22.4 months for patients with high levels, 71.8 months for those with normal levels, and 55.8 months for those with low levels (P = 0.05). OS was 23.9 months for patients with high levels, 97.6 months for those with normal levels, and 63.5 months for those with low levels (P < 0.001). In the multivariate analyses, high miR-16 levels emerged as an independent prognostic factor for poor DFS (P = 0.001) and OS (<0.001).
CONCLUSIONS: Our results provide the first hints that miR-16 levels in tumor samples may be a prognostic marker in NSCLC.
Copyright © 2010 Wiley-Liss, Inc.

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Year:  2010        PMID: 21400525     DOI: 10.1002/jso.21847

Source DB:  PubMed          Journal:  J Surg Oncol        ISSN: 0022-4790            Impact factor:   3.454


  32 in total

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7.  Applications of MicroRNAs in the Diagnosis and Prognosis of Lung Cancer.

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8.  Prognostic significance of microRNA-16 expression in human colorectal cancer.

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9.  Pathway-based serum microRNA profiling and survival in patients with advanced stage non-small cell lung cancer.

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10.  Histone deacetylases inhibitor trichostatin A increases the expression of Dleu2/miR-15a/16-1 via HDAC3 in non-small cell lung cancer.

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