Genes & development 1992, 6 (3) : 439–453 CrossRef 23 Miyata Y,

Genes & development 1992, 6 (3) : 439–453.CrossRef 23. Miyata Y, Fukuhara A, Matsuda M, Komuro R, Shimomura I: Insulin induces chaperone and CHOP gene expressions in adipocytes. Biochem Biophys Res Commun. 2008, 365 (4) : 826–832.CrossRefPubMed 24. Poitout V, Robertson RP: Glucolipotoxicity:

fuel excess and beta-cell dysfunction. Endocrine reviews 2008, 29 (3) : 351–366.CrossRefPubMed 25. Boru C, Silecchia G, Pecchia A, Iacobellis G, Greco F, Rizzello M, Basso N: Prevalence of cancer in Italian obese patients referred for bariatric surgery. Obesity surgery 2005, 15 (8) : 1171–1176.CrossRefPubMed 26. Pi-Sunyer FX: Comorbidities of overweight and obesity: current evidence and research issues. Med Sci Sports Exerc. 1999, 31 (11 Suppl) : S602-S608.PubMed Competing interests The authors declare that they have no competing interests. Authors’ contributions CG participated in study design, DNA EPZ5676 amplification, sequence BI 2536 order reading, project coordination and manuscript

TSA HDAC research buy drafting and revising. RM carried out the statistical analysis, reference collection, and manuscript drafting. NP and LP executed PCR set up, DNA amplification and sequence reading. All authors have read and approved the manuscript.”
“Background Lung cancer is the leading cause of death from cancer worldwide, and the care rate remains less than 15% despite improvements in surgery, radiotherapy and chemotherapy [1]. Insulin-like growth factor-I (IGF-I) and IGF-binding protein-3 (IGFBP-3) have been widely accepted that they may have key role on the genesis and development of many types of tumor including lung cancer [2–7]. Growth hormone Cyclin-dependent kinase 3 stimulates production of IGF-I in the liver and peripheral tissues. IGF-I is also released locally in response to damage, either directly or through the action of other factors associated with tissue responses to damage, including epidermal growth factor, fibroblast growth factor, and platelet-derived growth factor [8]. IGFBP-3 is the dominant circulating binding partner for both IGFs, accounting for 70 to 80% of their blood levels [8, 9]. Multiple lines of evidence suggest involvement

of the IGF pathway across a range of malignancies, including both non-small cell lung cancer (NSCLC) and small cell lung cancer [5, 10, 11]. Elevated plasma levels of IGF-I have been associated with an increased risk of lung cancer, and high plasma levels of IGFBP-3 associated with a reduced risk [5]. Similarly, IGFBP-3 promoter methylation in tumor cells has been linked to decreased survival in stage I NSCLC patients. These suggest that IGF-I may promote tumor cell growth, while IGFBP-3 acts as a tumor suppressor gene [12, 13]. At the same time, different results were obtained from other studies. Recently, many large-scale clinical prospective case-control studies on association between circulating levels of IGF-I, IGFBP-3 and the risk of lung cancer were performed [14–19].

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