Clin Cancer Res 2009, 15:3423–3432 PubMedCrossRef 30 Verrax J, P

Clin ARN-509 cancer Res 2009, 15:3423–3432.PubMedCrossRef 30. Verrax J, Pedrosa RC, Beck R, Dejeans N, Taper H, Calderon PB: In situ modulation of oxidative stress: a novel and efficient strategy to kill cancer cells. Curr Med Chem 2009, 16:1821–1830.PubMedCrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions NDF was responsible for all experimental data and helped draft the manuscript. RHS aided coordination of the study and helped draft the manuscript. AM conceived of the study, participated in its design and drafted the manuscript. All authors

read and approved the final manuscript.”
“Background Renal cell carcinoma (RCC) accounts for approximately 3% of cancers in adults as well as 85% of all primary malignant kidney tumors. It is the third most common urological cancer after prostate and bladder cancer but it has the highest mortality Rigosertib rate at over 40% [1, 2]. Clear cell (conventional) carcinoma is the most common subtype of RCC and accounts for approximately 75-80% of these tumors

[3]. Apart from surgery, it is both chemotherapy and radiotherapy resistant. The present absence of biomarkers for early detection and follow-up of the disease is responsible for late diagnosis and subsequent poor prognosis. It is necessary, therefore, to improve our understanding of RCC’s pathogenesis, identify new biomarkers enabling prediction of early metastasis after nephrectomy, and develop new targeted therapies. One of the most modern and progressive approaches for molecular characterization of tumors today is based on microRNA expression profiles. MicroRNAs (miRNAs) are short noncoding Veliparib Histone demethylase RNAs, 18-25 nucleotides in length, that post-transcriptionally regulate gene expression. Depending upon the extent of their complementarity with target mRNA, miRNAs act by two mechanisms of post-transcriptional regulation of gene expression, which lead to target mRNA degradation or repression

of its translation and consequent decrease of particular protein levels. Bioinformatics have predicted that miRNAs have the capacity to regulate one third of all mammalian genes, among which are included a significant number of important oncogenes and tumor suppressor genes [4, 5]. MiRNAs have been studied most intensively in the field of oncological research, and emerging evidence suggests that altered miRNA regulation is involved in the pathogenesis of cancer [6–8]. Changes in the expression of miRNAs have been observed in a variety of human cancers [9–11]. Several studies have focused on miRNAs’ significance in RCC [12]. These papers described the potential of miRNA profiles to distinguish tumor tissue from normal renal parenchyma [13–20], classify renal cell carcinomas according to histological subtypes [13–15], identify expression profiles to predict metastasis from primary tumors [13, 16], and determine prognosis for particular renal cell carcinoma patients [13, 16].

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