There were several limitations of this study. The sample size was relatively small and samples were not well matched. Besides, this study was not specifically designed to evaluate EGFR-TKIs treatment. Notwithstanding its limitations, this study demonstrates that EGFR mutations detected in blood of NSCLC patients by ARMS may be highly predictive of identical mutations

in corresponding tumor, as well as showing correlations with tumor response and survival benefit from EGFR-TKIs. However, due to the method’s low sensitivity in blood samples, tumor tissue remains the best sample for EGFR mutation analysis. Further investigations involving appropriate methodologies to decrease false negatives in cfDNA-based EGFR mutation analysis are warranted. This study was supported by grants from the National Natural Science Foundation of China (No.81172101) and the key project of the Science CP-690550 purchase and Technology Commission of Shanghai Municipality (No.11JC1411301). No conflicts of interests are present. The authors are grateful to all the patients and investigators for their participation in this study. “
“Epigenetics is the study of a stably heritable

phenotype resulting from changes in a chromosome without alterations in the DNA sequence [1]. DNA methylation and histone modifications are essential epigenetic processes of normal cellular differentiation and function. Dysregulation of epigenetic modifications can lead to neoplasia [2]. In cancer, aberrant regulation of DNA methylation leads to global SB431542 hypomethylation, though many gene promoters, including those of tumor suppressor genes are abnormally hypermethylated. Silencing of tumor suppressors by hypermethylation Arachidonate 15-lipoxygenase of their gene promoters, which inhibits transcription, is nearly universal in neoplasia. Genes encoding proteins that modify

histones have emerged to be some of the most commonly mutated sequences associated with neoplasia [3]. These various epigenetic changes are targetable. Efforts have focused on DNA-demethylating drugs and inhibitors of histone deacetylases (HDACs). Cytidine analogs such as 5-azacytidine (azacitidine) and 5-aza-deoxycytidine (decitabine) are demethylating agents, which inhibit DNA methyltransferases (DNMTs) [4]. These drugs have been approved for the treatment of myelodysplastic syndrome and are currently under investigation in solid tumors [5]. Their potential mutagenic properties prevent use for cancer prevention. HDACs remove acetyl groups from the histone lysine residues (as well as other nonhistone proteins), leading to the formation of a condensed and transcriptionally silenced chromatin. HDAC inhibitors that are used for cancer therapy include romidepsin and vorinostat, both of which have been approved for cutaneous T cell lymphoma. Belinostat is currently under review by the United States Food and Drug Administration (US FDA) for various indications.