Our study provides solid evidence to classify smoking as the most important behavioral risk factor for gastric cancer.

Purpose The purpose of our study was to determine whether the amounts of circulating DNA (cDNA) could discriminate between NSCLC patients and healthy individuals and assess its value as a prognostic marker of this disease. Methods We conducted a study of 309 individuals and the cDNA levels were assessed through real-time PCR methodology. Results We found increased cDNA levels in NSCLC patients compared to control individuals. We also found a decreased overall survival time in patients presenting high cDNA levels, when compared to lower cDNA concentrations. Conclusions Quantification of cDNA may be a good tool for NSCLC detection with potential for clinical applicability.

Genomes are continually subjected to DNA damage whether they are induced from intrinsic physiological processes or extrinsic agents. Double-stranded breaks (DSBs) are the most injurious type of DNA damage, being induced by ionizing radiation (IR) and cytotoxic agents used in cancer treatment. The failure to repair DSBs can result in aberrant chromosomal abnormalities which lead to cancer development. An intricate network of DNA damage signaling pathways is usually activated to eliminate these damages and to restore genomic stability. These signaling pathways include the activation of cell cycle checkpoints, DNA repair mechanisms, and apoptosis induction, also known as DNA damage response (DDR)-mechanisms. Remarkably, the homologous recombination (HR) is the major DSBs repairing pathway, in which RAD52 gene has a crucial repairing role by promoting the annealing of complementary single-stranded DNA and by stimulating RAD51 recombinase activity. Evidence suggests that variations in RAD52 expression can influence HR activity and, subsequently, influence the predisposition and treatment efficacy of cancer. In this review, we present several reports in which the down or upregulation of RAD52 seems to be associated with different carcinogenic processes. In addition, we discuss RAD52 inhibition in DDR-defective cancers as a possible target to improve cancer therapy efficacy.