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Background: Over- or underexpression of miR-146a has been reported in several different human tumor types, and a polymorphism in its precursor form (pre-miR-146a rs2910164 G/C) has been recently studied in connection with cancer susceptibility. The aim of the present study was to investigate the possible influence of the pre-miR-146a rs2910164 polymorphism on the risk of squamous cell carcinoma of the head and neck (HNSCC)., Patients and Methods: The study included 468 patients with HNSCC and 468 cancer-free, age-, gender-, and smoking-matched controls. The miR-146a genotypes were determined using polymerase chain reaction with confronting two-pair primers, and their distribution was compared by multivariate binary logistic regression analysis., Results: Occurrence of heterozygous (odds ratio, OR=1.46, 95% confidence interval, CI=1.10-1.95, p=0.009) and C/C homozygous (OR=2.37, 95% CI=1.01-5.60, p=0.048) individuals was significantly more frequent among patients with HNSCC than in the control group., Conclusion: The pre-miR/146a C allele may contribute to an increased susceptibility to HNSCC.

Background: Head and neck cancer is a significant current health problem in Hungary because the mortality of this cancer has increased by 387% in the last thirty-two years. Because of the important role of the XRCC1 gene in DNA repair, we wanted to test the effects of the Arg194Trp and Arg399Gln polymorphisms of XRCC1 on the clinical outcome of head and neck cancer., Patients and Methods: A polymerase chain reaction-restriction fragment lenght polmorphism (PCR-RFLP) method was used. A total of 108 samples were taken from intraoperatively removed formalin-fixed, and paraffin-embedded blocks of tissue. An age- and sex-matched cancer-free control group was used to compare the frequency of polymorph variants., Results: No significant difference was found between patients and controls in repect of the investigated polymorphisms. A significant difference was found between the patients with different XRCC1 194 polymorph status in clinical stage SIII. The survival proportion of patients with the Arg194Arg genotype was significantly lower than of those with the Arg194Trp genotype., Conclusion: The complex analysis of these factors may provide the basis for personal risk assessment and an opportunity for individualised therapy.

Background: Increased production of reactive oxygen species (ROS) by anticancer drugs has been described in patients with various malignancies, which might attribute to their nephrotoxicity., Materials and Methods: The effects of two epigenetic modifiers - trichostatin A (TSA) and 5-aza-deoxycytidine (5AZA) - on ROS production and cell injury alone or in combination with mild oxidative stress were studied in mouse renal proximal tubule cells., Results: Both agents increased mitochondrial ROS production and consequent lactate dehydrogenase (LDH) release either alone or in combination with a low dose of H(2)O(2). The antioxidant N-acetyl-cysteine (NAC) abolished LDH release. It was also found that CREB-mediated transcription, vital for survival of proximal tubule cells, is attenuated by these anticancer agents., Conclusion: The ROS-inducing activity of TSAI and 5AZA might explain the in vivo nephrotoxicity of epigenetic modifiers. The mechanisms that are responsible for this injury could involve attenuation of pro-survival signaling and/or activation of death signaling pathway(s) associated with mitochondrial ROS release.