Lung cancer is the leading cause of cancer mortality in Mexico and worldwide. In the past decade, there has been an increase in the number of lung cancer cases in young people, which suggests an important role for genetic background in the etiology of this disease. In this study, we genetically characterized 16 polymorphisms in 12 low penetrance genes (AhR, CYP1A1, CYP2E1, EPHX1, GSTM1, GSTT1, GSTPI, XRCC1, ERCC2, MGMT, CCND1 and TP53) in 382 healthy Mexican Mestizos as the first step in elucidating the genetic structure of this population and identifying high risk individuals. All of the genotypes analyzed were in Hardy-Weinberg equilibrium, but different degrees of linkage were observed for polymorphisms in the CYP1A1 and EPHX1 genes. The genetic variability of this population was distributed in six clusters that were defined based on their genetic characteristics. The use of a polygenic model to assess the additive effect of low penetrance risk alleles identified combinations of risk genotypes that could be useful in predicting a predisposition to lung cancer. Estimation of the level of genetic susceptibility showed that the individual calculated risk value (iCRV) ranged from 1 to 16, with a higher iCRV indicating a greater genetic susceptibility to lung cancer.
Background and Aims: Currently, treatments are being sought to improve the control of type II diabetes mellitus (T2DM), and inulin has been shown to be effective in reducing glucose levels and other metabolic control parameters. These effects on metabolic control may be associated with changes in the epigenetic modulation of genes of the insulin pathway. Therefore, our objective is to determine the effect of agave inulin in metabolic control parameters and in INS and IRS1 genes’ methylation in T2DM patients. Methods: This was a longitudinal experimental study with 67 Mexican participants who received an intervention of inulin agave (10 g daily) for 2 months. The methylation of the INS and IRS1 genes was determined by MSP. Results: For the INS gene, we found a significant decrease in the proportions of T2DM patients with methylated DNA after inulin intervention (p = 0.0001). In contrast, the difference in the proportions of the unmethylated IRS1 gene before and after the inulin intervention was not significant (p = 0.79). On the other hand, we observed changes in the number of T2DM patients’ recommended categories for metabolic control depending on the methylation of INS and IRS1 genes before and after treatment with inulin. Conclusion: For the first time, we report the modification in the methylation of two genes, INS and IRS1, of the insulin pathway and provide information on the possible relevant role of epigenetics as a key factor in positive changes in metabolic control parameters by inulin intake in T2DM patients.