Prominent genetic variants and epigenetic changes in post-traumatic stress disorder among combat veterans.

Post-traumatic stress disorder (PTSD) is one of the most widespread and disabling psychiatric disorders among combat veterans. Substantial interindividual variability in susceptibility to PTSD suggests the presence of different risk factors for this disorder. Twin and family studies confirm genetic factors as important risk factors for PTSD. In addition to genetic factors, epigenetic factors, especially DNA methylation, can be considered as a potential mechanism in changing the risk of PTSD. So far, many genetic and epigenetic association studies have been conducted in relation to PTSD. In genetic studies, many single nucleotide polymorphisms have been identified as PTSD risk factors. Meanwhile, the variations in catecholamines-related genes, serotonin transporter and receptors, brain-derived neurotrophic factor, inflammatory factors, and apolipoprotein E are the most prominent candidates. CpG methylation in the upstream regions of many genes is also considered a PTSD risk factor. Accurate identification of genetic and epigenetic changes associated with PTSD can lead to the presentation of suitable biomarkers for susceptible individuals to this disorder. This study aimed to delineate prominent genetic variations and epigenetic changes associated with post-traumatic stress disorder in military veterans who have experienced combat, focusing on genetic and epigenetic association studies.

Association Analysis of GSTP1-rs1695 Polymorphism with the Risk of Oral Cancer: A Literature Review, an Updated Meta- Analysis, and a Structural Assessment.

BACKGROUND: This study aimed to investigate the association of rs1695 polymorphism in glutathione S-transferase P1 (GSTP1) with risk of oral cancer in a meta-analysis which was followed by a bioinformatics approach. MATERIALS AND METHODS: Related articles were collected through a systematic search in PubMed, Google Scholar, and EMBASE databases up to June 2022 and then screened. Finally, seven studies, including 1249 cases of oral cancer and 1861 healthy individuals, were included in our meta-analysis. Seven different genetic models including G vs. A, GG+GA vs. AA, GG vs. GA+AA, GA vs. GG+AA, GG vs. GA, GG vs. AA, and GA vs. AA were used for the calculation of odds ratio and 95% confidence interval in order to assess the association between GSTP1-rs1695 polymorphism and oral cancer risk. Also, the ethnicity-based stratified analyses were performed using the seven mentioned models. Some bioinformatics software was used to investigate the effect of rs1695 polymorphism on the primary, secondary, and three-dimensional structure of GSTP1. RESULTS: Our results showed that rs1695 polymorphism was not associated with the risk of oral cancer in any seven genetic models (G vs. A: OR= 0.9331, 95%CI= 0.6339-1.3737, P= 0.726; GG vs. GA+AA: OR= 0.9112 , 95%CI= 0.6865-1.2093, P= 0.520; GG+GA vs. AA: OR= 0.9006, 95%CI= 0.5522-1.4690, P= 0.675; GA vs. GG+AA: OR= 0.8732, 95%CI= 0.5763-1.3230, P= 0.522; GG vs. AA: OR= 0.9516, 95%CI= 0.5503-1.6456, P= 0.859; GG vs. GA: OR= 1.0645, 95%CI= 0.7891-1.4359, P= 0.683; GA vs. AA: OR= 0.8825, 95%CI= 0.5499-1.4162, P= 0.604). Also, we did not observe any significant associations in ethnicity-based stratified analyses. But bioinformatics studies have shown that this polymorphism can alter the physicochemical properties and secondary structure of the protein. CONCLUSIONS: Based on results, the rs1695 polymorphism could not be considered a risk factor for oral cancer.