Cancer is a complex disease and the genetic susceptibility to it could be an outcome of the inherited difference in the capacity of xenobiotic metabolizing enzymes. Glutathione-S-transferases (GSTs) are phase II metabolizing enzymes whose various genotypes have been associated with increased risk of different types of cancer. Null mutations caused by the deletion of the entire gene result in the absence of the enzymatic activity and increase in the risk of developing cancer including chronic myeloid leukaemia (CML). In the present case-control study we evaluated the effect of null mutations in GSTM1 and GSTT1 genes on the risk of developing CML. The study included 75 CML patients (43 males and 32 females; age (mean ± S.D) 42.3 ± 13.4 years) and unrelated non-malignant controls (76 male and 48 females; age (mean ± S.D) 41.5 ± 12.9). The distribution of GSTM1 and GSTT1 genotypes in CML patients and controls was assessed by multiplex-PCR method. Logistic regression was used to assess the relationship between GSTM1 and GSTT1 genotypes and risk of CML. Chi-square test was used to evaluate the trend in modulating the risk to CML by one or more potential high risk genotype. Although GSTM1 null genotype frequency was higher in CML patients (41%) than in the controls (35%), it did not reached a statistical significance (OD = 1.32, 95% CI: 0.73-2.40; P value = 0.4295). The frequency of GSTT1 null genotypes was higher in the CML patients (36%) than in the controls (21%) and the difference was found to be statistically significant (OD = 2.12, 95% CI: 1.12-4.02; P value = 0.0308). This suggests that the presence of GSTT1genotype may have protective role against the CML. We found a statistically significant (OD = 3.09, 95% CI: 1.122-8.528; P value = 0.0472) interaction between the GSTM1 and GSTT1 null genotypes and thus individuals carrying null genotypes of both GSTM1 and GSTT1 genes are at elevated risk of CML.
The human intestinal microbiota is a plethora of diverse microbial species, wherein certain bacteria considered as driver bacteria with procarcinogenic features contribute directly toward colonic epithelium cell damage to initiate colorectal carcinogenesis. However, some bacteria, in particular Fusobacterium nucleatum, which is otherwise a normal resident of the oral microflora and a relatively poor colonizer of the healthy gut, have also been considered to play a role in the development of colorectal cancer. Many studies have reported that F. nucleatum is associated with colorectal adenomas and advanced-stage colorectal cancer, but its precise role in the early stages of colorectal tumorigenesis is poorly understood. Here, we review some of the important features of F. nucleatum, its association with inflammatory bowel disease, modulation of the tumor-immune microenvironment, and E-cadherin/β-catenin signaling.
Human Cytochrome P 450 3A, a variant of Cytochrome P-450-dependent monooxygenases is a major drug metabolizing enzyme. CYP3A has evolved to catalyze the biotransformation of its substrate. A great deal of inter-individual variation in expression levels exists for CYP3A5 gene. The common polymorphism in CYP3A5 that induces a cryptic splice site has been shown to cause a significant reduction in its expression. Variation in CYP3A enzyme activity contributes greatly to variation in systemic clearance of CYP3A substrates and its oral bioavailability. The present study was designed to study the CYP3A5*3 polymorphism in the Kashmiri population. CYP3A5*3 genotypic status of 400 unrelated individuals of the Kashmiri population wasevaluated by PCR-RFLP method. The frequency of CYP3A5 variant in Kashmiri population was found similar to Caucasian but higher than that in Chinese and Japanese population. Our finding suggest that approximately 89.5% of study population carry CYP3A5*3 genotype and thus might be at an increased risk. So, detection of CYP3A5 variant alleles and knowledge about their allelic frequency in ethnic Kashmiris might play a key player in improved therapeutic intervention in Kashmiri population.
Background: Hyperlipidemia is the primary risk factor for coronary artery disease and subsequently leading to morbidity and mortality in adulthood. It is a well-known fact that coronary artery disease can initiate in the fetal stage itself. The present study was planned to analyse cord blood lipoproteins and apolipoproteins levels and its association with gender and birth weight.Methods: This cross-sectional study was conducted in the Department of Biochemistry, in collaboration with Department of Gynecology and Obstetrics at SKIMS Medical College and Hospital, Bemina, Srinagar. A total 200 pregnant women who delivered by normal vaginal delivery and caesarean section were included in the study. 10 ml of umbilical cord blood was collected in a plain vial from the placental end within five minutes of delivery and serum lipoprotein and Apo-lipoprotein levels were measured.Results: Out of 200 newborns102 were males and 98 were females. Statistically significant difference was seen in parameters Apo A1, Apo B, Atherogenic index (Apo B/Apo A1) and LDL between the genders rest of the parameters were statistically. Also 32 newborns (16.0%) had <2500, 152 (76.0%) new born had 2500-4000 and 16(8.0%) > 4000 grams birth weight. The mean lipoprotein and Apo-lipoprotein levels in these new born were compared between the groups. The mean serum levels of TC, TG, LDL and HDL were statistically significant (<0.05) between the three groups were as Apo A1, Apo B, Atherogenic index (Apo B/Apo A1) and VLDL was insignificant (>0.05) respectively.Conclusions: CVD being a leading cause of morbidity and mortality in the developing countries, early screening of the at risk babies i.e. low birth weight newborns using cord blood lipoproteins and apolipoproteins levels helps in primordial and primary prevention of diseases.
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