Background: MDM2 is an important negative regulator of the TP53 pathway, over expressed in many cancers as oncoprotein. Polymorphisms in the promoter region of the MDM2 gene have been shown to alter protein expression and may, thus play an important role in carcinogenesis. Aim and methods:To test our hypothesis that the MDM2 promoter polymorphisms are associated with risk of non small cell lung cancer, we conducted a hospital-based, case-control study of 136 Indian patients diagnosed with NSCLC and 136 cancer-free controls and investigated the association between genetic variation in the promoter region of MDM2 (c.-51309G4T, rs2279744:g.G4T) and the risk of developing NSCLC by tetra-primer ARMS-PCR and ASO-PCR.Results: Compared with the MDM2-2580TT genotype, we found that the MDM2-309G variant genotypes were associated with an increased risk of NSCLC in Indian patients [

Background: Apoptotic inhibitor gene survivin regulates apoptosis and cell cycle progression. Functional polymorphism in the promoter region of survivin influences its expression may lead to the development of several cancers including lung cancer. Our study aimed to investigate the association of survivin-31G>C polymorphism with the risk of NSCLC in Indian population.Methods: A hospit al-based case control study of 136 cases and 136 age-gender matched healthy controls was performed by PCR-RFLP.Results: Our findings reveal that a statistically increased risk and poor survival was associated with the BIRC5 -31CC genotype (OR 3.13, 95% CI 1.57-6.25) compared to the genotype containing G allele GC (OR 1.22, 95% CI 0.69-2.14). In addition significant association was found with stage and distant metastasis status of NSCLC patients. Conclusions:Our results conclude that the function polymorphism (-31G>C) in the promoter of survivin gene is associated with risk and susceptibility to NSCLC.

Background: Ovarian cancer is the leading cause of death from gynecological malignancies. The early stages of this disease are asymptomatic and more than 75% of the cases are diagnosed with regional or distant metastases. P53 is a tumor suppressor gene and is involved in the etiology of ovarian cancer. Studies investigating the associations between the p53 codon 72 polymorphism and ovarian cancer risk showed conflicting results. A polymorphism at codon 72 of the human tumour-suppressor gene, p53, results in translation to either arginine or proline. To investigate the association of p53 codon 72 polymorphism with susceptibility to epithelial ovarian cancer in North Indian women and to correlate them with clinicopathological characteristics of disease. Methods: The study was conducted on 100 epithelial ovarian cancer patients and 100 healthy controls. Genotyping of p53 codon 72 polymorphism was examined by PCR with allele-specific primers. Results: The proportions of individuals homozygous for the arginine allele, homozygous for the proline allele, and heterozygous for the two alleles were 33%, 17%, and 50% among women screened for ovarian cancer; 62%, 6%, and 32% among the control group. A significant correlation was found between the arg/pro (p<0.0004) and pro/ pro (p<0.0006) genotypes with respect to the arg/arg genotype. Pro/pro genotype emerged as the risk factor with an OR of 5.3 and a RR of 2.5. Conclusion: Our study suggests that Pro/Pro genotype of 72 codon polymorphism could be an independent susceptibility marker in northern Indian women with ovarian carcinomas.