ABSTRACT
Prostate cancer is one of the most prevalent and least understood of all malignancies in men. The prevalence of histological prostate cancer is remarkably similar in the whole world, but clinical incidence widely varies. It indicates that although initiation rate of prostate cancer is the same, progression of clinically evident disease varies. This progress of carcinogenesis is likely to vary strongly between individuals because of the population variability in polymorphic genes that regulate these processes. Changes in the patterns of methylationhave been associated with the altered expression of a number of genes involved in cell cycle control and apoptosis, including p16, GSTP1, INK4a, RASSFIA, RAR-ß, FHIT, APC, MGMT, H-, and E-cadherins among many others in various carcinomas. Silencing of tumour suppressor and tumour-related genes by hypermethylation at promoter CpG islands is one of the major events in human tumourigenesis. Prostate cancer is the second most common cancer in Europe and the United States. Its incidence and mortality rates vary worldwide. It accounts for 33% of all the recently diagnosed malignancies among men in United States. Although Asian people have the lowest incidence and mortality rates of prostate cancer in the world, these rates have rapidly risen in the past two decades in most Asian countries. A Delhi urban resident population-based cancer registry reveals an age standardized rate (ASR) of 9.0 per 100,000 men in prostate cancer and the incidence of prostate cancer in males was the highest among the Indian registries. A number of genetic and environmental factors are known to influence individual susceptibility towards the formation of prostatic tumors. Unlike genetics, epigenetic mechanisms such as DNA methylation confer different functional status to the same genes under different environmental conditions. Knowledge of such gene-environment interaction may lead to established biomarkers that will perform better than the standards of PSA, Gleason score, and TNM staging.
