Polymorphisms, genomic imprinting and cancer susceptibility

Abstract

Polymorphisms have been identified in proto-oncogenes and tumor suppressor genes that predispose people to cancer. Recent evidence indicates that genomic imprinting, an epigenetic form of gene regulation that results in uniparental gene expression, can also function as a cancer predisposing event. Thus, cancer susceptibility is increased by both Mendelian inherited genetic and non-Mendelian inherited epigenetic events. Consequently, chemical and physical agents cannot only induce cancer through the formation of genetic mutations but also through epigenetic changes that result in the inappropriate expression of imprinted proto-oncogenes and tumor suppressor genes. The role of genomic imprinting in carcinogenesis and cancer susceptibility is examined in this review.