| Popis: |
During the pathogenesis of prostate cancer, prostate cells acquire both genetic and epigenetic alterations [1]. Genetic defects have long been considered hallmarks of cancer, but because such changes tend to accumulate during cancer pathogenesis, i.e., they are essentially irreversible, only a fraction are likely to act as drivers of the malignant phenotype at any given time [2]. In contrast, epigenetic changes, which affect gene function rather than gene sequence, are potentially reversible and thus tend to be maintained only when contributing to cancer growth and progression. During prostatic carcinogenesis, epigenetic alterations can be detected in the earliest of cancer precursor lesions, in localized cancer lesions, and at lethal disease progression [3]. Furthermore, new technologies for genome-wide characterization of chromatin structure and function in normal and neoplastic prostate cells have revealed broad corruption of the regulation of gene function [4, 5]. How the myriad somatic epigenetic alterations collaborate with genetic accidents to create prostate cancer has not yet been fully elucidated. Nonetheless, improved understanding of the nature, extent, and functional consequences of epigenetic defects in prostate cancer appears poised not only to provide new insights into the causes of the disease, but also to yield new diagnostic tests for disease detection and risk stratification and new treatment approaches for disease control. |
