Konishi N, Cho M, Yamamoto K, Hiasa Y
Second Department of Pathology, Nara Medical University, Japan.
Pathol Int. 1997 Nov;47(11):735-47. doi: 10.1111/j.1440-1827.1997.tb04451.x.
Recent advances in molecular biology have allowed us to understand that it is the accumulation of genetic alterations which leads to each step of tumorigenesis. What the specific alterations may be, however, often varies with each neoplasm. Prostate cancer is somewhat unique in its presentation to the pathologist of a bewildering array of histologies difficult to assign to diagnostic categories and contributing to misinterpretations of underlying molecular events. As with any malignancy, it is of utmost importance to thoroughly analyze and record the genetic aberrations found in prostate cancer with the objective of correlation to the pathology and natural history of the disease. Multiple oncogenes and tumor suppressor genes have been investigated in both clinical and latent cancer using conventional mutational analyses. To probe deeper into these genes and to uncover novel molecular events, genomic tumor DNA were examined using restriction landmark genomic scanning (RLGS), a method which allows the identification and comparison of specific genetic alterations within large segments and multiple samples of DNA at a time. This article reviews what has been identified based on numerous molecular studies, focusing on the genetic alterations peculiar to human prostate cancer.
