A substantial amount of evidence suggests that neoplastic transformation may result from alterations in tumor suppressor genes whose products negatively regulate cell growth. To date, a number of tumor suppressor genes (e. g., RB, p53, DCC, APC/MCC, NF1, NF2, WT1, VHL, BRCA1, MST1, and WAF1/CIP1 genes) have been identified and have been shown to be important in a variety of human malignancies such as cancers of the colon, lung, breast, and esophagus (see refs. 1 and 2 for reviews). Tumor suppressor genes are potential targets for various inactivational events leading to prostatic tumorigenesis. However, it is possible that the genes which play a critical role in cancer development of one cell type may not necessarily be involved in the carcinogenesis of other cell types. For example, certain proto-oncogenes are only expressed in a tissue and cell type specific manner, and thus the deregulation of the expression of these genes would result in cell type specific neoplastic transformation. Accumulative evidence supports the cell type specific involvement of tumor suppressor genes in human cancers. The retinoblastoma (RB) tumor suppressor gene is one such example. While allelic deletions or mutations of the RB gene were demonstrated in approximately 75% of retinoblastomas, similar molecular alterations of this gene were found in less than 10% of colorectal cancers. This suggests that the RB gene may not play an important role in the development of colorectal cancers. Investigations by Vogelstein and associates demonstrated allelic deletions of chromosome 5q, 17p, and 18p in more than 55–85% of colorectal cancer patients studied³. These results showed that such mutational events occurred in a majority of colorectal cancers and suggested that genes located on these subchromosomal regions may play key roles in the genesis of this cancer type.