Chin R K, Hawkins A L, Isaacs W B, Griffin C A
Johns Hopkins School of Medicine, Department of Pathology, Baltimore, MD, USA.
Cancer Genet Cytogenet. 1998 Jun;103(2):155-63. doi: 10.1016/s0165-4608(97)00407-x.
The difficulty of maintaining long-term prostate cell cultures has hindered the development of essential models for understanding prostate cancer. We report here the establishment of two 12S E1A transformed non-tumorigenic prostate epithelial cell strains, and their characterization. The two clonal cell strains, TP2 and TP4, proliferated for approximately 40 passages before senescence. Both exhibited a strong dependence on exogenous peptide growth factors and an immunophenotype characteristic of their prostate epithelial origin. Cytogenetic analysis revealed a consistent deletion on the q arm of chromosome 16 in TP2 with an otherwise normal karyotype. Band-specific microdissection generated region-specific probes from 16q23, which when used in fluorescence in situ hybridization (FISH) revealed that the region was deleted in 83% of metaphases analyzed. By cytogenetic analysis and FISH, the q arm of 16 was found deleted from the genome of TP4 in 60% of cells analyzed. Lost sequences on 16q-16q23 in particular--in prostate cancer have been observed by a variety of methods. Localization of common region of deletion has been determined from these studies to be distal to 16q23. Our findings suggest that 16q23 may be of major importance in the development of prostate cancer, and may harbor tumor suppressor elements.
