AI Article Synopsis
- The p16 gene, which normally helps regulate the cell cycle, is often deleted or mutated in various tumors, but its specific role in prostate cancer remains unclear.
- Five metastatic prostate cancer cell lines and 41 DNA samples from primary tumors and normal tissues were examined for p16 gene alterations using various molecular biology techniques.
- The study found only one missense mutation in a specific cell line while no significant mutations were identified in primary prostate cancer samples, suggesting that p16 mutations do not significantly contribute to the development of primary prostate cancer.
Article Abstract
Background: The p16 gene product is a negative regulator of cell cycle and has been shown to be deleted or mutated in a number of tumor cell lines and primary tumors. The role of p16 in prostate cancer is not defined. Prostate cancer tissues and cell lines were evaluated for p16 gene alterations.
Methods: Five metastatic prostate cancer cell lines were analyzed for p16 gene structure and its expression by Southern and Northern blot analyses. Forty-one DNA specimens from 18 microdissected primary tumor specimens, adjacent normal tissues, and cell lines were amplified by polymerase chain reaction for p16 protein coding and splice junction sequences. Mutations were analyzed by single strand conformation polymorphism and DNA sequencing.
Results: DU 145 cell line exhibited a missense mutation in codon 84 (GAC to TAC). With the exception of previously reported polymorphism, no mutation was detected in p16 coding or splice junction sequences in primary prostate cancer specimens.
Conclusions: Inactivation of p16 gene by mutations in the protein coding sequence does not play a major role in the genesis of primary prostate cancer.
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| http://dx.doi.org/10.1002/(sici)1097-0045(19970215)30:3<188::aid-pros7>3.0.co;2-i | DOI Listing |
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