The LOH in tumors was analyzed by PCR with fluorescently labeled primers and an ABI PRISM 377 DNA Sequencer. DNA was isolated from prostate biopsies and matched peripheral blood of 50 patients. To evaluate the contribution of RAD51 to sporadic prostate cancer, loss of heterozygosity (LOH) for chromosomal region 15q14-21.1 ( RAD51 locus) was determined and compared to LOH in 17q21.31 ( BRCA1 locus) and 13q12.3-13.1 ( BRCA2 region). RAD51 functioning depends on the indirect or direct interactions with BRCA1 and BRCA2. RAD51 is a central player in double-strand break repair via homologous recombination, and its alterations may confer and increase the risk of cancer. Accumulating evidence indicates that the fidelity of the response to DNA double-strand breaks is critical for maintaining genome integrity. DNA damage repair mechanisms have been implicated in human cancer. Although prostate cancer is one of the most common cancers in men, the genetic defects underlying its pathogenesis remain poorly understood.
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