In summary, we report a novel finding that the LPL gene is commonly methylated in prostate tumors, and our results suggest that biallelic inactivation of LPL by chromosomal deletion and promoter hypermethylation may play a role in human prostate cancer.
Loss of a part of chromosome 8p22, containing the gene LPL and amplifications of the field 8q24 comprising the c-myc oncogene are the most frequent chromosomal aberrations in prostate cancer.
Our results suggest that the LPLSer447stop polymorphism is a common genetic modifier for the development of prostate cancer, particularly that of high-grade and/or high-stage, in a Japanese population.