We found no statistically significant associations of ApoE variants with overall prostate cancer or Gleason sum ≤ 7 (3+4), Gleason sum ≥ 7 (4+3), clinically localized stage, or progression to metastasis or death.
In this investigation, we determined whether variants of the Apo E gene can trigger defective intracellular cholesterol efflux, which could promote aggressive prostate cancer.
In the 102-country subset of 102, per capita GDP, ApoE4 prevalence, and milk protein explained 62% of the variance of prostate cancer incidence, while lack of cereal consumption, ApoE4 prevalence and per capita GDP explained 55% of the variance of prostate cancer mortality rates.
Whereas the latter group of tumors expressed some proapoptotic genes, tumors with high FAS levels overexpressed, among other genes, its transcriptional regulator, steroid regulator binding protein, and apolipoprotein E. These data demonstrate (1) the consistent overexpression of FAS in prostate carcinoma compared with the adjacent normal tissue, (2) a strong association between FAS and prostate tumor initiation and progression, (3) the highest FAS expression occurring in androgen-independent bone metastases, (4) the transcriptional and posttranscriptional regulation of FAS in the majority and in a subset of prostate cancers, respectively, and (5) most importantly, the identification by FAS expression of prostate tumors with unique molecular signatures and potentially diverse biologic behavior.