Several studies indicate that DHEA may enhance cancer-promoting activities in several prostate cancer cell lines acting as agonist or antagonist for the intracellular AR
the estrogenic metabolites of DHEA, 5a-androstane-3b, 17b-diol (3b-Adiol) and E2 bind to estrogen receptors but not to AR
Different members of neurotrophins are expressed during cancer progression, suggesting their involvement in cell proliferation, anoikis protection, and malignancy
Regulation of the apoptotic machinery in prostate and colon cancer cells by testosterone occurs rapidly and is initiated at the plasma membrane level through specific membrane-binding sites not involving the classical cytoplasmic AR
testosterone exerts potent regulatory effects on prostate and colon cancer cell apoptosis
Testosterone increased cell death in a dose-dependent manner
testosterone antagonizes the prosurvival effects of DHEA in neuronal cells, blocking its binding to NGF receptors
treatment of cells with DHEA exerted a strong antiapoptotic effect,
Androgens hold a central role in prostate and colon cancer biology
elevated levels of DHEA or its sulfate ester DHEA-sulfate in young adults are associated to low incidence of androgen-dependent tumors
DHEA may play a protective role in young prostate
The decline of DHEA with aging may contribute to prostate cancer progression associated with advanced age
DHEA is an effective antiapoptotic factor, reversing the serum deprivation-induced apoptosis in prostate cancer cells (DU145 and LNCaP cell lines) as well as in colon cancer cells
NGF appears to exert similar antiapoptotic actions in both prostate and color cancer cells
exposure of prostate DU145 and colon Caco2 cancer cells to testosterone totally blocked the protective effects of both DHEA and NGF. These findings suggest that testosterone acts as an antagonist of DHEA and NGF
These findings support the hypothesis that testosterone may inhibit cancer cell growth by antagonizing the proliferative, antiapoptotic effects of endogenous factors, such as DHEA or NGF, in the case of prostate and colon cancer cells
intratumor hormonal microenvironment may play a critical role in tumor progression.
The paracrine interactions of androgens with locally produced NGF may define tumor cell fate
Full article of previously posted abstract. Cancers are unique. Not all cancers are alike. Whether they are tissue specific or not, cancers are unique. This article describes the uniqueness of DHEA and Testosterone cancer, with particular attention to colon.
DHEA-S shown to increase genetic expression of adiponectin in human adipose tissue. This has enormous implications on the link between DHEA and insulin resistance induce obesity. This is a peripheral tissue problem, not a central problem.
Polychlorinated biphenyl (PCBs) shown to disrupt thyroid hormone function through disruption of the transthyretin binding sites. Not only is it a xenoestrogen, but it disrupts thyroid function too.
Only abstract available here, but lower DHEA-S (still in reference normal range) associated with lower bone mineral density and increased osteoporosis risk.