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another awesome article dealing with hormone metabolites. Physicians that don't understand metabolites and receptors may be doing more harm than good.   One of the mainstays of the treatment of metastatic prostate disease is androgen deprivation therapy.  This article requires a reassessment of this due to the DHT metabolite 3-beta androstanediol.  This metabolite is produced from DHT production via the enzyme 3beta HSD.  This metabolite binds to ER beta, an estrogen receptor, and inhibits proliferation, migration, promotes adhesion (limits spreading), and stimulates apoptosis.  This is contrast to 3-alpha androstanediol.  Androgen deprivation therapy will decrease 3-beta androstanediol.  This is the likely reason for the increased aggressive prostate cancer found in those men using 5 alpha reductase inhibitors.

Different progesterone metabolites shown to have different tumor effects.  Implications are that, just as estrogen metabolism effects cancer risk, so does progesterone metabolism.

Study finds that ER beta inhibits invasion, proliferation and actually triggers cell death of prostate cancer cells.  This fits with the other data that loss of ER beta promotes carcinogenesis.

Good discussion of the different effects of progesterone metabolites in breast cancer cell lines (in vitro).  This article focused on the biochemical balance of 5alpha pregnane: 3alpha HP.  The increase in this ration promoted proliferation and metastasis, where a decreased ratio did the opposite

Animal study, finds that DHEA inhibited 11beta-HSD type I and thus improved glucose uptake and adipocyte proliferation.  This effect occurred peripherally.

Another mark for cucumin in the battle against cancer.  This article looked at the mechanism behind the inhibition of cell proliferation by curcumin.  The proposed mechanism is via Nrf2 induction in the MCF-7 cell culture lines.

Awesome article on progesterone metabolism in breast cancer.  The author, weibe, describes 2 categories of progesterone metabolites in breast tissue: 5alpha-pregnanes and 4-pregnenes.  The author describes 3 primary enzymes that control the balance between these 2 metabolites--5alpha reductase, 3alpha-HSO, and 20alpha-HSO.  The resultant balance of 5alpha-dihydroprogesterone and 3alpha-dihydroprogesterone helps to determine the cancer potential of breast tissue.

Estrogenic Potential of Progestins in Oral Contraceptives to Stimulate Human Breast Cancer Cell Proliferation1

Estrogenic potential of progestins in oral contraceptives to stimulate human breast cancer cell proliferation.

LDN inhibits cell proliferation through increased opioid growth factor and receptor translation.

study finds that BDNF is more associated with cell proliferation and neurogenesis with normal circulating Testosterone levels.  

Anandamide, an endogenous CBD ligand found to inhibited breast cell proliferation in breast cancer cell lines.

Ivermectin found to be pro-apoptotic for the epithelial ovarian cancer oncogene, KPNB1 in in Vivo study.  This effective anti-parasitic drug inhibits the KPNB1 oncogene.

Epigenetics plays a role, via disregulated miRNA, in increased cell growth, progression, and invasion in Lebanese women with breast cancer.  It is not just genetics that play a role, but epigenetics.

doxycycline useful in breast cancer animal model to reduce tumor burden through inhibition of tumor cell proliferation and inhibition of MMP.

Low dose procaine found to decrease tumor growth and proliferation.

Oxidative stress/inflammation via HIF-1alpha increase D3 which increases rT3 to increase proliferation in cancer; in contrast, there is a decrease in D1 and D2 to decrease T3 and T4. The question is the systemic versus the TME.

Mistletoe found to inhibit cancer cell proliferation and reduce chemo-resistance.

Peptide therapy effective in inhibits proliferation in TNBC.

Intratumoral mistletoe injections reduces proliferation and increases apoptosis in breast cancer mouse model.