Vitamin D may prevent and treat breast cancer through several mechanisms

[Lani]

in a multitude of ways--the most recently discovered of which is by TISSUE SPECIFIC diminution of aromatase (by two mechanisms)

it has cox2 inhibitory properties as well

I have quoted Dr. Feldman before and even posted a video of one of his lectures on vitamin D. His work was initially with NSAIDs+vitamin D vs prostate cancer. I believe they have started a similar trial for breast cancer @ Stanford. Not a lot of financial support for these trials as no big money to be made on NSAIDs and vitamin D

Here is the abstract of his latest paper:
J Steroid Biochem Mol Biol. 2010 Feb 12. [Epub ahead of print]
Vitamin D and Breast Cancer: Inhibition of Estrogen Synthesis and Signaling.
Krishnan AV, Swami S, Feldman D.

Division of Endocrinology, Department of Medicine, Stanford University School of Medicine, Stanford, California 94305.
Calcitriol (1,25-dihydroxyvitamin D(3)), the hormonally active metabolite of vitamin D, inhibits the growth and induces the differentiation of many malignant cells including breast cancer (BCa) cells. Calcitriol exerts its anti-proliferative activity in BCa cells by inducing cell cycle arrest and stimulating apoptosis. Calcitriol also inhibits invasion, metastasis and tumor angiogenesis in experimental models of BCa. Our recent studies show additional newly discovered pathways of calcitriol action to inhibit the growth of BCa cells. Calcitriol suppresses COX-2 expression and increases that of 15-PGDH thereby reducing the levels and biological activity of prostaglandins (PGs). Calcitriol decreases the expression of aromatase, the enzyme that catalyzes estrogen synthesis selectively in BCa cells and the breast adipose tissue surrounding BCa, by a direct repression of aromatase transcription via promoter II as well as an indirect effect due to the reduction in the levels and biological activity of PGE(2), which is a major stimulator of aromatase transcription through promoter II in BCa. Calcitriol down-regulates the expression of estrogen receptor alpha and thereby attenuates estrogen signaling in BCa cells including the proliferative stimulus provided by estrogens. We hypothesize that the inhibition of estrogen synthesis and signaling by calcitriol and its anti-inflammatory actions will play an important role in the use of calcitriol for the prevention and/or treatment of BCa. Copyright © 2010. Published by Elsevier Ltd.

PMID: 20156557 [PubMed - as supplied by publisher]