What I will add is that soy isoflavones both slow the breakdown
of activated vitamin D  and help upregulate the VDR
which in turn will help maintain
cellular differentiation. The following abstracts relate
to the prostate but in principle should apply to
breast health and disease as well.

1: Postepy Hig Med Dosw (Online). 2007;61:253-60.

[The influence of isoflavonoids on the antitumor activity of vitamin
D3]

[Article in Polish]

Wietrzyk J.

Laboratorium Doswiadczalnej Terapii Przeciwnowotworowej
Instytutu Immunologii i
Terapii Doswiadczalnej PAN im. L. Hirszfelda we
Wroclawiu, Poland.
wietrzyk@iitd.pan.wroc.pl

Isoflavonoids exert a regulatory function on the expression of
cytochrome P450 enzymes and also up-regulate the
vitamin D(3) receptor (VDR) on cancer cells,
which increase their sensitivity to 1,25-dihydroxyvitamin D(3) ,
the hormonally active form of vitamin D(3) . Isoflavonoids are also
able to raise the serum level of the active form of vitamin D(3) due
to their inhibitory activity on CYP24, the enzyme involved in
the degradation of 1,25-dihydroxyvitamin D(3) and
its precursor 25-OH-D(3) to inactive compounds.
Another enzyme, CYP27B1, involved
in the synthesis of 1,25-dihydroxyvitamin D(3) ,
is stimulated by isoflavonoids,
and this may result in a similar effect of increasing in
the serum level of 1,25-dihydroxyvitamin D3. CYP27B1
and CYP24 were found in kidneys (the main
location of 1,25-(OH) (2)D(3) synthesis) and
also in brain cells, osteoclasts, keratinocytes,
macrophages, intestine epithelial cells, and in
some cancer cells. The expression of VDR was
detected not only in the cells primarily targeted by
1,25-dihydroxyvitamin D3, but also in epithelial and
mesenchymal cells.  Therefore, combined treatment
with isoflavonoids and 1,25-dihydroxyvitamin D3
might be effective in both cancer prevention and treatment.

PMID: 17507873

1: J Nutr. 2007 Jan;137(1 Suppl):205S-210S.

Calcitriol and genistein actions to inhibit the
prostaglandin pathway: potential
combination therapy to treat prostate cancer.

Swami S, Krishnan AV, Moreno J, Bhattacharyya RB,
Peehl DM, Feldman D.

Department of Medicine,
Division of Endocrinology,
Stanford University School of
Medicine, Stanford, CA 94305, USA.

We present an overview of the prostaglandin (PG)
pathway as a novel target for the treatment of prostate
cancer (PCa) using a combination of calcitriol and
genistein, both of which have known antiproliferative
properties. Calcitriol inhibits the PG pathway in
PCa cells in 3 separate ways: by decreasing
cyclooxygenase-2 (COX-2) expression, stimulating
15-hydroxyprostaglandin dehydrogenase
(15-PGDH) expression, and decreasing EP (PGE2)
and FP (PGF(2alpha)) receptors. These actions of
calcitriol result in reduced levels of biologically
active PGE2, leading ultimately to growth
inhibition of the PCa cells. We also
demonstrate the advantages of using
calcitriol in combination with genistein for
the treatment of PCa. Genistein, a major
component of soy, is a potent inhibitor
of the activity of CYP24, the enzyme
that initiates the degradation of
calcitriol. This leads to increased half-life
of bioactive calcitriol, thereby
enhancing all of calcitriol's actions including
those on the PG pathway. In addition to inhibiting
CYP24 enzyme activity, genistein has its own
independent actions on the PG pathway in PCa cells.
Like calcitriol it inhibits COX-2 expression and
activity, leading to decreased synthesis of PGE2.
It also inhibits the EP and FP receptors, thereby
reducing the biological function of PGE2. Thus,
the combination of calcitriol and genistein acts
additively to inhibit the PG pathway. Both calcitriol
and genistein are relatively safe and have little
toxicity associated with their intake. We postulate
that the combination of calcitriol and genistein
is an attractive therapeutic option for the treatment of
PCa.

PMID: 17182827

Endocrinol. 2006 Nov;191(2):387-98.

Phytoestrogens regulate transcription
and translation of vitamin D receptor in
colon cancer cells.

Gilad LA, Tirosh O, Schwartz B.

Faculty of Agricultural,
Food and Environmental Quality Sciences, Institute of
Biochemistry, Food Science and Nutrition,
The Hebrew University of Jerusalem,
Rehovot 76100, Israel.

The present study assesses the effects of two isoflavones,
genistein and glycitein, and equol - a product of
intestinal bacterial metabolism of dietary
isoflavones, on vitamin D receptor (VDR) expression
in an intestinal HT29 cell line. Genistein and glycitein
significantly upregulated the VDR transcription and
translation in HT29 cells. The effect of equol was
less pronounced. Treating HT29 cells transfected with
a vector containing the VDR promoter next to a luciferase
reporter with genistein or glycitein resulted in significant
upregulation of VDR  promoter activity, in a manner
similar to that induced by 17beta-estradiol (E2).
Again, the effect of equol was less pronounced.
VDR luciferase promoter activity  was upregulated most
by genistein, then by glycitein and least by equol when the
VDR promoter was cotransfected with estrogen
receptor beta. Reporter gene and chromatin
immunoprecipitation (ChIP) assays demonstrated
that E2 upregulates AP-1 and Sp-1 sites present
on the VDR gene. In contrast, the same assays
demonstrated that the Sp-1, but not AP-1, site is
induced by the phytoestrogens. Similar to
E2, genistein, glycitein and the isoflavonoid
metabolite equol induced higher
concentrations of intracellular free calcium,
an event that could provide the
upstream mechanism(s) induced by E2
and phytoestrogens that initiates the
signaling cascade which results in the
activation of extracellular signal-regulated
kinase (ERK) signaling pathways and
modulation of Sp-1 sites of
the VDR gene, and culminates
in enhanced VDR expression.

PMID: 17088408