Re: Breast cancer - what to eat

On Nov 12, 6:32 am, "BASTARDO 65346354354" <n...@xxxxx> wrote: What
kind of food and food supplements should she eat? <<

Anticancer Res 2002 Sep-Oct;22(5):2685-92


Induction of apoptosis by iron depletion in the human breast cancer
MCF-7 cell
line and the 13762NF rat mammary adenocarcinoma in vivo.


Jiang XP, Wang F, Yang DC, Elliott RL, Head JF
Mastology Research Institute, Elliott-Hailey-Head Breast Cancer
Research and
Treatment Center, 17050 Medical Center Drive, 4th Floor, Baton Rouge,
LA 70816,
USA.


[Medline record in process]


It is known that the interruption of normal iron metabolism with
chelators of
iron, toxic metals, toxic metals bound to transferrin, or anti-
transferrin
receptor antibodies leads to significant inhibition of tumor cell
growth in
cell culture systems and animal models. In the present study, we found
that
iron depletion was produced by the iron chelator deferoxamine
mesylate, the
free toxic metals gallium or indium, and the toxic metals gallium or
indium
bound to transferrin in the MCF-7 human breast cancer cell line, and
this
induced the condensation and fragmentation of chromatin, and the
formation of
DNA fragments characteristic of apoptosis. The induction of apoptosis
was
quantitated with acridine orange and ethidium bromide staining of
apoptotic
cells, separation of fragmented DNA from radiolabeled cells, and in
situ
terminal deoxynucleotidyl transferase-mediated dUTP-digoxigenin nick
end
labeling (TUNEL) assays. The apoptosis, caused by deferoxamine
mesylate, and
gallium or indium bound to transferrin in the MCF-7 cells, can be
completely
inhibited by excess ferric chloride or equimolar iron-loaded
transferrin.
Gallium-transferrin and indium-transferrin complexes induced more
apoptosis
than their respective salts in the MCF-7 cells. Deferoxamine mesylate
induced a
small increase in the endogenous expression of both the bcl-2 and bax
genes in
the MCF-7 cells and this can be prevented by ferric chloride. In the
13762NF
rat mammary adenocarcinoma model, in situ TUNEL assays showed that
the
iron-deficiency following a low iron diet or intravenous injection of
deferoxamine mesylate produced 5.32 +/- 3.90% and 6.46 +/- 3.58% of
apoptotic
cells, respectively, compared to 2.01 +/- 1.20% of apoptotic cells in
the
control rats maintained on a normal diet (p < 0.05 and p < 0.01,
respectively,
Student's t-test). This is the first report of iron depletion caused
by a low
iron diet or deferoxamine mesylate treatment inducing apoptosis in
rats bearing
the 13762NF marnmary adenocarcinoma.


PMID: 12529982, UI: 22418357


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Crit Rev Oncol Hematol 2002 Jun;42(3):267-81


Iron chelators as therapeutic agents for the treatment of cancer.


Richardson DR
The Iron Metabolism and Chelation Group, The Heart Research Institute,
145
Missenden Road, Camperdown, 2050, Sydney, NSW, Australia


[Medline record in process]


A wide variety of studies in vitro, in vivo, and in clinical trials
have
demonstrated that the chelator currently used to treat iron overload
disease,
desferrioxamine, has anti-proliferative effects against both leukemia
and
neuroblastoma. However, the efficacy of desferrioxamine is severely
limited due
to its poor ability to permeate cell membranes and chelate
intracellular iron
pools. These studies have led to the development of other iron
chelators that
are far more effective than desferrioxamine. Some of these chelators
such as
3-aminopyridine-2-carboxaldehyde thiosemicarbazone (Triapine(R)) have
entered
phase I clinical trials, while other chelators such as
2-hydroxy-1-naphthylaldehyde isonicotinoyl hydrazone or tachpyridine
require
evaluation in animal models. The high anti-tumor activity observed
with these
ligands certainly suggests further development of chelators as anti-
cancer
agents is warranted.


PMID: 12050019, UI: 22045182


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