Re: You may want to look at more research on progesterone...

[Guest guest]

Lynn, I agree with you. I have not seen bioidentical progesterone

contribute to cancer growth. Sounds like a study backed by a pharmaceutical

company. Also the study was done in 2001 and we known a lot more about

bioidentical progesterone and how the body uses it than we did even in 2001.

Be Well

Dr.L

[ ] You may want to look at more research on

progesterone...

It is probably not a good idea to pick one article out on progesterone but

instead look at the preponderance of evidence.

_www.breastcancerchoices.org/progesterone_

(http://www.breastcancerchoices.org/progesterone)

Lynne

[Guest guest]

Enough research has been done on progesterone and

breast cancer to warrant high caution. I don't

use it and won't until I see a greater

consensus. I went to the website

suggested. This does not present a preponderance

of evidence, but a selection of evidence in

support of progesterone use. Good science and

its presentation should be a truth-seeking

venture, not a forum for polemics, the market,

unprincipled captiousness, nor

defensiveness. Few things bring me greater joy

than when I can change my mind or simply monitor

the coalescence of a justifiable conclusion over the months and years.

------------------------------------

Informa Healthcare

Membrane-initiated effects of progesterone on

proliferation and activation of VEGF in breast cancer cells

Authors: H. Neubauera; G. Adama; H. Seegera; A.

O. Muecka; E. Solomayera; D. Wallwienera; M. A. Cahillb; T. Fehma

Affiliations: a Department of Obstetrics and

Gynecology, University of Tuebingen,

b School of Biomedical Sciences, Sturt

University, Wagga, Wagga, Australia

DOI: 10.1080/13697130802635637

Publication Frequency: 6 issues per year

Published in:

journal

<http://www.informaworld.com/smpp/title%7Edb=all%7Econtent=t713605024>Climacteri\

c<http://www.informaworld.com/smpp/title%7Edb=all%7Econtent=t713605024%7Etab=iss\

ueslist%7Ebranches=12#v12>,

Volume

<http://www.informaworld.com/smpp/title%7Edb=all%7Econtent=t713605024%7Etab=issu\

eslist%7Ebranches=12#v12>12,

Issue

<http://www.informaworld.com/smpp/title%7Edb=all%7Econtent=g911141356>3

June 2009 , pages 230 - 239

First Published: June 2009

Subject:

<http://www.informaworld.com/smpp/browse%7Edb=all%7Ething=title%7Eby=subject%7Ea\

ppend=714595033,714594960,714594959,714595039#subject714595039>Menopause

& Hormone Replacement;

Formats available: HTML (English) : PDF (English)

Single Article Purchase: from €69.00 -

<http://www.informaworld.com/smpp/content%7Econtent=a910146463%7Edb=all%7Ejumpty\

pe=rss?action=showoptions & mode=content>view

purchasing options

Abstract

Objective Progesterone influences mammary gland

development and probably breast cancer

tumorigenesis and functions by regulating a broad

spectrum of physiological processes. We

investigated receptor membrane-initiated actions

of progesterone in MCF-7 breast cancer cells via

progesterone receptor membrane component 1 (PGRMC1).

Design and method The expression of PGRMC1 in

breast cancer was verified by immune fluorescent

analysis of paraffin sections. MCF-7 cells were

transfected with PGRMC1 (wild type) or PGRMC1

variants. These cells were stimulated with a

membrane-impermeable progesterone (P4) conjugate

(P4-BSA-fluorescein isothiocyanate, P4-BSA-FITC,

10-6 mol/l) or unconjugated progesterone (P4,

10-6 mol/l) in the presence or absence of the

progesterone receptor blocker RU-486 (10-6

mol/l). Additionally, the effects on the

expression of vascular endothelial growth factor

A (VEGF-A) were determined using quantitative

real-time polymerase chain reaction.

Results PGRMC1 is perinuclearly localized in

breast cancer cells. Western Blot analysis

suggests that PGRMC1 is phosphorylated at serine

180. MCF-7-PGRMC1 (S180A) cells show an

approximately 35% increase in proliferation after

incubation with P4-BSA-FITC compared to MCF-7

control and MCF-7-PGRMC1 (wild type) cells. This

effect cannot be blocked by RU-486. P4 reduced

proliferation of MCF-7-PGRMC1 cells by

approximately 10% compared to untreated controls.

P4-BSA-FITC treatment led to a roughly three-fold

activation of VEGF-A gene expression compared to MCF-7 cells.

Conclusion PGRMC1 is expressed in breast cancer

tissue and mediates an RU-486-independent

proliferative signal. It might also contribute to

VEGF-induced neovascularization in tumor tissue.

Thus, screening for PGRMC1 expression might be of

interest to identify women with a higher

expression of PGRMC1 and who might thus be

susceptible for breast cancer development under hormone replacement therapy.

--------------------------

Endocrinology, doi:10.1210/en.2005-0103

Google Scholar

PubMed

Endocrinology Vol. 146, No. 8 3632-3641

Copyright © 2005 by The Endocrine Society

Proliferation of Endothelial and Tumor Epithelial

Cells by Progestin-Induced Vascular Endothelial

Growth Factor from Human Breast Cancer Cells: Paracrine and Autocrine Effects

Yayun Liang and Salman M. Hyder

Dalton Cardiovascular Research Center and

Biomedical Sciences, University of Missouri, Columbia, Missouri 65211

Address all correspondence and requests for

reprints to: Dr. Salman M. Hyder, Dalton

Cardiovascular Research Center, University of

Missouri, 134 Research Park Drive, Columbia,

Missouri 65211. E-mail: <mailto:hyders@...>hyders@....

Angiogenesis, the formation of new blood vessels,

is essential for tumor expansion, and vascular

endothelial growth factor (VEGF) is one of the

most potent angiogenic growth factors known. We

have previously shown that natural and synthetic

progestins, including those used in hormone

replacement therapy and oral contraception,

induce the synthesis and secretion of VEGF in a

subset of human breast cancer cells in a

progesterone receptor-dependent manner. We now

report that conditioned medium from

progestin-treated breast tumor cells can induce

the proliferation of endothelial cells in a

paracrine manner and induce the proliferation of

tumor epithelial cells in a paracrine and an

autocrine manner. The use of an anti-VEGF

antibody and SU-1498, an inhibitor of VEGF

receptor-2 (VEGFR-2 or flk/kdr) tyrosine kinase

activity, demonstrated that these effects involve

interactions between VEGF and VEGFR-2. Also,

blockage of progestin-induced VEGF by the

antiprogestin RU-486 (mifepristone) eliminated

VEGF-induced proliferative effects. The ability

of VEGF to increase the proliferation of

endothelial cells and tumor cells, including

those that do not release VEGF in response to

progestins, suggests that these effects are

mediated by amplification of the progestin

signal, which culminates in angiogenesis and

tumor growth. These novel findings suggest that

targeting the release of VEGF from tumor

epithelial cells as well as blocking interactions

between VEGF and VEGFR-2 on both endothelial and

tumor epithelial cells may facilitate the

development of new antiangiogenic therapies for

progestin-dependent breast tumors. Furthermore,

these data indicate that it would be useful to

develop selective progesterone receptor

modulators that prevent the release of angiogenic

growth factors from breast cancer cells.

----------------------

Curr Cancer Drug Targets. 2004 Mar;4(2):183-9.

A rationale for inhibiting progesterone-related

pathways to combat breast cancer.

<http://www.ncbi.nlm.nih.gov/pubmed?term=%22%20MR%22%5BAuthor%5D> MR.

Department of Biochemistry and Molecular Biology,

Joan C. School of Medicine, Marshall

University, 1542 Spring Valley Drive, Huntington,

WV 25704, USA. moorem@...

Abstract

Inhibitors of estrogen-related pathways have been

used with some success in the treatment of breast

cancer. These include the antiestrogens

tamoxifen, more recently faslodex, and the

aromatase inhibitor anastrazole. However, failure

and recurrence rates are substantial with drugs

countering the effects of estrogens. Progestins,

unlike estrogens, have generally been considered

to oppose breast cancer and have been used with

reasonable efficacy after antiestrogen failure.

However, a building body of evidence, from cell

culture, animal studies, and, most recently,

several major clinical studies involving hormone

replacement therapy, strongly supports the notion

that progestins generally stimulate breast

cancer. Our studies and those of others suggest

that progestins increase the numbers of breast

cancer cells by both stimulating the rate of

proliferation and inhibiting cell death. These

data indicate that progestin-related pathways

might provide effective targets for breast cancer

therapy. This review addresses the rationale for

using inhibitors of progestin-related pathways to

treat breast cancer and comments on some possible points of attack.

PMID: 15032668 [PubMed - indexed for MEDLINE]

---------------------------

Gynecol Endocrinol. 2007 Oct;23 Suppl 1:32-41.

Progestins and breast cancer.

<http://www.ncbi.nlm.nih.gov/pubmed?term=%22Pasqualini%20JR%22%5BAuthor%5D>Pasqu\

alini

JR.

Hormones and Cancer Research Unit, Institut de

Puériculture et de Périnatalogie, Paris, France. .Pasqualini@...

Abstract

Progestins exert their progestational activity by

binding to the progesterone receptor (form A, the

most active and form B, the less active) and may

also interact with other steroid receptors

(androgen, glucocorticoid, mineralocorticoid,

estrogen). They can have important effects in

other tissues besides the endometrium, including

the breast, liver, bone and brain. The biological

responses of progestins cover a very large

domain: lipids, carbohydrates, proteins, water

and electrolyte regulation, hemostasis,

fibrinolysis, and cardiovascular and

immunological systems. At present, more than 200

progestin compounds have been synthesized, but

the biological response could be different from

one to another depending on their structure,

metabolism, receptor affinity, experimental

conditions, target tissue or cell line, as well

as the biological response considered. There is

substantial evidence that mammary cancer tissue

contains all the enzymes responsible for the

local biosynthesis of estradiol (E(2)) from

circulating precursors. Two principal pathways

are implicated in the final steps of E(2)

formation in breast cancer tissue: the 'aromatase

pathway', which transforms androgens into

estrogens, and the 'sulfatase pathway', which

converts estrone sulfate (E(1)S) into estrone

(E(1)) via estrone sulfatase. The final step is

the conversion of weak E(1) to the potent

biologically active E(2) via reductive

17beta-hydroxysteroid dehydrogenase type 1

activity. It is also well established that

steroid sulfotransferases, which convert

estrogens into their sulfates, are present in

breast cancer tissues. It has been demonstrated

that various progestins (e.g. nomegestrol

acetate, medrogestone, promegestone) as well as

tibolone and their metabolites can block the

enzymes involved in E(2) bioformation (sulfatase,

17beta-hydroxysteroid dehydrogenase) in breast

cancer cells. These substances can also stimulate

the sulfotransferase activity which converts

estrogens into the biologically inactive

sulfates. The action of progestins in breast

cancer is very controversial; some studies

indicate an increase in breast cancer incidence,

others show no difference and still others a

significant decrease. Progestin action can also

be a function of combination with other molecules

(e.g. estrogens). In order to clarify and better

understand the response of progestins in breast

cancer (incidence, mortality), as well as in

hormone replacement therapy or endocrine

dysfunction, new clinical trials are needed

studying other progestins as a function of the dose and period of treatment.

PMID: 17943537 [PubMed - indexed for MEDLINE]

At 10:54 AM 5/29/2010, you wrote:

>

>It is probably not a good idea to pick one article out on progesterone but

>instead look at the preponderance of evidence.

>

>_www.breastcancerchoices.org/progesterone_

>(http://www.breastcancerchoices.org/progesterone)

>

>Lynne

[Guest guest]

Please cite your sources.

Thanks so much.

Lynne

In a message dated 5/29/2010 8:54:23 P.M. Eastern Daylight Time,

vgammill@... writes:

Enough research has been done on progesterone and

breast cancer to warrant high caution.

[Guest guest]

, it appears that most of these abstracts used progestin. You know

that's not a bioidentical or natural replacement. Do you have the same type of

data for natural progesterone? Progestin and progesterone are not the same

thing, regardless of what the drs say.

xoo

[Guest guest]

All the sources were cited in the selfsame

post. They clearly lay it out that this is a

disputed area of research -- an unsettled area of science.

Additionally:

Benakanakere I, Besch-Williford C, Schnell JD & Hyder SM 2005

Natural and synthetic progestins accelerate tumor

development and increase VEGF production in a

chemically induced mammary tumor model: a

potentially novel target for anti-angiogenic therapeutics.

AACR Special Conference in Advances in Breast

Cancer, San Diego, CA. Abstract A15.

---------------

Hyder SM & Stancel GM 2002

Inhibition of progesterone-induced VEGF

production in human breast cancer cells by the pure antiestrogen ICI 182,780.

Cancer Letters 181

47–53.<http://erc.endocrinology-journals.org/cgi/external_ref?access_num=10.1016\

%2FS0304-3835%2802%2900048-4 & link_type=DOI>[CrossRef]<http://erc.endocrinology-j\

ournals.org/cgi/external_ref?access_num=000176629800006 & link_type=ISI>[Web

of

Science]<http://erc.endocrinology-journals.org/cgi/external_ref?access_num=12430\

178 & link_type=MED>[Medline]

-----------------------------

Liang Y, Wu J & Hyder SM 2005 p53-dependent

inhibition of progestin-induced VEGF expression

in human breast cancer cells. Journal of Steroid

Biochemistry and Molecular Biology 93

173–182.<http://erc.endocrinology-journals.org/cgi/external_ref?access_num=10.10\

16%2Fj.jsbmb.2004.12.011 & link_type=DOI>[CrossRef]<http://erc.endocrinology-journ\

als.org/cgi/external_ref?access_num=000229195200012 & link_type=ISI>[Web

of

Science]<http://erc.endocrinology-journals.org/cgi/external_ref?access_num=15860\

260 & link_type=MED>[Medline]

--------------------------

MR 2004 A rationale for inhibiting

progesterone-related pathways to combat breast

cancer. Current Cancer Drug Targets 4

183–189.<http://erc.endocrinology-journals.org/cgi/external_ref?access_num=10.21\

74%2F1568009043481515 & link_type=DOI>[CrossRef]<http://erc.endocrinology-journals\

..org/cgi/external_ref?access_num=000222364000005 & link_type=ISI>[Web

of

Science]<http://erc.endocrinology-journals.org/cgi/external_ref?access_num=15032\

668 & link_type=MED>[Medline]

---------------------

Cancer. 2004 Oct 1;101(7):1490-500.

Association of hormone replacement therapy to

estrogen and progesterone receptor status in invasive breast carcinoma.

<http://www.ncbi.nlm.nih.gov/pubmed?term=%22Chen%20WY%22%5BAuthor%5D>Chen

WY,

<http://www.ncbi.nlm.nih.gov/pubmed?term=%22Hankinson%20SE%22%5BAuthor%5D>Hankin\

son

SE,

<http://www.ncbi.nlm.nih.gov/pubmed?term=%22Schnitt%20SJ%22%5BAuthor%5D>Schnitt

SJ,

<http://www.ncbi.nlm.nih.gov/pubmed?term=%22Rosner%20BA%22%5BAuthor%5D>Rosner

BA,

<http://www.ncbi.nlm.nih.gov/pubmed?term=%22Holmes%20MD%22%5BAuthor%5D>Holmes

MD,

<http://www.ncbi.nlm.nih.gov/pubmed?term=%22Colditz%20GA%22%5BAuthor%5D>Colditz

GA.

Department of Medical Oncology, Dana-Farber

Cancer Institute, Boston, Massachusetts, USA. wychen@...

Abstract

BACKGROUND: Observational studies and randomized

trials have demonstrated that hormone replacement

therapy (HRT) increases the recipient's risk of

developing breast carcinoma. Because it is known

that some breast malignancies are hormonally

responsive and that others are not, it has been

hypothesized that HRT may be associated with the

development of estrogen receptor

(ER)-positive/progesterone receptor (PR)-positive

breast carcinoma more so than with the

development of ER-negative/PR-negative breast

carcinoma. METHODS: The Nurses' Health Study is a

prospective cohort study that enrolled 121,700

female registered nurses ages 30-55 years in

1976. In the current study, the authors analyzed

2548 malignancies that developed among eligible

postmenopausal women in that cohort between 1980

and 2000 and for which data on ER and PR status

were available. RESULTS: Compared with women who

had never used HRT, current long-term users of

HRT were more likely to develop

ER-positive/PR-positive breast carcinoma

(multivariate risk ratio [RR], 1.80; 95%

confidence interval [CI], 1.52-2.12) but were not

any more likely to develop

ER-negative/PR-negative disease (multivariate RR,

1.00; 95% CI, 0.72-1.39). This effect grew

stronger with increasing duration of current HRT

use and was also more pronounced among women with

body mass index < 25 kg/m2. Furthermore, the

association between HRT use and

ER-positive/PR-positive disease was stronger

among patients receiving combined HRT (CHRT)

regimens, which included estrogen and

progesterone, than among users of estrogen alone

(ERT). In addition, tumors tended to develop more

quickly in current users of CHRT than in ERT

users. CONCLUSIONS: The finding that current

users of HRT were more likely to develop

ER-positive/PR-positive tumors than they were to

develop ER-negative/PR-negative ones suggests

that both endogenous and exogenous hormonal

factors may influence breast tumor

characteristics. In analyses of the effects of

hormonal factors on breast tumor development,

ER-positive/PR-positive tumors and

ER-negative/PR-negative tumors should be

considered separately from each other. © 2004 American Cancer Society.

PMID: 15378477 [PubMed - indexed for MEDLINE]Free Article

---------------------

Breast Cancer Res. 2002;4(6):240-3. Epub 2002 Sep 12.

Progesterone receptors--animal models and cell

signalling in breast cancer. Diverse activation

pathways for the progesterone receptor: possible

implications for breast biology and cancer.

<http://www.ncbi.nlm.nih.gov/pubmed?term=%22Lanari%20C%22%5BAuthor%5D>Lanari

C,

<http://www.ncbi.nlm.nih.gov/pubmed?term=%22Molinolo%20AA%22%5BAuthor%5D>Molinol\

o

AA.

Laboratory of Hormonal Carcinogenesis, Instituto

de Biología y Medicina Experimental, Consejo

Nacional de Investigaciones Científicas y Técnicas, Buenos Aires, Argentina.

Abstract

Progesterone and estradiol, and their nuclear

receptors, play essential roles in the physiology

of the reproductive tract, the mammary gland and

the nervous system. Estrogens have traditionally

been considered associated with an increased risk

of breast cancer. There is, however, compelling

evidence that progesterone plays an important

role in breast cell proliferation and cancer.

Herein, we review the possible role of progestins

and the progesterone receptor-associated

signaling pathways in the development of breast

cancer, as well as the therapeutic possibilities

arising from our growing knowledge of the

activation of the progesterone receptor by other proliferative mechanisms.

PMID: 12473170 [PubMed - indexed for MEDLINE]PMCID: PMC137940Free PMC Article

-------------------------

Breast Cancer Res Treat. 2003 Jun;79(3):287-99.

Progesterone receptors A and B differentially

affect the growth of estrogen-dependent human breast tumor xenografts.

<http://www.ncbi.nlm.nih.gov/pubmed?term=%22Sartorius%20CA%22%5BAuthor%5D>Sartor\

ius

CA,

<http://www.ncbi.nlm.nih.gov/pubmed?term=%22Shen%20T%22%5BAuthor%5D>Shen

T,

<http://www.ncbi.nlm.nih.gov/pubmed?term=%22Horwitz%20KB%22%5BAuthor%5D>Horwitz

KB.

Department of Medicine, University of Colorado

Health Sciences Center, Denver, CO 80262, USA. carol.sartorius@...

Abstract

Sixty to seventy percent of all primary human

breast cancers are estrogen-dependent and express

both estrogen (ER) and progesterone receptors

(PR). Whereas expression of the two naturally

occurring PR isoforms, PR-A and PR-B, is close to

equimolar in normal human tissues, the ratio of

the two receptors varies extensively in tumors.

This is important since the two PR are

functionally distinct and have differential

repressor effects on ER. The PR isoform content

may, therefore, affect the outcome of endocrine

therapies targeted at ER. Study of PR isoforms is

difficult because the two receptors are

co-expressed in cells under estradiol

stimulation. We have engineered four sets of T47D

human breast cancer cells that, independent of

estrogen: (i) express only PR-A; (ii) express

only PR-B; (iii) are PR-negative; or (iv) contain

both PR isoforms. Each of these cell lines was

grown into solid tumors in nude mice in a

strictly 17beta-estradiol-dependent manner.

Results show, first, that PR-A expressing cells

grow into tumors that are approximately half the

size of PR-B expressing tumors, and second, that

the reduced growth of PR-A tumors occurs in the

absence of PR ligand. Tamoxifen treatment

preferentially inhibited the growth of PR-A

tumors, whereas PR-B tumors were unaffected.

Thus, PR are not just passive markers of

functional ER; the prevalence of PR-A or PR-B may

differentially influence tumor phenotype.

PMID: 12846413 [PubMed - indexed for MEDLINE]

---------------------------------

Breast Cancer Res. 2002;4(6):244-8. Epub 2002 Oct 7.

Progesterone receptors--animal models and cell

signalling in breast cancer. Implications for

breast cancer of inclusion of progestins in hormone replacement therapies.

<http://www.ncbi.nlm.nih.gov/pubmed?term=%22Schairer%20C%22%5BAuthor%5D>Schairer

C.

National Cancer Institute, Division of Cancer

Epidemiology and Genetics, Rockville, land

20852, USA. schairec@...

Comment in:

*

<http://www.ncbi.nlm.nih.gov/pubmed/12473167>Breast

Cancer Res. 2002;4(6):222-3.

Abstract

Progestins are included in menopausal hormone

replacement therapy to counteract the increased

risk for endometrial cancer associated with

estrogen replacement therapy. Studies of hormone

replacement therapy and breast cancer risk and of

changes in mammographic density according to

different regimens of hormone replacement therapy

suggest that, for the most part,

estrogen-progestin replacement therapy has a more

adverse effect on breast cancer risk than does

estrogen replacement therapy. Many questions

remain unresolved, however, including risk

associated with different regimens of

estrogen-progestin replacement therapy, and

whether the effects vary according to tumor

characteristics, such as histology, extent of

disease, and hormone receptor status.

PMID: 12473171 [PubMed - indexed for MEDLINE]PMCID: PMC137941Free PMC Article

------------------------

I think these (and the earlier citations) clearly

show that progesterone or progestin use for

breast cancer treatment is not something that

should be rushed in to. The biology is complex.

Even some clinicians who like progesterone cream express reservations:

http://www.womentowomen.com/breasthealth/progesteronebreastcancer.aspx

" Breast cancer, progestins and natural progesterone ­ is there a link?

by Dixie Mills, MD, FACS

" Who should not use natural progesterone cream?

" Women with breast cancer or a past history of breast cancer:

" This is the only group of women at any age that

I advise to avoid using even low doses of

transdermal progesterone or Prometrium capsules

without consulting with their oncologist

beforehand. We simply don’t know enough about the

outcome either way. It’s quite possible that

certain tumors may not be affected, but until we

know more, I think it is clear that the possible

risks could outweigh the benefits here.

" Women who note adverse effects with use of natural progesterone:

" Some women will metabolize extra progesterone

into estrogen ­ we call these women “highly

estrogenic.” They tend to respond quickly to

supplemental progesterone with increased breast

tenderness (particularly during ovulation) and

irregular spotting or bleeding. The closer this

kind of woman is to menopause, the more cautious

she should be with any form of progesterone. With

the right medical practitioner and a deep

understanding of her whole health picture, it can

be possible for such a woman to actually change

the way she metabolizes progesterone to make it

safe to supplement with bioidentical forms.

" Post menopausal women:

" Out of an abundance of caution, it is best not

to use any form of progestogen, including

progesterone, if a woman is more than two years

beyond her last period, unless she is on estrogen.

" It would also seem most prudent (at this stage

of scientific knowledge) for a woman to not take

additional hormones, including progesterone, for

more than a total of five years. In this case,

the reason for avoiding progesterone has more to

do with the natural evolution of hormones in the

body than with any identifiably increased risk.

After menopause, it is natural for your body’s

estrogen levels to taper off ­ so, fittingly, should your progesterone levels.

" If, however, you are using estrogen and have a

uterus, you must also use some form of

progestogen to counter the effects of the

estrogen on the uterine cells. The use of

(bioidentical) Prometrium is recommended for this

circumstance, as studies using progesterone cream

are conflicting and very few. As with estrogen

supplementation, our recommendation is that it be

used for a short period and no longer than five

years, at least until more information is available. "

-----------------------

also:

http://www.medicalnewstoday.com/articles/161348.php

Progesterone Leads To Inflammation, A Breast

Cancer Risk Factor, Research Reveals

21 Aug 2009

Scientists at Michigan State University have

found exposure to the hormone progesterone

activates genes that trigger inflammation in the mammary gland.

This progesterone-induced inflammation may be a

key factor in increasing the risk of breast cancer.

Progesterone is a naturally occurring steroid

hormone and promotes development of the normal

mammary gland. Progesterone previously has been

identified as a risk factor for breast cancer,

and in a study published in the Journal of

Steroid Biochemistry and Molecular Biology, MSU

scientists examined the genes activated by

progesterone and the effects of their activation in a mouse model system.

Exposure to progesterone in normal amounts and in

normal circumstances causes inflammation, which

promotes breast development. However, exposure to

progesterone in menopausal hormone therapy is

known to increase breast cancer risk.

" Progesterone turns on a wide array of genes

involved in several biological processes,

including cell adhesion, cell survival and

inflammation, " said physiology professor

Haslam, co-author of the paper and director of

the Breast Cancer and the Environment Research

Center at MSU. " All of these processes may be

relevant to the development of breast cancer. "

The study shows progesterone significantly

regulates 162 genes in pubertal cells, 104 genes

in adult cells and 68 genes at both developmental

stages. A number of these genes make small

proteins, called chemokines, which control the process of inflammation.

Inflammation is a process where white blood cells

move into a tissue. One type of white blood cell

which moves to the breast during inflammation is

a macrophage. Macrophages normally enter growing

glands and help them develop, building blood

vessels and reshaping growing tissue.

" Macrophages also may promote the development of

tumors, such as breast cancer, as they make blood

vessels to deliver nutrients and can clear the

way for tumors to grow, " Haslam said. " Long-term

exposure to progesterone, such as that which

occurs in menopausal hormone therapy, may encourage growth of tumors. "

Haslam noted that as the link between

progesterone and increased breast cancer risk was

identified in recent years, women have been

taking less hormone therapy after menopause and

the rate of breast cancer in older women has gone down.

" This study reveals the targets of a specific

form of the progesterone receptor, called PRA, in

mammary cell development, " said microbiology

professor Schwartz, a co-author of the

paper and associate dean in the College of

Natural Science. " The linkages identified provide

targets for future work in reducing the influence

progesterone has on developing breast cancer.

" Understanding the genes that regulate

inflammation in the mammary gland will help us to

better understand normal breast growth and also

may help us devise better treatments for the abnormal growth in cancer. "

A collaborative team of 10 scientists in MSU's

departments of Physiology and Microbiology and

Molecular Genetics contributed to the findings.

The team's work was published in the July 2009 issue of the journal.

The team of faculty is part of MSU's Breast

Cancer and the Environment Research Center, one

of four centers nationwide funded by the National

Institute of Environmental Health Sciences and

the National Cancer Institute. The center brings

together researchers from MSU's colleges of

Natural Science and Human Medicine to study the

impact of prenatal-to-adult environmental

exposures that may predispose a woman to breast

cancer, as well as researchers in the College of

Communication Arts and Sciences to study how to

best communicate breast cancer health messages to the public.

----------------------

There are many things that those without cancer

can do without carefully sorting out the

consequences. With cancer everything changes. I

am very cautious if there seems to be risks

involved. For example, transdermal testosterone

can be used to fight breast cancer, but as much

as I would love to quickly regain my lost weight

I am not willing to take that step. Likewise, I

think that progesterone or the progestins are

dicey for women with a history of breast cancer

-- minimally the issues of inflammation and of

VEGF and angiogenesis stimulation should be resolved.

At 06:04 PM 5/29/2010, you wrote:

>

>Please cite your sources.

>

>Thanks so much.

>Lynne

>

>

>In a message dated 5/29/2010 8:54:23 P.M. Eastern Daylight Time,

><mailto:vgammill%40adelphia.net>vgammill@... writes:

>

>Enough research has been done on progesterone and

>breast cancer to warrant high caution.

[Guest guest]

excuse my ignorance, but I think that hormones come from

mare urine.....how is natural progesterone made ?

this is very important topic for women...

karla

>

> , it appears that most of these abstracts used progestin. You know

that's not a bioidentical or natural replacement. Do you have the same type of

data for natural progesterone? Progestin and progesterone are not the same

thing, regardless of what the drs say.

>

> xoo

>

>

[Guest guest]

Karla, the stuff made from mare urine is Premarin, an estrogen replacement

xoo

> >

> > , it appears that most of these abstracts used progestin. You know

that's not a bioidentical or natural replacement. Do you have the same type of

data for natural progesterone? Progestin and progesterone are not the same

thing, regardless of what the drs say.

> >

> > xoo

> >

> >

>

[Guest guest]

>

> Karla, the stuff made from mare urine is Premarin, an estrogen replacement

>

> xoo

>

>

One more step to clarify this subject: Premarin is made from PREGNANT MARE

URINE, hence it's name Pre-Mar-In...

During pregnancy, female animals get their estrogen kicked up to a high degree.

So Big Pharma got smart, they decided to strap the poor pregnant horses in a

stable attached to a tube that collects it's urine all day, then they process

the estrogen out of the sample. There are several hormones in horse urine, none

of which is identical to human estrogen, and several which the human body can't

use. But one is close enough to help with our hot flashes so they slip it to us

as something resembling natural hormones. Needless to say the horse lovers of

the world are absolutely sick about this cruel treatment and protest constantly

to deaf ears.

Contrary to this, bio-identical hormones are made identical to the ones the body

uses. Haven't any of you read Sommers' books? First you need to read Dr.

Lee's books, then 's. That will tell it all,.

Incidentally, Dr. Lee, many years ago, warned women NOT to take Fosomax for

osteoporosis... explaining that it worked by interfereing with the body's bone

replacement process... and if you don't remove old bone you don't make holes in

your bones. Instead you just keep the old bone that after 4 or 5 years begins

to deteriorate. But Sally Fields is correct, Boniva did reduce bone loss as she

gleefully says on TV... she didn't reduce the bad bone at all. Neither did she

replace the bad bone with new bone. The pharma companies stopped testing the

bones in their studies after 4 years. Just when the weakenss begins to show up.

Dr. Lee knew all about this ten years ago. Get his book... all you women... for

sooner or later you are going to start with the night sweats and call for

to tell you what to do. Be prepred. For both natural estrogen and

progesterone... and toss in a little testosterone to improve your libido and

keep your man happy while you're at it.

Marji

[Guest guest]

>

> Greetings,

>

> And sometimes the night sweats come back, after you think you are all

> done. Do you have any information on the bio-identical harmones, as to

> drug reactions. I have major reactions to almost everything, herbs,

> supplements, and pharma drugs. So far I have managed my health by whole

> foods, but it is not working well right now.

>

>

I have been told that the reason the hot flashes come back is not due to hormone

deficiency itself, but hormone imbalance including other than the sex hormones.

The idea, also advanced by acupuncture authorities, is that the liver has become

" congested, sluggish, toxic " pick your adjective... and accounts for the

imbalance. I don't know the science of all this, but if the liver is involved

in the hot flashes problem it probably is involved in why you can't process

other herbs and things. The liver just won't break things down correctly so

there may be residual toxicity.

Note, this is not a scientific description... just my colorful way of picturing

what may be going on.

Marji