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N Engl J Med 2012; 367:1998-2005
Effect of Three Decades of Screening Mammography on Breast-Cancer Incidence

Altern Ther Health Med. 2017 Nov;23(6):24-32.
In Defense of Progesterone: A Review of the Literature

CANCERactive 17 April 2022
Progesterone - The Natural Protector

Cancer Research UK Tuesday 17 January 2012
Researchers defend HRT breast cancer study

Emory University, Woodruff Health Sciences Jul. 13, 2011
Progesterone Inhibits Growth of Neuroblastoma Cancer Cells

MOL MED 17(9-10)1084-1094, SEPTEMBER-OCTOBER 2011
Progesterone Inhibits the Growth of Human Neuroblastoma: In Vitro and In Vivo Evidence

Hematology. 2011 Sep;16(5):278-83.
Serum 25-hydroxyvitamin D levels are associated with prognosis in hematological malignancies

CANCERactive 2010
DO SCREENING MAMMOGRAMS INCREASE THE RISK OF BREAST CANCER?

Natural News Monday, January 11, 2010
The Data Behind the New Mammogram Recommendations - Explained

Molecular Endocrinology 2008, 22 (8): 1812-1824
Progesterone Receptor Inhibits Aromatase and Inflammatory Response Pathways in Breast Cancer Cells via Ligand-Dependent and Ligand-Independent Mechanisms

Arch Intern Med. 2008;168(21):2311-2316
The Natural History of Invasive Breast Cancers Detected by Screening Mammography

Medscape February 29, 2008
Hormone Therapy Compromises Mammograms and Breast Biopsies

Medscape March 29, 2007
MRI Detects Breast Cancer Missed by Mammography

Cancer Epidemiol Biomarkers Prev May 2006 15; 967
The Association of Plasma DHEA and DHEA Sulfate with Breast Cancer Risk in Predominantly Premenopausal Women

CANCERactive 2005
Thermography: The Secret Weapon In Breast Cancer Detection?

The Lancet, Volume 365, Issue 9453, Pages 7 - 8, 1 January 2005
False-positive mammogramscan the USA learn from Europe?

BMJ 2003; 327 : 101
Women need better information about routine mammography

JNCI J Natl Cancer Inst (2000) 92 (20): 1657-1666
Predicting the Cumulative Risk of False-Positive Mammograms

Am. J. Epidemiol. (1981) 114 (2): 209-217
BREAST CANCER INCIDENCE IN WOMEN WITH A HISTORY OF PROGESTERONE DEFICIENCY

Fox Chase Cancer Center April 3, 2012
Scientists at Fox Chase Discover Link between Estrogen and Tobacco Smoke

Arch Intern Med. 2008;168(21):2311-2316.
The Natural History of Invasive Breast Cancers Detected by Screening Mammography

BMJ 2019;367:l5928
HRT and breast cancer risk - progesterone vs. progestins

Cancer Epidemiology Biomarkers & Prevention
17, 614-620, March 1, 2008. Published Online First March 6, 2008;

Reproductive Steroid Hormones and Recurrence-Free Survival in Women with a History of Breast Cancer

British Journal of Nutrition
April 2008, Volume 99, Issue 04, pp 723-731

"Trans-fatty acids induce pro-inflammatory responses and endothelial cell dysfunction"

Diabetes Care 30:561-567, 2007
Prospective Study of Hyperglycemia and Cancer Risk

J. Biol. Chem, March 12, 2007 10.1074/jbc.M611370200
Epinephrine protects cancer cells from apoptosis via activation of PKA and BAD phosphorylation

Breast Cancer Research and Treatment
Volume 101, Number 2, January 2007 , pp. 125-134(10)

Effects of estradiol with micronized progesterone or medroxyprogesterone acetate on risk markers for breast cancer in postmenopausal monkeys

Eur Urol, 2006 Nov; 50(5):935-9.
Testosterone and Prostate Cancer

Cancer Research 65, 54-65, January 1, 2005
Xenoestrogen Action in Prostate Cancer: Pleiotropic Effects Dependent on Androgen Receptor Status

Reproductive Sciences, Vol. 12, No. 4, 285-292 (2005)
Progesterone-Induced Inhibition of Growth and Differential Regulation of Gene Expression in PRA- and/or PRB-Expressing Endometrial Cancer Cell Lines

JNCI Journal of the National Cancer Institute 2005 97(10):755-765
Serum Sex Steroids in Premenopausal Women and Breast Cancer Risk Within the European Prospective Investigation into Cancer and Nutrition

Journal of Steroid Biochemistry & Molecular Biology 97 (2005) 441-450
Pregnancy, progesterone and progestins in relation to breast cancer risk

BIOLOGY OF REPRODUCTION 73, 586–590 (2005)
Carcinogenic Potential of Ovulatory Genotoxicity

JAMA. 2004;291:1701-1712, 1769-1771
Effects of Conjugated Equine Estrogen in Postmenopausal Women With Hysterectomy

International Journal of Cancer Volume 114, Issue 3 , Pages 448 - 454
Breast cancer risk in relation to different types of hormone replacement therapy in the E3N-EPIC cohort

J Endocrinol. 2003 Oct;179(1):55-62.
'Overexpression of wild-type p53 gene renders MCF-7 breast cancer cells more sensitive to the antiproliferative effect of progesterone.'

Oncogene. 2003 Oct 9;22(44):6883-90.
'Progesterone-induced apoptosis in immortalized normal and malignant human ovarian surface epithelial cells involves enhanced expression of FasL'.

BMJ Publishing Group Ltd 2003
'Women need better information about routine mammography'

JNCI J Natl Cancer Inst (2002) 94 (8): 606-616
Endogenous Sex Hormones and Breast Cancer in Postmenopausal Women: Reanalysis of Nine Prospective Studies

Clinical Chimica Acta, 2002; vol. 322: 21-8
'Hyperhomocysteinemia is a risk factor for cancer and a new potential tumour marker'

Cancer. 2002 Mar 15;94(6):1867-75
'An estimate of premature cancer mortality in the U.S. due to inadequate doses of solar ultraviolet-B' radiation.'

Clinical Cancer Research September 2001 7; 2880
Effect of Progesterone on the Invasive Properties and Tumor Growth of Progesterone Receptor-transfected Breast Cancer Cells MDA-MB-23

J Cell Biochem. 2001;82(3):445-51.
'Apoptosis induced by progesterone in human ovarian cancer cell line SNU-840.'

Anticancer Res. 2001 Nov-Dec;21(6A):3871-4.
'Progesterone induces apoptosis in malignant mesothelioma cells.'

Int J Oncol. 2001 Jul;19(1):31-8.
Steroid receptors and hormones in relation to cell proliferation and apoptosis in poorly differentiated epithelial ovarian tumors.

Kim JJ, Chapman-Davis E. Semin Reprod Med. 2010;28(1):81–90. doi:10.1055/s-0029-1242998
Role of Progesterone in Endometrial Cancer

Molecular and Cellular Biochemistry
Volume 202, Numbers 1-2 / December, 1999 Pages 53-61

Bcl-2, survivin and variant CD44 v7-v10 are downregulated and p53 is upregulated in breast cancer cells by progesterone: Inhibition of cell growth and induction of apoptosis

Journal of the National Cancer Institute, 1998, Vol. 90: 1774-86, No. 23,
Hormonal Etiology of Epithelial Ovarian Cancer, With a Hypothesis Concerning the Role of Androgens and Progesterone

Ann Clin Lab Sci. 1998 Nov-Dec;28(6):360-9.,
'Progesterone inhibits growth and induces apoptosis in breast cancer cells: inverse effects on Bcl-2 and p53.'

Cancer. 1997 May 15;79(10):1944-50.,
'Progesterone induces apoptosis and up-regulation of p53 expression in human ovarian carcinoma cell lines.'

Breast Cancer Res. 2002;4(2):70–76. doi:10.1186/bcr426
The p53 pathway in breast cancer.

J Am Diet Assoc. 1995 Jun; 95(6):693-7.
'Implementing a ketogenic diet based on medium-chain triglyceride oil in pediatric patients with cancer.'

J Am Coll Nutr. 1995 Apri14(2):202-8.
'Effects of a ketogenic diet on tumor metabolism and nutritional status in pediatric oncology patients: two case reports.'

New England Journal of Medicine 332:1589-1593 June 15, 1995 Number 24
'The Use of Estrogens and Progestins and the Risk of Breast Cancer in Postmenopausal Women'

Web sites

canceractive.com
mercola.com

Research papers...

Hormonal Etiology of Epithelial Ovarian Cancer, With a
Hypothesis Concerning the Role of Androgens and
Progesterone

Harvey A. Risch

"Progesterone
Evidence for a possible protective role of progesterone in the etiology of ovarian cancer starts with consideration of the increased sex hormone activity during pregnancy. Over the first month of pregnancy, maternal LH and FSH decline strongly with the increase in trophoblast hCG (162). The hCG also stimulates the corpus luteum to continue producing progesterone and not regress (102). After the seventh week, the luteal-placental shift occurs in which the functional capacity of the corpus luteum of pregnancy drops, while the massive placental production of progesterone during pregnancy begins (102). In addition, the placenta extracts maternal (and later, fetal) adrenal androgens, which remain at stable maternal serum concentrations while both production and utilization rates increase; maternal serum estrone and estradiol are made from the adrenal androgens (102). During pregnancy, the placental synthesis thus causes 10-fold increases in maternal circulating progesterone levels (102). Maternal testosterone and androstenedione levels increase some twofold to threefold, although most of the testosterone is bound to the pregnancy-induced higher levels of sex hormonebinding globulin, preventing virilization of female fetuses (102). These maternal ovarian androgens are in any case dwarfed by the huge estrogen and progesterone concentrations. In terms of the pathogenesis of ovarian cancer, we suggest that the additional protective aspect of pregnancy not mediated through suppression of ovulation may be due to the 8–9 months of elevated progesterone. As we have noted, it seems unlikely to be due to the pregnancy estrogens, since most of the evidence relating estrogens to risk of ovarian cancer (as well as to endometrial cancer and perhaps breast cancer) points either to no effect or to increase in risk."

2. Journal of Steroid Biochemistry & Molecular Biology 97 (2005) 441–450
Pregnancy, progesterone and progestins in relation to breast cancer risk.
Carlo Campagnoli, Chiara Abba, Simona Ambroggio, Clementina Peris

Abstract
In the last two decades the prevailing opinion, supported by the “estrogen augmented by progesterone” hypothesis, has been that progesterone contributes to the development of breast cancer (BC). Support for this opinion was provided by the finding that some synthetic progestins, when added to estrogen in hormone replacement therapy (HRT) for menopausal complaints, increase the BC risk more than estrogen alone. However, recent findings suggest that both the production of progesterone during pregnancy and the progesterone endogenously produced or exogenously administered outside pregnancy, does not increase BC risk, and could even be protective. The increased BC risk found with the addition of synthetic progestins to estrogen in HRT seems in all likehood due to the fact that these progestins (medroxyprogesterone acetate and 19-nortestosterone-derivatives) are endowed with some non-progesterone-like effects which can potentiate the proliferative action of estrogens. The use of progestational agents in pregnancy, for example to prevent preterm birth, does not cause concern in relation to BC risk."
Conclusion
Available data suggest that progesterone produced during pregnancy does not have deleterious effects on BC risk; conversely, it could have a predominant role in the long term protective effect against BC shown by full-term pregnancies. Even outside pregnancy, the balance of the in vivo evidence is that progesterone does not have a cancer-promoting effect on breast tissue. The greater BC risk related to the use of HRT preparations containing estrogen and synthetic progestins seems in all likelihood to be due to the fact that many of the progestins used have several nonprogesterone like actions that potentiate the proliferative effect of estrogens on breast tissue and estrogen-sensitive cancer cells. Particularly relevant seem to be the metabolic and hepatocellular effects (decreased insulin sensitivity, increased levels and activity of IGF-I, and decreased levels of SHBG), which oppose the opposite effects induced by oral estrogen. The use of progestational agents in pregnancy, e.g. to prevent preterm birth [107,108], does not cause concern in relation to BC risk. On the contrary, progestational agents could even be protective, especially when they succeed in avoiding preterm delivery, a well documented risk factor for the subsequent development of BC"

3. Int J Oncol. 2001 Jul;19(1):31-8.
Steroid receptors and hormones in relation to cell proliferation and apoptosis in poorly differentiated epithelial ovarian tumors.
Lindgren P ,Bäckström T ,Mählck CG ,Ridderheim M ,Cajander S .
Department of Obstetrics and Gynecology, Umeå University, Umeå, Sweden

4. Cancer Volume 83, Issue 1 , Pages 111 - 121
Published Online: 9 Nov 2000
Copyright © 1998 American Cancer Society
Progesterone therapy for endometrial carcinoma reduces cell proliferation but does not alter apoptosis
Makoto Saegusa, M.D. *, Isao Okayasu, M.D.
Department of Pathology, Kitasato University School of Medicine, Kanagawa, Japan

5. Reproductive Sciences, Vol. 12, No. 4, 285-292 (2005)
Progesterone-Induced Inhibition of Growth and Differential Regulation of Gene Expression in PRA- and/or PRB-Expressing Endometrial Cancer Cell Lines
Ellen Smid-Koopman, MD, PhD
Liesbeth C. M. Kuhne
Eline E. Hanekamp, PhD
Susanne C.J.P. Gielen, MD
Petra E. De Ruiter, BSc
J. Anton Grootegoed, PhD
Theo J.M. Helmerhorst, MD, PhD
Curt W. Burger, MD, PhD
Albert O. Brinkmann, PhD
Frans J. Huikeshoven, MD, PhD
Departments of Obstetncs and Gynecology, and Reproduction and Development, Erasmus Medical Center, Rotterdam; Department of Obstetncs and Gynecology, Ruwaard van Putten Hospital, Spijkemsse, The Netherlands

6. Source: Breast Cancer Research and Treatment , Volume 101, Number 2, January 2007 , pp. 125-134(10)
Effects of estradiol with micronized progesterone or medroxyprogesterone acetate on risk markers for breast cancer in postmenopausal monkeys
Authors: Wood, Charles 1; Register, Thomas; Lees, Cynthia; Chen, Haiying; Kimrey, Sabrina; Mark Cline, J.

7. International Journal of Cancer
Volume 114, Issue 3 , Pages 448 - 454
Published Online: 18 Nov 2004
Breast cancer risk in relation to different types of hormone replacement therapy in the E3N-EPIC cohort
Agnès Fournier 1, Franco Berrino 3, Elio Riboli 2, Valérie Avenel 1, Françoise Clavel-Chapelon 1*
1Equipe E3N, Institut National de la Santé et de la Recherche Médicale (INSERM), Villejuif, France
2Unit of Nutrition and Cancer, International Agency for Research on Cancer (IARC-WHO), Lyon, France
3Department of Preventive and Predictive Medicine, Istituto Nazionale Tumori, Milan, Italy

8. Brigham and Women's Hospital, Harvard Medical School
News

Press Release - Jun 11, 2008

Low Melatonin Associated with Increased Risk of Breast Cancer in Postmenopausal Women

Researchers from Brigham and Women's Hospital have shown in a new study that low melatonin levels are associated with an increased risk of breast cancer in postmenopausal women. This research is published in the June 11, 2008 issue of the Journal of the National Cancer Institute._Melatonin is primarily secreted during the dark hours of a light-dark cycle and has been shown to be low in some night workers. Previous research has found that low melatonin levels in premenopausal women are associated with an increased risk of breast cancer.

Schernhammer and colleagues compared melatonin levels in 178 postmenopausal women and 710 matched controls. All of the women were enrolled in the Hormones and Diet in the Etiology of Breast Cancer Risk study. Researchers report that women with the lowest levels of melatonin had a significantly higher incidence of breast cancer than those with the highest levels.

“Further studies are needed to confirm these data and investigate the mechanisms that underlie the association between melatonin levels and breast cancer risk,” concluded Schernhammer.

This research was funded through a grant from the Department of Defense.

Brigham and Women's Hospital is a 747-bed nonprofit teaching affiliate of Harvard Medical School and a founding member of Partners HealthCare, an integrated health care delivery network. BWH is committed to excellence in patient care with expertise in virtually every specialty of medicine and surgery. BWH is an international leader in basic, clinical and translational research on human diseases, involving more than 860 physician-investigators and renowned biomedical scientists and faculty supported by more than $416 M in funding. BWH is also home to major landmark epidemiologic population studies, including the Nurses' and Physicians' Health Studies and the Women's Health Initiative.

How to best absorb progesterone

A good skin cream (such as Natpro) is the most user friendly of all the ways progesterone can be taken. Oral progesterone is a waste as 80-90% is destroyed in the digestive system and liver. Injections are inconvenient and painful. Buccal drops or pills are very bitter and suppositories are not much fun!

The cream can be applied anywhere... in the vagina or nose for dryness, on piles or painful, achy or itchy areas. Its the best thing for burns and wonderful on the face and elsewhere.

All the successful studies done on progesterone use between 100mg to 200mg per day. This equates to 3ml to 6ml of Natpro per day. Some authorities suggest as high as 400-600mg/day. Orally administered forms need 5 to 10 times as much to compensate for the digestive losses. The cream is best applied twice a day, to keep levels up.



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