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Breast Cancer and Natural Progesterone

On This Web Page:
PROGESTERONE DECREASES CELL PROLIFERATION
NATIONAL CANCER INSTITUTE'S SYMPOSIUM ON ESTROGEN AS A- MAJOR CAUSE OF CANCER

Progesterone Decreases Cell Proliferation: Estrogen Increases It
If You Want To Increase Cell Proliferation Use Estrogen If You Want To Decrease Cell Proliferation Use Progesterone
Progesterone Levels At Time of Breast Cancer Surgery Affect Survival Rates
Method of Measuring Cell Proliferation
Progesterone Levels at the Time of Surgery
Estrogen a Major Cause of Cancer
National Cancer Institute's Symposium on Estrogen
Estrogens as Endogenous Carcinogens in the Breast and Prostate

Progesterone Decreases Cell Proliferation: Estrogen Increases It

The Fertility and Sterility Journal article was particularly interesting, as it was the first double blind, placebo controlled, randomized study using transdermal progesterone and transdermal estrogen (estradiol) on real women (40 of them) who were having breast biopsies. They had one at the beginning of the study and another biopsy 13 days later, and were able to check on several interesting things.

The first thing of note was that even though the estrogen and the progesterone did not show up in the serum, it showed up in the breast tissue at over 100% increased levels above the placebo cream.

The most interesting finding was what happened to cell proliferation during this 13 day test. The following chart shows two ways of measuring cell proliferation. The PCNA (proliferating cell nuclear antigen) is the most accurate, but both methods were used.

Based on PCNA numbers (these tend to be the most accurate measurement) the numbers in the above chart showing increase or decrease of cell proliferation showed up in only 13 days. Translated into percentages the following 3 sentences summarize it.

Method of Measuring cell Proliferation	Placebo	Progesterone	Estrogen	Estrogen & Progesterone
Mitosis per 1000 Cells	0.51	0.17	0.83	0.52
PCNA	7.8	1.9	17.4	6.5

Topical Progesterone reduced cell proliferation by 410%
Topical Estrogen increased cell proliferation by 223%
Topical Estrogen/Progesterone combination reduced cell proliferation by 16%

The numbers on this chart were excerpted from the Fertility and Sterility Journal, Vol. 63, No. 4, April, 1995. The exact reference is: Chang KJ, Lee TTY , Linares-Cruz G, Fournier S, de Lignieres B. Influences of percutaneous administration of estradiol on human breast epithelial cell cycle in vivo. Fertility and Sterility 1995; 63; 7865-7891.

If You Want To Increase Cell Proliferation Use Estrogen If You Want To Decrease Cell Proliferation Use Progesterone

The conclusion seems to be: if you want increased cell proliferation use estrogen. If you want decreased cell proliferation use progesterone. The entire study is worth reading, and is an excellent affirmation that what Dr. John Lee has been saying and writing is correct. This is not secret information, but it is being denied to the typical doctor of conventional medicine, even though similar information is in the AMA journal.

It is Dr. John Lee's contention that progesterone prevents breast cancer, and if you already have breast cancer progesterone protects you against reoccurrence or late metastases. In his medical practice he treated many women who had had mastectomies. In the 20 years since he started recommending the use of progesterone, not one of the hundreds of women he treated has died of breast cancer. Think about what the odds are on that number when you compare it to normal post mastectomy figures.

Progesterone Levels At Time of Breast Cancer Surgery
Affect Survival Rates

In 1976 Dr. Mohr started a test at two major hospitals in London that did breast surgery. He requested that every time they had a breast surgery that they take a blood test and save it so that he could test the progesterone level at the time of surgery. He tested testosterone, progesterone and estrogen. He found that progesterone level at the time of surgery was correlated with better survival. The survival record was reviewed 18 years after breast cancer surgery in node positive patients: this means that the cancer had already spread, was already metastasizing.

Summary of Dr. Mohr's findings

Progesterone Level at The Time of Surgery	Survival percentage after 18 year
Adequate Progesterone (4ng/ml or more)	62%
Low Progesterone (less than 4 ng/ml)	30%

This was written up in the British Journal of Cancer in 1996. The title of the article is: “Serum Progesterone and Prognosis in Operable Breast Cancer.” This is over a 100% improvement just by having adequate progesterone level at the time of surgery. There is no treatment that provides that degree of benefits. Progesterone is the treatment.

Estrogen a Major Cause of Cancer

Dr. Ercole Cavalieri, the head of cancer research at the University of Nebraska Medical Center (also one of the speakers at the NCI program shown below). He calls estrogen the angel of life, the angel of death. It is necessary at the beginning to create a successful pregnancy, and if you have estrogen dominance later in your life it is the angel of death. When the body tries to metabolize estradiol and estrone it is possible to end up in this pathway which ends up in cancer. This is real human estrogen, and the body is trying to get rid of it. If the body does it correctly it methylates it, and it is safely excreted. But if the person has been eating margarine or transfatty acids, things that are not real and are missing the essential fatty acids it falls into another pathway. If the same person is not getting the sulfated amino acids like methionine and cysteine that is in garlic and beans, it continues on in this pathway and binds to DNA, causes a mutation, and creates cancer and kills the person.

National Cancer Institute's Symposium on Estrogen as a Cause of Cancer

Estrogen is the cause of the cancer that women fear, and yet there are many doctors still giving them unopposed estrogen. The recent National Cancer Institute symposium March 16-17, 1998 basically states that estrogen is the cause of the cancer that is killing women. If you look at the following program to see some of the major medical research organizations stating this in their presentations, it sort of make you wonder why we didn't hear any of this on the news in any of the major media. It makes you wonder why unopposed estrogen is still being so widely used. Look at the following program:

Estrogens as Endogenous Carcinogens in the Breast and Prostate

This symposium has been planned to explore the role of endogenous estrogens in the etiology of human breast and prostate cancer. An international group of scientists will share viewpoints and construct a more holistic understanding of the way estrogens induce cancer. Topics will include metabolic activations of estrogens to carcinogenic forms, deactivation of carcinogenic metabolites, and the role of estrogen receptor-mediated processes in tumor induction. One of the goals of this symposium is to provide the attendees with an overview of the direction of research on estrogen-induced cancer. Another goal is to identify biomarkers that can be useful in studies of cancer risk among humans and in the future development of preventive strategies. The overview of the role of estrogens in cancer obtained from this symposium will be useful for scientists engaged in a variety of cancer-related studies, as well as for epidemiologists, health planners, journalists and members of advocacy groups for breast and other human cancers.

The Program

Welcoming Remarks

Dr. David Longfellow
Chemical and Physical Carcinogenesis Branch
Division of Cancer Biology, NCI

Overview of Estrogens as Endogenous Carcinogens Introduction and Remarks
Co-Chairs:

Dr. David Longfellow
Dr. Richard Santen, University of Virginia Health Science Center

Cellular and Molecular Interactions in Breast Cancer: Role of Estrogen and Its Receptors
Dr. Joe Russo, Fox Chase Cancer Center

Endogenous Estrogens as Carcinogens Through Metabolic Activity
Dr. James Yager, The Johns Hopkins University

Estrogens as Endogenous Genotoxic Agents: DNA Adducts and Mutations Remarks:
Dr. Joachim Liehr, Stehlin Foundation for Cancer Research
Dr. Ercole Cavalieri, University of Nebraska Medical Center

Catechol Estrogen -3,4-Quinones and Apurinic Sites in Cancer Initiation
Dr. Ercole Cavalieri, University of Nebraska Medical Center

Endogenous Oxidants and DNA Damage
Dr. Krystyna Frenkel, New York University Medical Center

Estrogen-induced Gene Mutations
Dr. Deodutta Roy, University of Alabama at Birmingham

Tissue-Specific Synthesis and Oxidative Metabolism of Estrogens
Co-Chairs:

Dr. James Yager Dr. Colin Jefcoate, University of Wisconsin-Madison

Estrogen Formation by Aromatase in Breast Tissue
Dr. Richard Santen Metabolic Activation of Estrogens by 4-Hydroxylation
Dr. Joachim Liehr

Estrogen 4-Hydroxylation by Cytochrome P4501B1
Dr. Thomas Sutter, The Johns Hopkins University

Estrogen Metabolism by Conjugation
Co-Chairs:

Dr. Richard Weinshilboum, Mayo Medical School
Dr. Julius Axelrod, National Institute of Mental Health, Emeritus

Methylation of Catechol Estrogens by Catechol-O-methyltransferase (COMT)
Dr. Cyrus Creveling, National Institute of Diabetes and Digestive and Kidney Diseases

COMT Genetic Polymorphism and Breast Cancer
Dr. Patricia Thompson, National Center for Toxicological Research, FDA

COMT, CYP17, SRD5A Polymorphisms in Breast and Prostate Cancer
Dr. Douglas Bell, National Institute of Environmental Health Sciences

Estrogen Receptor-Mediated Processes in Normal and Cancer Cells
Co-Chairs:

Dr. George Stancel, University of Texas Medical School
Dr. Robert Dickson, Lombardi Cancer Center Dissection of the ER Signaling Pathway: Insights into the Mechanism of Tamoxifen Resistance
Dr. Donald McDonnell, Duke University Medical Center

Investigating the Role of ER-Alpha in Carcinogenesis Through the Use of Transgenic Mouse Models with Altered Levels of Receptor Expression
Dr. John Couse, National Institute of Environmental Health Sciences

Structure and Function of Estrogen Receptor-Beta
Dr. Jan-Ake Gustafsson, Karolinska Institute

Estrogen Receptor Structure, Modulators, and Targets in Hormone Responsive Tissues and Cancers
Dr. Geoffry Green, University of Chicago

Regulation of the Cell Cycle and Cell Death in Mammary Cancer
Dr. Robert Dickson

Estrogens and Cancer in Human Populations
Co-Chairs:

Dr. Louise Brinton, Environmental Epidemiology Branch Division of Cancer Epidemiology and Genetics, NCI
Dr. Shukmei Ho, Tufts University

Estrogen Levels and Breast Cancer Risk
Dr. Paolo Toniolo, New York University School of Medicine

Study Design Considerations in the Assessment of Cancer Risk in Relation to Genetic Polymorphisms
Dr. Montserrat Garcia-Closas, Environmental Epidemiology Branch, DCEG, NCI

Estrogens and Estrogen Metabolites: Technical Hurdles in Population Studies
Dr. Susan Hankinson, Brigham and Women's Hospital

DNA Biomarkers for Predicting Human Breast, Ovarian, and Prostate Cancer
Dr. Donald Malins, Pacific Northwest Research Foundation

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