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The following article was not written by Dr. Lee, but is drawn from information that he presented in his lectures. To learn more about hormones and breast cancer, read Dr. Lee’s book, What Your Doctor May Not Tell You About Breast Cancer.
Breast cancer is considered to be a hormone dependent cancer, which means that hormones have something to do with the growth and development of breast cancer. About two years ago, Time magazine had an article referring to apoptosis in reference to looking for something that would work against cancer. In the 1/28/98 issue of the Journal of the American Medical Association (JAMA), there was a reference to apoptosis in reference to cancer.
Almost all the cells in your body are being created, live a certain length of time, and then die to make place for the new cells coming along. White blood cells last only two days. Red blood cells last 120 days. Your skin cells are being made new all the time. They are the ones that flake off when you take a bath and make a ring in your tub. If you've had your arm in a cast for 6 weeks, when you take the cast off you can flake off a lot of old, dead cells. They die on their own. It is a planned cell suicide. They are designed to do this because the new cells are coming.
What has been discovered is that the cells that become cancer cells are not only those that are multiplying rapidly, because the white blood cells multiply rapidly, and they don't become cancer cells. It's the ones that don't die on time; they don't go through this programmed cell suicide. Programmed cell suicide is called apoptosis. It means “without dropping away.” Ptosis means “dropping.” If you have one eyelid that won't go up; that's called ptosis. The dropping away refers to the programmed cell suicide.
Research has looked into what it is that makes a cell do this. It is not told to by some other cell. It is built into the DNA of the genes of that cell. It's designed that way. It turns out that there's a gene that will block apoptosis and try to get the cell to live longer. That gene is called BCL2. It leads to the cell becoming a cancer cell.
The cancer cell doesn't think of itself as a bad cell. It thinks of itself as a cell that outsmarted you, and it is going to live on. You might die, but it is going to try to live on. But the gene that normally functions to cause that cell to commit programmed cell suicide is the gene called P53.
In the 1/28/98 issue of the Journal of the American Medical Association (JAMA) is an article entitled “To Die or Not to Die.” They are not talking about your life, though they well could be. They are talking about the cell and what controls and determines if it dies on time as it ought to. They refer to gene P53 as the gene that tells the cell to die on time, and BCL2 is the gene that blocks this. So if BCL2 is the dominant one you'll develop cancer. If P53 is the dominant one you won't.
Inside your breast you have skin cells that line the milk ducts. You have miles of milk ducts in your breasts. These cells are like skin cells. They are being made; then they are supposed to die, and the specialized blood cells (macrophages) go and eat them up, because new cells are coming along all the time. Imagine that they didn't die on time, and your breast just retained all these cells that are being made all the time. Pretty soon your breasts would be dragging on the ground. The only way you keep normal size breasts is to have last month's cells die, because this month new cells are coming along. This doesn't happen to brain cells or muscle cells, but in all the other cells in your body this goes on all the time. What keeps you young and healthy is the new cells coming along.
What they are admitting in the JAMA article is that the war on cancer has been a failure. The war on cancer has been trying to find medicine that stops rapidly growing cells from multiplying so rapidly, but in the process they are stopping your own white blood cells, your hair follicles and everything else. So if they give you a medicine strong enough to kill the cancer cells, they are in the process killing you. They admit that chemotherapy is a failure, except for some leukemias and lymphomas in young children. Young children that have a real strong immune system will survive the chemotherapy and come back. But for those of us who are adults, the chemotherapy strong enough to kill the cancer would have to be strong enough to kill us first. So now, the new treatment goal is how to control apoptosis to bring on cell death of the cancer cells. “New cancer therapies that aim to induce apoptosis, specifically in cancer cells and cells becoming cancer, are the source of much excitement and renewed hope for cure.” You can cure cancer if you can control apoptosis.
Last year Dr. Ben Formby and Dr. T.S. Wiley at the University of California in Santa Barbara proved how to do that very thing. Dr. Ben Formby is from Copenhagen, Denmark. He is a molecular biologist who has learned how to build cell cultures, and how to tell the products of specific genes like BCL2 and P53. So he took the cell cultures of breast, endometrium, ovary and prostate, and he grew them in culture. On some he added a little estrogen (estradiol). Guess what happened? The estradiol turned on BCL2, and the cells grew rapidly and didn't die. Then he added some progesterone to it. Guess what happened? They stopped growing so rapidly; they died on time, and the cancer all disappeared. He did that for all these types of cancer.
What do we have? The gene BCL2 stimulates the risk of cancer. Gene P53 decreases the risk of cancer. Estradiol upregulates BCL2. Progesterone upregulates P53. Therefore, progesterone decreases cancer. Unopposed estradiol causes the cancer. Simple. Estrogen dominance is the cause of the cancer growing and the inability of the body to cure it.
Progesterone and Estrogen Functions in Breast Cancer Supported by Major Medical Journals
The critics are saying that they don't see anything about this in the medical journals that they read. Maybe they aren't reading the correct journals. There are 12 references to tests on BCL2 and P53, and the difference between progesterone and estrogen. Here are some of the places these articles have occurred:
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