We now come face to face with what is perhaps the most important question that directly affects the relationship between the two medical terms, hormone therapy and breast cancer. The relationship is simply that the concept hormone therapy is applied for the treatment of breast cancer which has been successfully performed for millions of people especially women who have suffered from this insidious disease. You’d learn even more about this unique relationship if you continue reading.
A brief description of hormones
Hormones can be described as substances that exist in the body which act as chemical messengers.
They can directly affect the actions of cells as well as tissues located at various places in the body, after they reach their targets as they travel in the bloodstream.
You should know that the hormones estrogen and progesteroneare continuously produced by the ovaries in premenopausal women.
They are also produced by some other tissues found in your body such as fat and skin, in both premenopausal and postmenopausal women and also men.
What estrogen does is it develops and maintains the unique female sexual traits and it also helps long bones in the body to flourish.
For its part, the hormone progesterone plays out its role in the monthly menstrual cycle in women and pregnancy.
Both hormones also encourage the growth of some breast cancers which are labeled hormone-sensitive (or hormone dependent) breast cancers.
The hormone-sensitive breast cancers also contain proteins called hormone receptors(estrogen receptors or ERs as well as progesterone receptors, or PRs which are activated when hormones bind to them.
The active receptors can cause changes in certain genes which in turn can stimulate cell growth.
To find out whether or not hormone receptors are present in breast cancer cells, doctors test samples of tumor tissue removed by surgery.
If the tumor tissue contains estrogen receptors, the cancer is labeled as estrogen receptor positive (ER positive), estrogen sensitive, or estrogen responsive.
If the tumor tissue contain progesterone receptors, the cancer is called progesterone receptor positive (PR or PgR positive).
Sometimes, tumors in the breast that contain estrogen and/or progesterone receptors are called hormone receptor positive (HR positive). Most ER positive breast cancers are also PR positive.
You should note that breast cancers that are lacking in ERs are termed ER negative, and if they don’t have both ER and PR can be called HR negative.
It’s medically known that about 67% ‒ 80% of breast cancers in women are ER positive. In men, about 90% of breast cancers are ER positive about 80% are PR positive.
The nature of hormone therapy
Hormone therapy can also be referred to as hormonal therapy, endocrine therapy or hormone treatment.
Its function is to impede the growth of hormone-sensitive tumors by blocking the ability of the body of producing hormones or by directly interfering with the effects of hormones on breast cancer cells.
All hormones that are not sensitive to hormones lack the hormone receptors and are not responsive to hormone therapy.
You should note that hormone therapy is not the same as menopausal hormone therapy (MHT), which is a treatment with estrogen alone or combined with progesterone that helps in relieving menopausal symptoms.
The difference between the two hormone therapies produce opposite effects for the following reasons:
- Hormone therapy for breast cancer blocks the growth of HR – positive breast cancer, whereas
- MGT is able to stimulate the growth of HR – positive breast cancer.
It’s for this reason that when a woman treated for MHT is diagnosed with HR – positive breast cancer, she is usually asked to end the therapy.
Types of hormone therapy used for breast cancer
Hormone – sensitive breast cancer can be treated in several ways:
Blocking of ovarian function – the ovaries are the main source of estrogen in premenopausal women. For this reason, it’s possible to reduce the levels of estrogen in these women by reducing the function of the ovaries.
This blocking of the ovarian function is called ovarian oblationand it can be done through the removal of the ovaries by a surgical operation called oophorectomy or an alternative treatment by radiation. In most known case, the result of ovarian oblation is usually permanent.
Ovarian function can also be suppressed by drug treatments known as gonadotropin-releasing hormone (GnRH) agonists, also known as luteinizing hormone-releasing hormone (LHRG) agonists.
These medications copy the GnRH by interfering with signals that stimulate the ovaries to make estrogen.
Estrogen and progesterone production in premenopausal women
In premenopausal woman the production of estrogen and progesterone in the ovaries is controlled by the luteinizing hormone (LH) and luteinizing hormone-releasing hormone (LHRH).
Hypothalamus in the brain releases LHRH causing the pituitary gland and make and secrete LH and a hormone that stimulates your follicles.
Both LH and FSH stimulate the ovaries to make estrogen and progesterone that act on the inner lining of the uterus (endometrium).
When levels of estrogen and progesterone reach a certain during your menstrual cycle, the two hormones act on the hypothalamus and your pituitary gland cease their production of LHRH, LH, and FSH.)
How does ovarian suppression pan out?
FDA approved Gasorelin (Zoladex) and leuprolide (Lupron) are the main drugs used along with other drugs in triggering ovarian suppression.
Blocking production of estrogen: drugs known as aromatase inhibitors are utilized to block the activities of an enzyme called aromatase.
This enzyme is used by the body to manufacture estrogen in a woman’s ovaries and other body tissues.
It’s also mainly used in postmenopausal women since the ovaries in premenopausal women produce an excessive amount of aromatase to allow inhibitors to offer effective blockage.
Even so, these two drugs can be used for premenopausal women if they are taken in combination with a drug that interferes with ovarian function.
FDA approved anastrozole (Arimidex) and letrozole (Femara), which temporarily deactivates aromatase and exemstane (Aromasin) which permanently deactivates aromatase.
Blocking the effects of estrogen: There are several drug types that can and do interfere with estrogen’s ability to facilitate the growth of breast cancer cells:
- Selective estrogen receptor modulator (SERMs) – these bind themselves to estrogen receptors and thereby prevent estrogen from binding. Examples of these SERMS are FDA approved treatments of breast cancer are tamoxifen (Novaldex) and toremifene (Fareston).
Since they bind to estrogen receptors, SERMs are able to not only block estrogen to act (by stopping estrogen from binding to its receptors) but they also copy estrogen’s effects, in some parts of the body and not in others
For instance SERMs act as estrogen acts against estrogen in breast tissues, but functions in the same manner as estrogen in a woman’s uterus and bone.
- Other anti-estrogen drug medications – for example, fulvestrant (Faslodex), works differently to block estrogen’s effects. Like SERMs, fulvestrant binds to estrogen receptor and acts as to block estrogen.
But unlike SERMs the drug does not copy the actions of estrogen and is therefore given the status of a pure anti-estrogen drug.
When fulvestrant binds to an estrogen receptor, the receptor will inevitably be destroyed completely.
Conclusion
The best way of fully understanding how a drug medication works in treating a specific condition (breast cancer), is to really delve into how it’s used and how it actually works in treating that condition. This is the purpose behind what has been written in this first part of the article, followed by a second part. We sincerely hope your knowledge and understanding of how hormone therapy is used in treating breast cancer has been enhanced.