Dangers of Tamoxifen: Tell your story with the drug

california_artist said:

Elective preventive surgeries
What thoughts do any of you have on the current trend to offer removal of the breasts for those with Bra c 1 (not sure how to type that), and the refusal to offer or even consider a hysterectomy for those who have taken tamoxifen? There has been clear evidence of the connection of tamo to uterine cancer, and not the general version, but to UPSC specifically.

Would it not be the same reasoning. Can you have it if you pay for it yourself? Is it an insurance thing do you think? Could one lobby or file civil suits based perhaps on discrimination, to get the same sort of treatment based on the premise of how the genetic testing is allowing women to have preventative surgeries.

There is quite a bit of info on the discussion of tamox and uterine cancer. This site has a very long article, lots of info and additionally a great reference with full text and abstracts of many articles.

Just a bit of the article. Tamox has proven to be highly effective in further cancer developments in breast tissue. It's just the other problem that is-well-the problem.

Might there be therapeutic choices one could make to enhance the effectiveness and counteract the risks. Yerp, I do mean some sort of food thing.

Article: Is tamoxifen a genotoxic carcinogen in women?

Quote from this article: "...This review spans the clinical justification for tamoxifen as a chemopreventive agent, through to the very latest information on the mechanisms considered responsible for tamoxifen-induced tumours in rat liver and how these relate to women..."

From the Oxford Journal

http://mutage.oxfordjournals.org/content/24/5/391.full

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Abstract
The anti-oestrogen tamoxifen, which is widely used in the treatment of breast cancer and is also approved for the prevention of this disease, causes an increased incidence of endometrial cancer in women. The ability of tamoxifen to induce endometrial tumours and the underlying carcinogenic mechanisms have been a subject of intense interest over the last ∼20 years. They are central to the assessment of risks versus benefits for the drug, especially in a chemopreventive context. This review outlines the clinical justification for using tamoxifen as a chemopreventive agent and describes the genotoxic mechanisms considered responsible for tamoxifen-induced tumours in rat liver and how these might relate to women. In rat hepatic tissue, tamoxifen is metabolically activated via α-hydroxylation and sulphate conjugation to give a reactive species that binds to DNA predominantly at the N2-position of guanine, producing pro-mutagenic lesions. Whether tamoxifen–DNA adducts contribute similarly to the development of cancers in women depends on whether they can be formed in human tissues and the type of specific molecular and cellular responses they induce, if present. This review discusses the current data relating to these issues and highlights areas where further research is needed.


Introduction
The anti-oestrogen tamoxifen ((Z)-1,2-diphenyl-1-[4-[2-(dimethylamino)ethoxy]phenyl]-1-butene) was the first of a class of drugs, now referred to as selective oestrogen receptor modulators (SERMs), to be used clinically. Originally developed as an oral contraceptive, tamoxifen was actually found to induce ovulation in subfertile women and was marketed for this indication instead. In the early 1970s, following promising preliminary results in post-menopausal breast cancer patients (1), tamoxifen was reinvented as an anticancer drug and is now the most widely used adjuvant therapy in the treatment of breast cancer. Randomized clinical trials have demonstrated that adjuvant tamoxifen results in increased disease-free survival and a decrease in breast cancer recurrence rates saving thousands of lives each year (2). For oestrogen receptor (ER)-positive disease, 5 years adjuvant tamoxifen reduces the annual breast cancer death rate by 31% (3). Furthermore, in this setting, 5 years of tamoxifen lowers the risk of developing contralateral breast cancer by ∼47%, with shorter treatment durations associated with proportionately smaller reductions (4). Five years of therapy currently appears to be optimal, and remarkably, the benefit persists for at least a decade after ceasing treatment (3).

Pharmacology


The pharmacological properties of tamoxifen are complex, being both species and tissue specific, and potentially dependent on the duration of use. Tamoxifen is generally classified as a partial oestrogen antagonist in humans, where it functions by blocking the action of oestrogen in the breast by binding to the ER and inducing conformational changes that prevent interaction of the receptor with coactivator proteins (5). In contrast, in post-menopausal women, tamoxifen exerts oestrogenic activity in the endometrium, vaginal epithelium, bone and on serum lipids, which manifests as protective effects against both cardiovascular disease (6,7) and osteoporosis in breast cancer patients (8).

Adverse effects include an increase in the occurrence of deep vein thrombosis or pulmonary embolism (9), whilst a stimulatory action on the endometrium due to tamoxifen-activated gene transcription may be a contributing factor to the elevated incidence of endometrial tumours in women treated with this drug (10,11). The ability of tamoxifen to induce endometrial tumours and the underlying carcinogenic mechanisms have been subjects of intense interest over the last ∼20 years and are central to the assessment of risks versus benefits for the drug, especially in a chemopreventive context. This review spans the clinical justification for tamoxifen as a chemopreventive agent, through to the very latest information on the mechanisms considered responsible for tamoxifen-induced tumours in rat liver and how these relate to women. Emphasis is also placed on the potential for DNA adduct formation in human tissues and the subsequent biological effects these might elicit, with discussion of the approaches currently available for assessing the significance of DNA damage.

Kaleena said:

Claudia:
One cannot force
Claudia:

One cannot force doctors or insurance companies to use the latest methods. There are a lot of "small print" to allow "errors" or to deny or allow certain procedures. When a patient signs those documents that we sign, we sign that we know of the dangers, etc., of taking drugs or that the treatment we are receiving we approve and understand there could be circumstances beyond the control of physicians, etc. etc.

However, that is not to say that one could make a petition to allow such a procedure. You can appeal the insurance companies decision if you got a denial. Sometimes they will allow such a procedure if the case is presented to them.

With regard to a general allowance, it takes a lot of time and effort on many to do this. I further believe this is already started through the breast cancer because many woman who had family history of breast cancer wanted to have their breasts removed. You may want to look into how that is going to see if they got anywhere with that.

Kathy