
Estrogen [also sometimes spelled oestrogen] does not CAUSE uterine LMS. But ALL endometrial uterine cancers have a relationship with estrogen levels. Estrogen can stimulate the cells of the endometrium [the lining of the uterus] to grow, so it might increase the chance that cancerous cells develop and grow. 

All cancers develop from DNA damage. This might be genetic [for example, faulty repair enzymes that are inherited], or due to viruses, or chemical carcinogens, or radiation. Estrogen does not cause DNA damage. 

LMS uterine primary tumors often have estrogen receptors on their cells. Sometimes NONgenital LMS cells will have estrogen receptors on their cell membranes. <b>Estrogen can  stimulate cells with estrogen receptors on them to grow and reproduce.</b>  You might have your tumor tested for estrogen and progestogen receptors, and if positive, consider ANTI hormone treatment. 

<b>Estrogen Levels and Cancer Development</b>
	* Oral contraceptives which have a very low level of hormones, might actually lower the level of estrogen in a person's blood. In fact, this might be the reason for the protective effect that oral contraceptives have against some "female" cancers.  
	* It is also interesting that cigarette smoking, which induces certain liver enzymes that metabolize estrogen, lowers the level of estrogen in the blood.  Groups of women who smoke have a lower risk of uterine cancer than women who don't.  We are NOT recommending smoking as a preventative for uterine cancer, however, because of the damage it does to the rest of the body.
	* There is also some question about groups of people who eat a lot of soy phytoestrogens.  These are weaker estrogens than those we produce in our body, and the lower estrogen stimulation they provide in competition with our own estrogen, might protect some vegans and Asian population groups from developing some estrogen dependent cancers.
	* There is also some question about hormone levels in meat contributing to the development of some cancers.

<b>In Summary So Far</b>

	* LMS patients with a uterine primary that is estrogen positive run a risk of HRT stimulating any remaining tumor cells.
	* 7.5% of LMS patients are at risk for developing a second primary cancer.  HRT might promote breast or genital cancers.
	* Therefore, HRT might not be a good idea for any female LMS patients whether their primary is estrogen receptor positive or not.


<b>Jim wrote to the ACOR LMS LIST: </b>
OK here is my simple interpretation about receptors and LMS. Please note this is an oversimplification. I'll talk about oestrogen but these general observation apply to progesterone also. 

Oestrogen is a hormone produced in large amounts by the ovaries. Hormones are chemical messengers used by the body to control parts that may be widely separated [eg 'Womens bits']. 

Some cells have receptors on their surface that bind oestrogen. When the oestrogen binds to the cell surface a change occurs within the cell - even though the oestrogen doesn't enter it - a bit like ringing the doorbell to wake the cell up.  This is not the place to go into the details, but whole libraries have been written on what happens when a hormone binds to a cell! For example, the growth/shedding of the lining of the uterus is controlled by the levels of hormones leading to the monthly cycle - this is well understood and in just about any basic textbook. 

THIS IS THE IMPORTANT BIT. If a cell which is normally partly controlled by oestrogen becomes cancerous (eg breast cancer or SOME cases of uterine LMS) then the stimulation of these receptors MAY cause the tumour to grow faster - oestrogen may increase the rate of growth of the cancer. So it is a bad idea to give it any more oestrogen (by HRT) if the ovaries have been removed. Small amounts of oestrogen are produced by other tissues (men have low but measurable levels). 

It has been established in breast cancer that blocking oestrogen is beneficial if the cancer cells have estrogen receptors. The usual drug for breast cancer is Tamoxifen which stops the oestrogen from binding to the cells.  But Dr Judson (Royal Marsden) suggested that Tamoxifen  may not be ideal for uterine LMS as there is evidence that Tamoxifen may actually stimulate uterine endometrium and possibly therefore uterine LMS.

 Letrozole interferes with Oestrogen production so should be effective in slowing down cells that are stimulated by oestrogen. OK now these anti-oestrogens haven't been around long enough for anyone to know of the effects - Dr Judson said he is just starting to think about putting together a trial to see if they really work. They won't kill LMS but they may slow it down and as they do not appear to have any major side effects (but remember they are new) why not try them? 

My personal view is this:  
My wife's LMS grew back in a year and the main mass was removed again by surgery - but she was on HRT (a different story) so maybe without HRT it MIGHT take 2 years to grow to the same size and maybe with Letrozole it MIGHT take 4 years. Having had 6 courses of Adriamycin (with horrible side effects) that reduced it by 5%--- then the Letrozole looks like a real bargain. 

I would urge everyone with uterine LMS to have the tumor that was removed at operation tested for oest/prog receptors. Testing can be done on the wax embedded tumor that is preserved and stored in the laboratory. I would be very unhappy if my oncologist didn't see the point. 

Anti-oestrogen therapy will not cure you and if you have a large mass then surgery (including RFA etc) or possibly chemotherapy is probably the only option. If however you have Uterine LMS and had a recurrence removed then anti-hormone looks a good bet - it is untested but I don't think that there is anything else - I wouldn't go for adjuvant radio/chemotherapy. 

If you are clear after initial surgery then I'd probably wait and see. This is based on a 40% chance of a recurrence if there are clear margins; once you have a recurrence however then you are probably 90% certain to get more. Hope that I've pitched this at the right level feel free to e-mail me on or off list with any questions and I'll keep the list updated with my wife's progress. As always the above is not a medical opinion. I post to help everyone with LMS to understand it and to help YOU make a decision in consultation with YOUR medical advisor. 

In summary, Jim wrote:
"It is my understanding that oestrogens can stimulate Uterine LMS cells to grow quicker. As hormones closely control many cells of the uterus, this is only to be expected. Remember that LMS cells are not aliens - they are just cells of our own body that don't respond correctly to the signals and so grow out of control. If a tumour arises from uterine tissue it would be expected to still show many of its parent cell's characteristics."   

Search Pubmed for &&url
Search Pubmed for &&url 
