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Jul 19, 2012 08:34PM
Jul 19, 2012 09:12PM
Your July 17th statement is a little confusing, I understand what an ER receptor measure is however the last part of your last statement:
"It is based on the structure of those cells and is not affected by whether or how much estogen is available to those cells. "
The "It" you are referring to, ER staus, is directly affected by measurements of estrogen....so to calrify-
If you are ER+, your tumor cells respond to estrogen and thrive on it. By having an ooph, taking Tamoxifen and/or AI's, you are depriving the tumor cells of the estrogen they desire. Some estrogen will always be in your body, but there's less of it. Therefore there's less fuel for the cancer cells. When an estrogen molecule enters a cell and passes into the nucleus, it binds to its receptor. That causes the shape of the receptor to change. The estrogen-receptor complex binds to coactivator proteins. This causes nearby genes to become active. The active genes make molecules of messenger RNA. These guide the synthesis of specific proteins. The proteins can then influence cell behavior in different ways. How depends on the type of cell involved.
From the BCO website:
"It's also worth noting that some breast cancers that are hormone-receptor-positive can lose their receptors over time. The opposite is also true: hormone-receptor-negative cancers can gain receptors. If the breast cancer recurs in the future as advanced disease, doctors should order a repeat biopsy and retest the cancer for hormone receptors. If the cancer cells no longer have receptors, hormonal therapy is unlikely to help treat the cancer. If the cells have gained hormone receptors, however, then hormonal therapy may be helpful. "
It's the same concept as antiangiogenesis: tumors need a blood supply in order to thrive, and when the blood supply is diminished, they do not thrive as well as they would with a large blood supply.
And what Mina Bissell is stating in her talk, and I believe she is very correct, the tumor's microenvironment is very important. It's just that it is really not a revolutionary idea. The guys doing cell function analysis have known this for years (Nagourney and Weisenthal) and have gelled this idea into their drug selection technology. Please listen to her lecture, it is very important to know how the cells work in order to understand their language.
8/8/2011 IDC, 5 cm, Stage 3C, ER+PR+Her- grade 2, 11/19 Pos nodes; 1 Adriamycin-allergic,no more chemo; 32 Rad's; Tamo&Lupron failed, Hyster May 2012, Arimidex june-aug,Sept 2012, small mets L1/L4,May 2013 5mm tumor on left lobe of liver
8/8/2011, IDC, 5cm, Stage IIIC, Grade 2, 11/19 nodes, mets, ER+/PR+, HER2-