Link: Cholesterol vs Tamoxifen Resistance
Did anybody see this? This research is also based on ILC.
http://www.medicalnewstoday.com/articles/146945.php
".........
The researchers are trying to understand why some women with estrogen receptor-positive (ER+) invasive lobular breast cancer do not benefit as much from hormonal therapy such as tamoxifen when compared to women with other forms of ER+ breast cancer. Each year in the U.S., approximately 127,000 women develop ER+ breast cancer, and an increasing percentage of these are specifically diagnosed with invasive lobular breast cancer. ......"
Comments
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QAnna, This article is very interesting. When I started taking Femara my cholesterol level, usually in the normal range, shot up to over 300. A low dose of the statin Lipitor keeps it at a level even lower than I had before breast cancer. I wonder what is going on. This doesn't happen to everyone who takes Femara, but it is a side effect that is seen.
I was reading an article recently about IDC vs ILC gene expression profiles. Notice that "lipid" is mentioned for ILC. This indicates cholesterol, I think.
"In particular genes overexpressed in IDCs correspond preferentially to promoters of cell proliferation (e.g. tyrosine kinase receptor ERBB2, JAK2, transcription factor ANKRD32 and calmodulin-binding NRGN), whereas those overexpressed in ILCs code for proteins involved in cell adhesion (VWF, ELN, DPT, EMCN) or lipid (FABP4, CAV1, ADIPOG) and retinoic acid metabolism (ALDH1A1).
SFRP1, TGFBR2 and IGF1, whose functions are associated with cell differentiation rather than proliferation, were also upregulated in ILCs."
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Hi, Gitane,
Those "ERBB2, JAK2..." things look too complicated for now...:)
What was your cholesterol level before BC? -
My cholesterol level was about 160.
What this gene study seems to show, if I interpret it correctly, is that proliferation (how fast cells are dividing) seems to be important in IDC. However, in ILC how sugar and fat is metabolized, among other things, seems to be more important than proliferation. This is interesting because the OncotypeDX is heavily based on proliferation genes, the survivin gene (which is expressed at a much lower level in ILC than IDC), and Stromolysin 3 gene (also expressed at much lower level in ILC than IDC). This leads me to believe that the OncotypeDX may be much less prognostic in ILC than it is in IDC. I hope doctors are making this information available to patients. Mine didn't. He also didn't blink an eye when my cholesterol shot up.
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Hi, Gitane,
I am trying hard to digest all of these new info. eg. those genes stuff..... What was your Oncotype score? Then did they work out your treatment plan based on it?
This article was just published on Apr.24 which is very new, you see it earlier than your doctor. Are you going to show it to him? -
I had finished chemo, had bilat. mastectomies, reconstruction and been on Femara long before I knew what my Oncotype score was. I asked my oncologist if he would send in for the Oncotype score; he was as curious as I was to see what it would be since my cancer is unusual. It came back with score of 23. If I had known this before treatment it wouldn't have changed anything for me.
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I am thinking that your high cholesterol level after BC was fake score? (created by BC cells actually?)
Does Tamoxifen work well for you? -
My doctors said it was related to how my liver metabolized Femara since I didn't have cholesterol issues otherwise, no history, the triglycerides were low, good cholesterol was great, just bad cholesterol went up. It had nothing to do with treatments other than Femara according to the doctors. I never took Tamoxifen so never had any tests to see how it would work in me, so I don't know.
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