I see Robin's point why ER would down-regulate under unimpeded proliferation but....if you are taking herceptin, most research indicates up-regulation of ER through the survival instinct of x-talk. Lapatinib for example, has re-sensitizing effects on ER+ tamoxifen resistance BC cells. This is because the cancer has a multi-pathway fail-safe survival system. The goal of targetted therapies is to shutdown enough pathways to cause tumor death, as opposed to cellular death alone.
If I were the king of the cancer fighters, in HER2 cancers I would block HER1, HER2, and hopefully HER3 (either with pertuzumab or a combo of lapatinib and herceptin), P13K (which we try with curcumin, but there are better drugs under development), cox2 inhibitor (celebrex), ER (Faslodex seems to have the best results), VEGF (with avastin and maybe even add in some lucentis which is used in adult macular degeneration), c-myn and P53 inhibitors and probably a cyto-toxic drug such as xeloda (which is really a pro-drug there it isn't systemic) along with neupogen support (neupogen has been shown to mobilize anti-cancer t-cells).
OK, I just left the cat out of the bag because that is what I am going to push for a treatment regime for Linda. She has an appointment in Seattle on Jan 25 with one of their specialists. I'm sure she won't get the whole bag and alot has to do with $$$ BUT, I am going to ask for each of these pathways to be addressed with either a logical "can't do that " explanation of or tx. I know that we can't cover all the bases in one regime but......
Thanks for starting this thread,
A
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Primary care-giver to and advocate for Linda, who passed away April 27, 2006.
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