[Lani]

All the series on molecular profiling have a special subclass of breast cancer which is her2+ er- but didn't know where to classify her2+ er+ (sometimes in luminal B. sometimes totally ignored as they hadn't a clue)

Four years ago the literature refelcted that only 10% of her+ breast cancers were er+--now they usually quote 45% or so of her2+s are er+..

Many more studies are done of breast cancer cell line SKBr3 which is her2+er- than of BT474 which is her2+er-

So I don't know where you get your impression.

Perhaps because I go out of my way to try report what they are learning about her2+er+ as it is a complicated task of discovering how best to treat it ie, should fulvestrant be given rather than rather than tamoxifen, is it OK to give tamoxifen or AIs alone without herceptin after the year of herceptin ends, since tykerb has been shown to upregulate ER, does herceptin also.

It seems much more difficult to "cure" her2+ ER+ breast cancer in mice as Drs Osbourne and Schiff have as it requires blocking EGFR, her2, her3 and
may also require estrogen deprivation if it does not happen quickly.

I have been posting on her2+ER+ particularly as I felt it had been getting short-shrift in terms of research. The treatment of her2+er- breast cancer seemed much better studied with results much more straightforward.

I specifically made the effort to find papers on her2+er+ breast cancer because I had exactly the opposite impression than you did--ie that there was a scarcity of research/knowledge re her2+er+ breast cancer compared with her2+er- breast cancer. Jean and others had asked me to be on the outlook for papers comparing the efficacy of various antihormonal treatments for her2+ breast cancer.

Let me know why you think your perception and my perception are at opposite ends of the pole