Becky,
I read the abstract for this several times, and thank you very much for explaining the talk that went along with it, because it is difficult to "tease" such information out of a few paragraphs (i.e., the concluding sentence, "breast cancer subtypes by IHC may not fully overlap with those defined by gene expression profiling" does not convey nearly the depth of information contained in your post.)
I also saw this abstract:
http://www.abstracts2view.com/sabcs/...ABCS07L_999930 about "Biomarking the estrogen responsiveness of bc," wherein it is stated, "a global index of dependence on estrogen (GIDE) which integrates the transcriptional changes that occur with estrogen deprivation varies more than 30-fold among ER+ tumors . . .Despite compelling preclinical data, markers such as PgR and HER2 do not appear to define patients with a particularly high relative benefit of an aromatase inhibitor over tamoxifen. Further study of the molecular changes that occur with estrogen deprivation and association of these with clinical outcome may be expected to identify the hallmarks of breast cancer that are supported by estrogen stimulation."
This seems to piggyback on what you are asking Lani to comment on, I think - i.e., that having a positive or negative hormone receptor is not necessarily an indication of response to endocrine therapy, even though the therapy does what it is supposed to do (in the case of AI's, almost total ER deprivation) because the bc itself "looks and acts" like its receptor-opposite.
These seem to me to be profound findings that are not getting much airplay.
I will be interested in Lani's response, as well.
Hopeful
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