Here is a link to the full article:
http://www.springerlink.com/content/...5/fulltext.pdf
And the graphs:
http://www.springerlink.com/content/...MOESM1_ESM.ppt
One paragraph in particular stands out to me:
"These findings suggest that ER-negativity interacts with Her2-overexpression to cause a more aggressive clinical behavior, and that the acquisition of of ER-positivity in Her-2 positive disease affects the disease course of Her2-positive breast cancer and ameliorates the aggresiveness of Her2+/ER- diseases. There is increasing evidence that HER2 amplification may be the biological driver of Her2-positive diseases, overriding the influence of HR, and that acquisition of ER expression may be a late event in pathogenesis. However, maintaining ER-positivity independent of HER2 status may be more closely related to intrinsic dormancy, which is regulated by the microenvironment of the host and could be part of later events in tumorigenesis. This elucidation was supported by relapse curves according to HER2 status in the ER-positive and ER-negative patients. Apparently, favorable outcomes of ER-positive patients are not only due to hormonal therapy, but also from the less aggressive biologic behavior of the tumor, irrespective of the presence or absence of HER2."
This is a very strong statement. I am wondering how this can be reconciled with the concept that "biology drives treatment," and also with the high Oncotype scores seen for hormone positive, Her2 positive patients.
Thanks, Lani, for posting this interesting article.
Hopeful