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I have been looking for the paper I read that talked about one of the mechanisms for Tamoxifen resistance in Her2+ bc patients to give the citation. Apparently, in the lab (could have been in mice, not sure) they found that the ER receptor, normally located in the cell nucleus, was displaced to the outer surface of the cell by Her2 signaling. Apparently, the ER receptor has to be in the cell nucleus for Tamoxifen to work. Blocking the Her2 receptor with Herceptin caused the ER receptor to move back to the nucleus, where it belongs, and allowed the Tamoxifen to work. When I find this paper (as I am looking for another one, that's how it always happens) I will post the link.
Hopeful
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