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The difference I see between AI's and Tamoxifen is that Tamoxifen is both an angonist and an antagonist for ER receptors. While it is supposed to be strictly an antagonist for bc, in Her2+ patients in particular, it has the capacity to act as an agonist, to actually promote the growth of the cancer. The GUNN study from Naples was the first to recognize this, when their data showed that ER+ Her2+ bc patients fared worse on Tamoxifen than those that received no hormonal treatment.
I have not yet read any papers that intimate that AI's have a similar result. I think this is most likely because they work by removing ER rather than manipulating it.
Hopeful
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