Hyperactive mTOR and MNK1 phosphorylation of eIF4E confer tamoxifen resistance and estrogen independence through selective mRNA translation reprogramming.

Given the fact that mTORC1 is already highly active and that eIF4E is already overexpressed as a driver of breast cancer, it is not surprising that there was only a trend toward increased mTORC1 activity (P-4E-BP1) and slightly increased eIF4E levels with tamoxifen or aromatase resistance that did not reach statistical significance.

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