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Collateral-resistance to estrogen and HER-activated growth is associated with modified AKT, ERα, and cell-cycle signaling in a breast cancer model.

Kate M Moore, Vera Cerqueira,Kenneth G MacLeod,Peter Mullen,Richard L Hayward,Simon Green,David J Harrison,David A Cameron,Simon P Langdon

Exploration of targeted anti-tumor therapy（2022）

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Abstract
Multiple changes occur with progression of endocrine resistance in this model with AKT activation contributing to E insensitivity and loss of ERα(Ser118) phosphorylation being associated with full resistance. Cell cycle regulation is modified in endocrine-resistant breast cancer cells, and seliciclib is effective in both endocrine-sensitive and resistant diseases.
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Key words
Breast cancer,endocrine resistance,erbB receptor,estrogen,seliciclib
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