Advanced breast cancers that initially respond well to tamoxifen treatment eventually become refractory to this compound. Several mechanisms of acquired resistance have been hypothesized, including crosstalk between ER and growth factor receptor tyrosine kinase pathway. The cumulative data from clinical studies show that overexpression of HER-2 and/or EGFR, and high levels of phosphorylated Akt or ERK, contribute to tamoxifen resistance in some patients. HER-2, EGFR, Akt and ERK are all ...
Reports by Author
