Syed K. Mohsin

TL;DR: C Crosstalk between ER, HER-2, p38, and ERK may contribute to tamoxifen resistance and may provide molecular targets to overcome this resistance.

TL;DR: A recent review as mentioned in this paper discusses histological models of human premalignant breast disease that provide the framework for scientific investigations into the biological alterations behind them and examples of specific biological alterations that appear to be particularly important.

TL;DR: The hypothesis that poorly differentiated DCIS gradually evolve from well-differentiated DCIS by randomly acquiring genetic defects resulting in increasingly abnormal cellular features is supported.

TL;DR: A monoclonal antibody useful for the detection of ERbeta at the protein level in archival, formalin-fixed breast tumors is generated and ERbeta expression is found to be not a surrogate for ERalpha in clinical breast tumors and, as such, could be a useful biomarker in its own right.

TL;DR: The epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor gefitinib significantly delayed the emergence of resistance to both estrogen deprivation and fulvestrant, but reactivation of HER-2/neu and signaling through AKT leads to tumor regrowth.