Mechanisms of tamoxifen resistance: increased estrogen receptor-HER2/neu cross-talk in ER/HER2-positive breast cancer.

By J. Shou, S. Massarweh, C. Osborne, A. Wakeling, Simale Ali, H. Weiss, R. Schiff. Journal of the National Cancer Institute, 2004

1,223 citations recorded by the source corpus.

Subfields: Cancer Research, Genetics, Oncology

View Paper: https://www.semanticscholar.org/paper/6ccbe8488181051eccb20107375982d053e01873

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Citations in the corpus

Human Epidermal Growth Factor Receptor 2 (HER2) in Cancers: Overexpression and Therapeutic Implications (2014, neutral): “Even estrogen, working via the nongenomic activity of estrogen receptor (ER) outside the nucleus, has been shown to activate HER2 signaling [20].”
Integration of the extranuclear and nuclear actions of estrogen. (2005, background): “When ErbB2 is experimentally overexpressed, tamoxifen activates both ER and ErbB2 to signal downstream through ERK and PI3K to AIB1 phosphorylation (98).”
Drug Resistance in Cancer: An Overview (2014, background): “, HER2 amplification), tamoxifen may lose its estrogen antagonist activity and acquire more agonist-like activity, resulting in tumor growth stimulation [34].”
Tamoxifen-induced ER- a –SRC-3 interaction in HER2 positive human breast cancer; a possible mechanism for ER isoform speciﬁc recurrence (2006, background): “Recently, in tamoxifen-resistant cell lines engineered to overexpress HER2, tamoxifen-induced recruitment of SRC-3 to the promoter region of the ER target gene pS2 was demonstrated (Shou et al. 2004).”
Meeting highlights: international expert consensus on the primary therapy of early breast cancer 2005. (2005, background): “It may indicate a lower probability of response to tamoxifen [21] and perhaps suggest treatment with taxanes or anthracyclines [102], rather than CMF (cyclophosphamide, methotrexate and 5-fluorouracil).”
ERBB receptors and cancer: the complexity of targeted inhibitors (2005, background): “Tamoxifen, a selective ER modifier (SERM) was shown to transactivate EGFR and ERBB2, and in ERBB2-overexpressing breast cancer cells this reduced the antiproliferative activity of the SER”