2014
DOI: 10.1016/j.clbc.2013.10.008
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Extending the Clinical Benefit of Endocrine Therapy for Women With Hormone Receptor–Positive Metastatic Breast Cancer: Differentiating Mechanisms of Action

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Cited by 26 publications
(24 citation statements)
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“…5B, ER-positive or PR-positive patients tended to express low levels of CXCL2/8/13 and high levels of CXCL12/14 compared with ER-negative or PR-negative patients. ER-positive and PR-positive cancer cells depend on estrogen for their growth, so they can be treated with drugs to block estrogen effects (e.g., tamoxifen) and generally have a better prognosis [24]. Therefore, these results indicate that low expression of CXCL2/8/13 and high expression of CXCL12/14 may predict a better prognosis.…”
Section: Resultsmentioning
confidence: 99%
“…5B, ER-positive or PR-positive patients tended to express low levels of CXCL2/8/13 and high levels of CXCL12/14 compared with ER-negative or PR-negative patients. ER-positive and PR-positive cancer cells depend on estrogen for their growth, so they can be treated with drugs to block estrogen effects (e.g., tamoxifen) and generally have a better prognosis [24]. Therefore, these results indicate that low expression of CXCL2/8/13 and high expression of CXCL12/14 may predict a better prognosis.…”
Section: Resultsmentioning
confidence: 99%
“…Evidence exists that ER+ MBC may either be unresponsive to ET (de novo resistance) or lose endocrine responsiveness by upregulating other signaling pathways involved in cell survival and proliferation (i.e., acquired endocrine resistance) . Several mechanisms may be responsible for acquired endocrine resistance, including downregulation or loss of ER expression, ER mutations generating mutant ER isoforms, or altered expression or activity of ER coregulators . Phosphorylation, methylation, ubiquitination, and additional posttranslational modifications of ER and its coregulators have been shown to influence ER activity and sensitivity to ET .…”
Section: Resultsmentioning
confidence: 99%
“…Preclinical data suggest that crosstalk between growth factor receptor and ER pathways may mediate the development of resistance to ET in ER+ MBC . Growth factor receptor pathways may act as ER‐independent drivers of tumor growth and survival, leading to the expression of ER‐target genes independently of estrogen binding to ER, therefore conferring resistance to ET . Epidermal growth factor receptor, HER2 epidermal growth factor receptor, and insulin growth factor receptor have been recognized as the most prominent factors contributing to endocrine resistance .…”
Section: Resultsmentioning
confidence: 99%
“…Two phase III clinical trials exploring this issue in postmenopausal women in first-line treatment for MBC, using a combination of anastrozole and fulvestrant, produced diverging results [1 positive: SWOG 0226 [51] (HR (hazard ratio): 0.81; 95% confidence interval: 0.65-1.00), and 1 negative: Review articles: [102,103] Progressive disease without initial response to treatment…”
Section: Is There Evidence For Suggesting That a Combination Of Severmentioning
confidence: 99%