Abstract
One of the best-characterized oncogenic mechanisms in breast cancer is the aberrant activation of phosphatidylinositol-3-kinase, protein kinase B, and mammalian target of rapamycin signaling. In both endocrine-resistant disease and breast cancer stem cells, this is commonly caused by specific genetic lesions or amplification of key pathway components or both. These observations have generated two interesting hypotheses. Firstly, do these genetic anomalies provide clinically significant biomarkers predictive of endocrine resistance? Secondly, do tamoxifen-resistant breast cancer cells emerge from a stem-like cell population? New studies, published in Breast Cancer Research, raise the possibility that these hypotheses are intrinsically linked.
Publication types
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Editorial
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Research Support, Non-U.S. Gov't
MeSH terms
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Antineoplastic Agents, Hormonal / therapeutic use
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Breast Neoplasms / drug therapy*
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Breast Neoplasms / genetics
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Breast Neoplasms / metabolism
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Drug Resistance, Neoplasm / genetics
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Female
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Humans
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Mutation
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Neoplastic Stem Cells / drug effects
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Neoplastic Stem Cells / metabolism
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Neoplastic Stem Cells / pathology
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Phosphatidylinositol 3-Kinase / genetics
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Phosphatidylinositol 3-Kinase / metabolism*
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Proto-Oncogene Proteins c-akt / metabolism*
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Signal Transduction / drug effects*
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TOR Serine-Threonine Kinases / metabolism*
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Tamoxifen / therapeutic use*
Substances
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Antineoplastic Agents, Hormonal
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Tamoxifen
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Phosphatidylinositol 3-Kinase
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Proto-Oncogene Proteins c-akt
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TOR Serine-Threonine Kinases