Abstract
Tamoxifen is the drug most used for early breast cancer treatment in oestrogen receptor (ER) positive patients. Unfortunately, despite high ER tumour levels in a tumour, resistance to endocrine therapy, either de novo or acquired after prolonged treatment, can occur. In this review, we will try to summarise the postulated mechanisms of hormonal-resistance, namely, the role of co-regulators and the crosstalk between the HER-2, IGF-IR, Cox-2 and ER pathways. Other predictive markers of tamoxifen-resistance/response, such as cyclin E and UPA/PAI-1, are also discussed.
MeSH terms
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Antineoplastic Agents, Hormonal / therapeutic use
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Biomarkers, Tumor / analysis
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Breast Neoplasms / drug therapy*
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Breast Neoplasms / metabolism
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Cyclin E / metabolism
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Drug Resistance, Neoplasm*
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Estrogen Antagonists / therapeutic use*
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Female
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Humans
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Oncogene Proteins v-erbB / metabolism
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Proto-Oncogene Proteins c-bcl-2 / metabolism
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Receptors, Estrogen / metabolism
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Receptors, Progesterone / metabolism
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Somatomedins / metabolism
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Urokinase-Type Plasminogen Activator / metabolism
Substances
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Antineoplastic Agents, Hormonal
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Biomarkers, Tumor
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Cyclin E
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Estrogen Antagonists
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Oncogene Proteins v-erbB
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Proto-Oncogene Proteins c-bcl-2
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Receptors, Estrogen
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Receptors, Progesterone
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Somatomedins
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Urokinase-Type Plasminogen Activator