Abstract
Drugs that target the reliance of tumor cells upon estrogen signalling have revolutionised the treatment of breast cancer. Despite this, resistance to these endocrine therapies limits their utility. While the study of individual genes has contributed greatly to understanding drug resistance, relatively unbiased screening approaches may also be illuminating. The results of a high-throughput RNA interference screen identifying novel determinants of tamoxifen resistance support this conjecture and demonstrate that such approaches can identify clinically relevant genes, such as CDK10.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Antineoplastic Agents, Hormonal / metabolism
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Antineoplastic Agents, Hormonal / therapeutic use*
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Breast Neoplasms / drug therapy*
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Breast Neoplasms / metabolism
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Cell Cycle / drug effects
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Cell Line, Tumor
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Cyclin-Dependent Kinases / genetics
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Cyclin-Dependent Kinases / metabolism*
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Drug Resistance, Neoplasm*
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Estrogens / metabolism
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Humans
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Mammary Neoplasms, Experimental / drug therapy
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Mammary Neoplasms, Experimental / metabolism
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Neoplasms, Hormone-Dependent / drug therapy
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RNA Interference
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Receptors, Estrogen / metabolism
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Tamoxifen / analogs & derivatives*
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Tamoxifen / metabolism
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Tamoxifen / therapeutic use*
Substances
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Antineoplastic Agents, Hormonal
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Estrogens
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Receptors, Estrogen
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Tamoxifen
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afimoxifene
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CDK10 protein, human
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Cyclin-Dependent Kinases