Abstract
MYB is highly expressed in almost all estrogen receptor (ER)-positive breast tumours and is a direct target of estrogen/ER signalling. Our recent studies have shown that MYB is also required for the proliferation of ER-positive breast tumour cell lines, and have shed further light on the mechanism of ER regulation of MYB expression. Here we discuss the rationale for therapeutic targeting of MYB in breast cancer and consider a number of approaches to developing an anti-MYB therapeutic.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Antineoplastic Agents / pharmacology*
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Antineoplastic Agents / 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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Cell Division
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Cell Line, Tumor / metabolism
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Cell Line, Tumor / pathology
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Drug Design
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Estrogens* / physiology
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Female
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Gene Expression Regulation, Neoplastic / physiology
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Genes, myb
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Humans
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Neoplasm Proteins / analysis
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Neoplasm Proteins / antagonists & inhibitors
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Neoplasm Proteins / chemistry
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Neoplasm Proteins / physiology
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Neoplasms, Hormone-Dependent / genetics
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Neoplasms, Hormone-Dependent / metabolism
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Neoplasms, Hormone-Dependent / therapy*
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Nucleic Acid Synthesis Inhibitors / therapeutic use
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Oncogene Proteins v-myb / antagonists & inhibitors
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Oncogene Proteins v-myb / chemistry
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Oncogene Proteins v-myb / physiology*
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Peptides / pharmacology
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Peptides / therapeutic use
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Protein Binding / drug effects
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Protein Interaction Mapping
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RNA Interference
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Receptors, Estrogen / analysis
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Receptors, Estrogen / chemistry
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Receptors, Estrogen / physiology
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Transcription, Genetic / drug effects
Substances
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Antineoplastic Agents
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Estrogens
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Neoplasm Proteins
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Nucleic Acid Synthesis Inhibitors
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Oncogene Proteins v-myb
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Peptides
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Receptors, Estrogen