Abstract
Heat-shock factor 1 (HSF1) is a transcription factor that is activated upon proteotoxic stress and coordinates induction of the heat-shock response. In this issue, Dai et al. (2007) show that HSF1 is a potent modifier of tumorigenesis and is required for tumor initiation and maintenance in a variety of cancer models. These findings add HSF1 to a growing list of non-oncogenes that could be exploited as cancer drug targets.
MeSH terms
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Animals
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Carcinogens
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Cell Line, Tumor
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Cell Proliferation
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Cell Survival
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Cell Transformation, Neoplastic / genetics
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Cell Transformation, Neoplastic / metabolism*
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Cell Transformation, Neoplastic / pathology
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DNA-Binding Proteins / deficiency
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DNA-Binding Proteins / genetics
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DNA-Binding Proteins / metabolism*
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Gene Expression Regulation, Neoplastic*
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Genotype
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Glucose / metabolism
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Heat Shock Transcription Factors
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Humans
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Mice
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Mice, Knockout
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Mutation
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Phenotype
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Protein Biosynthesis
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Proto-Oncogene Proteins c-sis / genetics
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Proto-Oncogene Proteins c-sis / metabolism
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Signal Transduction / genetics
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Skin / metabolism*
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Skin / pathology
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Skin Neoplasms / chemically induced
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Skin Neoplasms / genetics
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Skin Neoplasms / metabolism*
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Skin Neoplasms / pathology
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Stress, Physiological / genetics
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Stress, Physiological / metabolism*
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Stress, Physiological / pathology
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Time Factors
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Transcription Factors / deficiency
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Transcription Factors / genetics
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Transcription Factors / metabolism*
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Tumor Suppressor Protein p53 / genetics
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Tumor Suppressor Protein p53 / metabolism
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ras Proteins / genetics
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ras Proteins / metabolism
Substances
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Carcinogens
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DNA-Binding Proteins
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HSF1 protein, human
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Heat Shock Transcription Factors
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Hsf1 protein, mouse
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Proto-Oncogene Proteins c-sis
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Transcription Factors
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Tumor Suppressor Protein p53
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ras Proteins
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Glucose