Abstract
The retinoblastoma tumour suppressor (RB) is a crucial regulator of cell-cycle progression that is invoked in response to a myriad of anti-mitogenic signals. It has been hypothesized that perturbations of the RB pathway confer a synonymous proliferative advantage to tumour cells; however, recent findings demonstrate context-specific outcomes associated with such lesions. Particularly, loss of RB function is associated with differential response to wide-ranging therapeutic agents. Thus, the status of this tumour suppressor may be particularly informative in directing treatment regimens.
Publication types
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Research Support, N.I.H., Extramural
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Review
MeSH terms
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Animals
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Antineoplastic Agents / therapeutic use
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Biomarkers / analysis
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Cell Cycle
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Cell Death
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E2F Transcription Factors / metabolism
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Gene Expression Regulation, Neoplastic
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Genes, Tumor Suppressor
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Humans
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Mice
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Neoplasms / metabolism*
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Neoplasms / therapy
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Neoplasms, Hormone-Dependent / genetics
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Organ Specificity
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Protein Kinase Inhibitors / pharmacology
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Retinoblastoma Protein / deficiency
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Retinoblastoma Protein / physiology*
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Signal Transduction
Substances
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Antineoplastic Agents
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Biomarkers
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E2F Transcription Factors
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Protein Kinase Inhibitors
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Retinoblastoma Protein