Abstract
The promyelocytic leukaemia gene PML was originally identified at the t(15;17) translocation of acute promyelocytic leukaemia, which generates the oncogene PML-retinoic acid receptor α. PML epitomises a subnuclear structure called PML nuclear body. Current models propose that PML through its scaffold properties is able to control cell growth and survival at many different levels. Here we discuss the current literature and propose new avenues for investigation.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Cell Cycle / genetics
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Cell Death / genetics
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Cell Differentiation
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Cell Nucleus
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Gene Expression Regulation, Neoplastic
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Humans
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Leukemia, Promyelocytic, Acute / genetics*
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Leukemia, Promyelocytic, Acute / metabolism
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Leukemia, Promyelocytic, Acute / pathology
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Mice
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Neoplastic Stem Cells / metabolism
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Neoplastic Stem Cells / pathology
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Nuclear Proteins / genetics*
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Nuclear Proteins / metabolism
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Oncogene Proteins, Fusion / genetics*
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Oncogene Proteins, Fusion / metabolism
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Promyelocytic Leukemia Protein
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Receptors, Retinoic Acid / genetics*
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Receptors, Retinoic Acid / metabolism
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Retinoic Acid Receptor alpha
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Signal Transduction / genetics
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Transcription Factors / genetics*
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Transcription Factors / metabolism
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Transcription, Genetic
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Translocation, Genetic*
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Tretinoin / metabolism
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Tumor Suppressor Proteins / genetics*
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Tumor Suppressor Proteins / metabolism
Substances
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Nuclear Proteins
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Oncogene Proteins, Fusion
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Promyelocytic Leukemia Protein
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RARA protein, human
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Rara protein, mouse
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Receptors, Retinoic Acid
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Retinoic Acid Receptor alpha
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Transcription Factors
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Tumor Suppressor Proteins
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PML protein, human
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Tretinoin