Abstract
The three most common genetic abnormalities occurring in malignant lymphomas involve alterations resulting in the deregulated expression of the c-myc and bcl-2 oncogenes and the inactivation of the p53 tumor suppressor gene. Relevant strains of genetically engineered mice, including bcl-2-Ig and E mu-myc transgenic mice and p53 knockout mice, have been used to prospectively examine the regulation of apoptotic cell death by these genes, individually and in combination, and their contribution to in vivo lymphomagenesis. The potential importance of the therapeutic induction of apoptosis is discussed.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Apoptosis / genetics*
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Cell Division / genetics
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Chromosomes, Human, Pair 14 / genetics
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Chromosomes, Human, Pair 18 / genetics
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Chromosomes, Human, Pair 8 / genetics
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Gene Expression Regulation, Neoplastic / genetics
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Genes, Tumor Suppressor / physiology*
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Genes, myc / physiology
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Genes, p53 / physiology
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Humans
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Lymphoma / genetics*
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Lymphoma / pathology
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Mice
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Mice, Transgenic
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Mutation / genetics
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Proto-Oncogene Proteins / physiology
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Proto-Oncogene Proteins c-bcl-2
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Proto-Oncogene Proteins c-myc / physiology
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Proto-Oncogenes / physiology*
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Translocation, Genetic / genetics
Substances
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Proto-Oncogene Proteins
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Proto-Oncogene Proteins c-bcl-2
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Proto-Oncogene Proteins c-myc