Abstract
Because normal lymphoid tissue homeostasis depends on a balance between cell proliferation and cell death, lymphomas can arise from mutations that interfere with the normal cell death process. We here discuss some circumstances in which lymphoid cell overexpression of a cell death antagonist, the Bcl2 protein, in E mu-bcl2 transgenic mice can contribute to the development of lymphomas and plasmacytomas.
MeSH terms
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Animals
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Cell Differentiation
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Cell Survival
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Crosses, Genetic
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Genes, abl*
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Homeostasis
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Humans
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Incidence
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Lymphoma / epidemiology
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Lymphoma / genetics*
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Lymphoma, T-Cell / epidemiology
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Lymphoma, T-Cell / genetics
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Lymphoma, T-Cell / pathology
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Mice
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Mice, Inbred C57BL
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Mice, Inbred Strains
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Mice, Transgenic
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Plasmacytoma / epidemiology
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Plasmacytoma / genetics
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Proto-Oncogene Proteins c-bcl-2 / biosynthesis*
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Proto-Oncogene Proteins c-bcl-2 / genetics
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Thymus Neoplasms / epidemiology
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Thymus Neoplasms / genetics
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Tumor Cells, Cultured
Substances
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Proto-Oncogene Proteins c-bcl-2