Abstract
The pathogenesis of human T-cell leukemia virus (HTLV)-induced adult T-cell leukemia-lymphoma (ATLL) was explored using an infectious molecular viral clone and a transgenic mouse model. Activation of nuclear factor-kappaB by the HTLV transcriptional transactivator protein Tax was found to be important for lymphocyte immortalization and tumorigenesis. Interferon-gamma regulates tumor development owing primarily to angiostatic effects. Translational clinical studies of chemotherapy, interferon-alpha, and nucleoside reverse transcriptase inhibitors have also assisted in identifying the pathogenic features of ATLL.
MeSH terms
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Animals
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Anti-Retroviral Agents / administration & dosage
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Antineoplastic Agents / administration & dosage
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Disease Models, Animal
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Gene Products, tax / metabolism
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Genes, pX
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HTLV-I Infections / drug therapy
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HTLV-I Infections / etiology*
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HTLV-I Infections / immunology
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Human T-lymphotropic virus 1 / genetics
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Human T-lymphotropic virus 1 / immunology
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Human T-lymphotropic virus 1 / pathogenicity
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Humans
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Leukemia-Lymphoma, Adult T-Cell / drug therapy
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Leukemia-Lymphoma, Adult T-Cell / etiology
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Leukemia-Lymphoma, Adult T-Cell / immunology
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Mice
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Mice, Transgenic
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NF-kappa B / metabolism
Substances
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Anti-Retroviral Agents
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Antineoplastic Agents
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Gene Products, tax
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NF-kappa B