Abstract
Chronic lymphocytic leukemia is a malignant disease characterized by clonal expansion of relatively mature B-lymphocytes with a high percentage of cells arrested in the nonproliferative G0/G1 cell cycle phase. Possibly reflecting the clinical heterogeneity observed in patients, various signaling pathways may become affected during the initiation and course of this disease. This review discusses frequent alterations concerning proliferative, differentiation-inducing, and apoptotic pathways elucidated in the recent years that have improved our understanding of this disease.
MeSH terms
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Animals
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Apoptosis / physiology
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Caspases / metabolism
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Cell Division / physiology*
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Cell Survival
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Cyclins / metabolism
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Cytokines / metabolism
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DNA-Binding Proteins / metabolism
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Humans
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Leukemia, Lymphocytic, Chronic, B-Cell / metabolism*
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Leukemia, Lymphocytic, Chronic, B-Cell / pathology*
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Proto-Oncogene Proteins c-bcl-2 / genetics
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Proto-Oncogene Proteins c-bcl-2 / metabolism
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Receptors, Adrenergic, beta-2 / metabolism
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Receptors, Antigen, B-Cell / metabolism
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STAT1 Transcription Factor
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Signal Transduction*
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Trans-Activators / metabolism
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Tumor Suppressor Protein p53 / genetics
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Tumor Suppressor Protein p53 / metabolism
Substances
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Cyclins
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Cytokines
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DNA-Binding Proteins
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Proto-Oncogene Proteins c-bcl-2
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Receptors, Adrenergic, beta-2
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Receptors, Antigen, B-Cell
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STAT1 Transcription Factor
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STAT1 protein, human
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Trans-Activators
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Tumor Suppressor Protein p53
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Caspases