Abstract
Leukaemia is characterized by the accumulation of malignant haematopoietic precursors. Recent studies have revealed that acquired alterations in genes that regulate normal haematopoiesis are frequently detected in leukaemia. The progression to leukaemia depends on additional mutations that promote the survival of developmentally arrested cells. This review describes three examples of this general paradigm of leukaemogenesis: RUNX1 abnormalities in acute leukaemias, GATA1 mutations in the leukaemias of Down syndrome, and SCL and LMO2 ectopic expression in T cell acute lymphoblastic leukaemia.
MeSH terms
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Adaptor Proteins, Signal Transducing
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Cell Cycle / genetics
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Cell Death / genetics
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Cell Division / genetics
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Core Binding Factor Alpha 2 Subunit
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DNA-Binding Proteins / genetics
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Erythroid-Specific DNA-Binding Factors
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GATA1 Transcription Factor
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Gene Expression
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Hematopoiesis / genetics*
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Humans
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LIM Domain Proteins
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Leukemia / genetics*
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Leukemia-Lymphoma, Adult T-Cell / genetics
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Metalloproteins / genetics
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Oncogene Proteins / genetics
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Proto-Oncogene Proteins / genetics
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Transcription Factors / genetics
Substances
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Adaptor Proteins, Signal Transducing
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Core Binding Factor Alpha 2 Subunit
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DNA-Binding Proteins
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Erythroid-Specific DNA-Binding Factors
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GATA1 Transcription Factor
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GATA1 protein, human
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LIM Domain Proteins
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LMO1 protein, human
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LMO2 protein, human
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Metalloproteins
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Oncogene Proteins
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Proto-Oncogene Proteins
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RUNX1 protein, human
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Transcription Factors