Abstract
The great majority of patients with chronic myeloid leukaemia (CML) have a Philadelphia (Ph) chromosome which has proved at molecular level to be associated with the production of chimeric BCR-ABL gene which in turn is expressed as a fusion protein (P210) with tyrosine kinase activity. An equivalent but somewhat smaller chimeric gene and fusion protein (P190) is found in some cases of Ph-positive acute leukaemia. Though the consistency of these abnormal findings in patients with Ph-positive leukaemia is strong evidence for their pathogenetic role, there are still many unanswered questions.
MeSH terms
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Blast Crisis / genetics
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Blast Crisis / pathology
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Chromosomes, Human, Pair 21 / ultrastructure
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Fusion Proteins, bcr-abl
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Hematopoiesis
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Humans
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Leukemia, Myelogenous, Chronic, BCR-ABL Positive / etiology*
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Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics
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Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology
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Neoplasm Proteins / genetics
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Neoplasm Proteins / physiology
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Neoplastic Stem Cells / pathology
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Philadelphia Chromosome
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Protein-Tyrosine Kinases / genetics
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Protein-Tyrosine Kinases / physiology
Substances
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Neoplasm Proteins
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Protein-Tyrosine Kinases
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Fusion Proteins, bcr-abl