Abstract
Deletions of the CDKN2A/B tumor suppressor locus and of the IKAROS and PAX5 genes that promote B-lineage development occur frequently in lymphoid, but not myeloid leukemias initiated by the BCR-ABL tyrosine kinase. Why is this the case, and how do these genetic lesions contribute to an aggressive disease that fails to durably respond to targeted kinase inhibitors?
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Cell Lineage
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Drug Delivery Systems
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Drug Resistance, Neoplasm / genetics*
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Fusion Proteins, bcr-abl
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Gene Deletion
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Genes, p16*
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Humans
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Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
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Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics*
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Protein Kinase Inhibitors / therapeutic use
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Protein-Tyrosine Kinases / genetics*
Substances
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Protein Kinase Inhibitors
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Protein-Tyrosine Kinases
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Fusion Proteins, bcr-abl