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PERSPECTIVE

Failure of CDKN2A/B (INK4A/B–ARF)-mediated tumor suppression and resistance to targeted therapy in acute lymphoblastic leukemia induced by BCR-ABL

¹ Department of Pathology, St. Jude Children’s Research Hospital, Memphis, Tennessee 38105, USA; ² Department of Oncology, St. Jude Children’s Research Hospital, Memphis, Tennessee 38105, USA; ³ Department of Genetics and Tumor Cell Biology, St. Jude Children’s Research Hospital, Memphis, Tennessee 38105, USA; ⁴ Howard Hughes Medical Institute, St. Jude Children’s Research Hospital, Memphis, Tennessee 38105, USA

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?

[Keywords: SNP genomic microarrays; acute lymphoblastic leukemia (ALL); chronic myeloid leukemia (CML); imatinib (Gleevec); dasatinib (Sprycel); targeted therapy]

E-MAIL sherr{at}stjude.org; FAX (901) 495-2381.

Article is online at http://www.genesdev.org/cgi/doi/10.1101/gad.1673908.

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