BCR-ABL1 promotes leukemia by converting p27 into a cytoplasmic oncoprotein

Author:

Agarwal Anupriya1ORCID,Mackenzie Ryan J.1,Besson Arnaud2,Jeng Sophia3,Carey Alyssa1,LaTocha Dorian H.1,Fleischman Angela G.1,Duquesnes Nicolas2,Eide Christopher A.14,Vasudevan Kavin B.1,Loriaux Marc M.15,Firpo Eduardo6,Cortes Jorge E.7,McWeeney Shannon3,O’Hare Thomas89,Roberts James M.6,Druker Brian J.14,Deininger Michael W.89

Affiliation:

1. Division of Hematology and Medical Oncology, Knight Cancer Institute, Oregon Health & Science University, Portland, OR;

2. Cancer Research Center of Toulouse, INSERM Unité Mixte de Recherche 1037, Université de Toulouse, Toulouse, France;

3. Division of Bioinformatics & Computational Biology, Knight Cancer Institute,

4. Howard Hughes Medical Institute, and

5. Department of Pathology, Knight Cancer Institute, Oregon Health & Science University, Portland, OR;

6. Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA;

7. Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX; and

8. Division of Hematology and Hematologic Malignancies and

9. Huntsman Cancer Institute, The University of Utah, Salt Lake City, UT

Abstract

Key Points Coordinated BCR-ABL1 kinase-dependent and -independent mechanisms convert p27 from a nuclear tumor suppressor to a cytoplasmic oncogene. Oncogenic functions of p27 that persist despite effective BCR-ABL1 inhibition may contribute to resistance to tyrosine kinase inhibitors.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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