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Advances in Hematology
Volume 2015, Article ID 612567, 6 pages
Review Article

Protein Kinase CK2: A Targetable BCR-ABL Partner in Philadelphia Positive Leukemias

1Department of Clinical and Biological Sciences, University of Turin, 10043 Orbassano, Italy
2Department of Oncology, University of Turin, 10043 Orbassano, Italy

Received 27 October 2015; Accepted 20 December 2015

Academic Editor: Estella M. Matutes

Copyright © 2015 Alessandro Morotti et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


BCR-ABL-mediated leukemias, either Chronic Myeloid Leukemia (CML) or Philadelphia positive Acute Lymphoblastic Leukemia (ALL), are the paradigm of targeted molecular therapy of cancer due to the impressive clinical responses obtained with BCR-ABL specific tyrosine kinase inhibitors (TKIs). However, BCR-ABL TKIs do not allow completely eradicating both CML and ALL. Furthermore, ALL therapy is associated with much worse responses to TKIs than those observed in CML. The identification of additional pathways that mediate BCR-ABL leukemogenesis is indeed mandatory to achieve synthetic lethality together with TKI. Here, we review the role of BCR-ABL/protein kinase CK2 interaction in BCR-ABL leukemias, with potentially relevant implications for therapy.