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Role of calcium-dependent protein kinases in chronic myeloid leukemia: combined effects of PKC and BCR-ABL signaling on cellular alterations during leukemia development

Authors Mencalha A, Corrêa S, Abdelhay E

Received 18 March 2014

Accepted for publication 29 April 2014

Published 8 July 2014 Volume 2014:7 Pages 1247—1254


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 3

André L Mencalha,1 Stephany Corrêa,2 Eliana Abdelhay2

1Biophysics and Biometry Department, Roberto Alcântara Gomes Biology Institute, Rio de Janeiro's State University (UERJ), Rio de Janeiro, Brazil; 2Bone Marrow Transplantation Unit (CEMO), National Cancer Institute (INCA), Rio de Janeiro, Brazil

Abstract: Calcium-dependent protein kinases (PKCs) function in a myriad of cellular processes, including cell-cycle regulation, proliferation, hematopoietic stem cell differentiation, apoptosis, and malignant transformation. PKC inhibitors, when targeted to these pathways, have demonstrated efficacy against several types of solid tumors as well as leukemia. Chronic myeloid leukemia (CML) represents 20% of all adult leukemia. The aberrant Philadelphia chromosome has been reported as the main cause of CML development in hematopoietic stem cells, due to the formation of the BCR-ABL oncogene. PKCs and BCR-ABL coordinate several signaling pathways that are crucial to cellular malignant transformation. Experimental and clinical evidence suggests that pharmacological approaches using PKC inhibitors may be effective in the treatment of CML. This mini review summarizes articles from the National Center for Biotechnology Information website that have shown evidence of the involvement of PKC in CML.

Keywords: PKC signaling, chronic myeloid leukemia, pharmacological inhibitors, malignant transformation

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