Author/Authors :
Babashah ، Sadegh نويسنده Department of Molecular Genetics, Faculty of Biological Sciences, Tehran , , Rezaei-Tavirani، Mostafa نويسنده , , Zamanian-Azodi ، Mona نويسنده Proteomics Research Center, Faculty of Paramedical Sciences, Shahid Beheshti University of Medical Sciences, Tehran , , Saki، Najmaldin نويسنده Department of Hematology and Blood Banking School of Medical Sciences, Tarbiat Modares University, Tehran, Iran ,
Abstract :
Chronic myeloid leukemia (CML) is a myeloproliferative disease of the hematopoietic stem cells, characterized by the presence of the Philadelphia (Ph) chromosome. Although imatinib inhibits the BCR-ABL kinase activity, clinical experiences confirm that imatinib may not target CML stem cells in vivo. The identification of signaling pathways responsible for the self-renewal properties of leukemic stem cells in CML will help in the discovery of novel therapeutic targets. Here we review signaling pathways including Wnt/B-catenin, Hedgehog, Alox5, and Foxo which play crucial roles in the maintenance of stem cell functions in CML. It is thought that inhibition of key genes that are part of self-renewal associated signaling pathways may provide an effective way to reduce aberrant stem cell renewal in CML.
