Crosstalk between bcr-abl and protease-activated receptor 1 (par1) suggests a novel target in chronic myeloid leukemia

Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm characterized by the presence of the Philadelphia chromosome (Ph) and the BCR-ABL1 oncogene [1]. This gene encodes the chimeric BCR-ABL oncoprotein, which has constitutive kinase activity and is responsible for the malignant phenotype of leukemic cells [2-3]. Activation of various signaling pathways by BCR-ABL can lead to the malignant transformation of cells by interfering with basic cellular processes, such as cell proliferation, differentiation, adhesion and survival [4-5].

Source: Experimental Hematology - August 1, 2018 Category: Hematology Authors: Camilla de S. Borges, Aline F. Ferreira, Vitor H. Almeida, Fausto G. Gomes, Maria Gabriela Berzoti-Coelho, Maira da Costa Cacemiro, Natalia S. Nunes, Lorena L. Figueiredo-Pontes, Belinda P. Sim ões, Fabíola A. Castro, Robson Q. Monteiro Source Type: research