作者: Luciana Pizzatti , Carolina Panis , Gabriela Lemos , Moisés Rocha , Rubens Cecchini
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摘要: Chronic myeloid leukemia (CML) is a pluripotent hematopoietic disorder that currently considered incurable. The tyrosine kinase product of the Philadelphia chromosome, P210 BCR-ABL, provided pathogenetic explanation for initiation CML chronic phase and molecular therapeutic target disease. Imatinib mesylate, an orally available BCR-ABL inhibitor, can induce haematologic cytogenetic remission CML. However, imatinib resistance occurs frequently, resulting in relapse. New treatment strategies are focusing on resistant stem cells bone marrow stroma. identification novel pathways mechanisms microenvironment could significantly contribute to development such strategies. In this work, we used high-resolution label-free MSE proteomic approach identify differential protein expression plasma responsive patients. Oxidative lipid metabolism regulation switch from canonical noncanonical WNT signaling may compartment.