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Alterations in the profile of metabolites from blast crisis chronic myeloid leukemia during the development of resistance to imatinib.


The discovery of tyrosine kinase inhibitors (TKIs) brought a major breakthrough in the treatment of patients with chronic myeloid leukemia (CML). But the emerging resistance to TKI therapy is a major challenge in CML treatment. Malignant cells exhibit metabolic changes when compared to their normal counterparts, owing to both genetic and epigenetic alterations. Whether the altered levels of metabolic enzymes result in alteration in total enzyme activity in TKI resistant CML clones which can be assessed from the number of their metabolites produced. LC-MS-based metabolomics approach is a sophisticated way to detection and quantification of altered metabolites to extract the meaningful information of regulatory pathways involved in TKI resistance in CML and tumorigenesis. Metabolic profiling of CML clones sensitive to TKI therapy and their resistant counterpart will ultimately yield clinically useful diagnostic biomarkers for drug resistance and novel metabolic target for CML therapy.

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