Detection of twelve nucleotides insertion in the BCR-ABL kinase domain in an imatinib-resistant but dasatinib-sensitive patient with bi-phenotypic acute leukemia.

in normal lymphocytes (Figure 2E). In samples from ALL patients, however, equivalent expression levels of PKM1/2 and PKM2 were present (Figure 2F). Analogous to the Q-PCR results, no significant difference in protein levels were observed between prednisolone-resistant and prednisolone–sensitive cases, suggesting that pyruvate kinase isoform M2 is not responsible for glucocorticoid resistance in childhood leukemia. Whether the difference in expression between different isoforms of pyruvate kinase that was detected between normal bone marrow and leukemic cells reflects a difference in glycolytic rate is not known, since patient cells do not grow in vitro and we can not detect glucose consumption. Thus, although pyruvate kinase might play a role in the regulation of glycolysis in childhood ALL, glucocorticoid resistance is unlikely to be caused by selective expression of PKM2.