HRONIC myeloid leukemia （CML） is characterized by the presence of the BCR/ABL fusion gene, which is the result of a reciprocal translo cation between chromosomes 9 and 22, calledPhiladelphia （Ph） chromosome. Imati...HRONIC myeloid leukemia （CML） is characterized by the presence of the BCR/ABL fusion gene, which is the result of a reciprocal translo cation between chromosomes 9 and 22, calledPhiladelphia （Ph） chromosome. Imatinib mesylate （imatinib）, a specific small molecular inhibitor of BCR/ABL, could improve the prognosis of CML and is now the standard drug applied in all phases of this disease} Despite the efficacy of imatinib, the development of resistance and the persistence of minimal residual disease have seriously impaired the efficiency of this medicine. Resistance may develop through several different mechanisms, such as mutations in the Abl kinase domain, BCR/ABL overexpression, or compensatory phosphatidylinositol 3 kinase （PI3K）/Akt/ mammalian target of rapamycin （mTOR） activation.2,3 Rapamycin, with mTOR as a potential therapeutic target, has been studied in patients with hematologic malignancies. Here we report a case of refractory CML myeloid blast crisissuccessfully treated by the combination of rapamycin and imatinib.展开更多
基金Supported by Key Provincial Talents Program of Jiangsu(H201126)the Priority Academic Program Development of Jiangsu Higher Education Institutions(PAPD)
文摘HRONIC myeloid leukemia （CML） is characterized by the presence of the BCR/ABL fusion gene, which is the result of a reciprocal translo cation between chromosomes 9 and 22, calledPhiladelphia （Ph） chromosome. Imatinib mesylate （imatinib）, a specific small molecular inhibitor of BCR/ABL, could improve the prognosis of CML and is now the standard drug applied in all phases of this disease} Despite the efficacy of imatinib, the development of resistance and the persistence of minimal residual disease have seriously impaired the efficiency of this medicine. Resistance may develop through several different mechanisms, such as mutations in the Abl kinase domain, BCR/ABL overexpression, or compensatory phosphatidylinositol 3 kinase （PI3K）/Akt/ mammalian target of rapamycin （mTOR） activation.2,3 Rapamycin, with mTOR as a potential therapeutic target, has been studied in patients with hematologic malignancies. Here we report a case of refractory CML myeloid blast crisissuccessfully treated by the combination of rapamycin and imatinib.
