Division of Hematology, Department of Cellular Biotechnologies and Hematology, Sapienza University of Rome, Italy.
Haematologica. 2011 Oct;96(10):1548-51. doi: 10.3324/haematol.2011.043786. Epub 2011 Jul 26.
The CD33 antigen is expressed on the blast cells of most cases of acute myeloid leukemia and represents a suitable tumor-associated target antigen for antibody-based therapies. The aim of this study was to investigate the relationship between the CD33 levels quantified by mean fluorescence intensity and antibody binding capacity, and the presence/absence of NPM1 and FLT3 gene mutations in 99 newly diagnosed acute myeloid leukemia cases. The CD33 intensity evaluated as mean fluorescence intensity and antibody binding capacity was significantly higher in the NPM1-mutated acute myeloid leukemia cases compared to the NPM1-unmutated cases (P=0.0001 and P=0.0088, respectively). On the contrary, FLT3 gene mutations did not influence the levels of CD33 expression on the leukemic cells. These results establish a rational basis for the therapeutic use of anti-CD33 antibodies in NPM1-mutated acute myeloid leukemia patients.
CD33 抗原在大多数急性髓细胞白血病的原始细胞上表达,是抗体为基础的治疗的合适的肿瘤相关靶抗原。本研究旨在探讨 99 例新诊断的急性髓细胞白血病患者中,CD33 水平(以平均荧光强度量化)与抗体结合能力与 NPM1 和 FLT3 基因突变的关系。与 NPM1 未突变的病例相比,NPM1 突变的急性髓细胞白血病病例的 CD33 强度(以平均荧光强度评估)和抗体结合能力显著更高(P=0.0001 和 P=0.0088)。相反,FLT3 基因突变并不影响白血病细胞上 CD33 的表达水平。这些结果为 NPM1 突变的急性髓细胞白血病患者使用抗 CD33 抗体治疗提供了合理的依据。