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Blood, 15 February 2006, Vol. 107, No. 4, pp. 1582-1590.
Prepublished online as a Blood First Edition Paper on October 25, 2005; DOI 10.1182/blood-2005-06-2318.
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NEOPLASIA
Coordination of intrinsic, extrinsic, and endoplasmic reticulum-mediated apoptosis by imatinib mesylate combined with arsenic trioxide in chronic myeloid leukemia
Yanzhi Du,
Kankan Wang,
Hai Fang,
Junmin Li,
Dakai Xiao,
Peizheng Zheng,
Yulong Chen,
Huiyong Fan,
Xiaoling Pan,
Chunjun Zhao,
Qinghua Zhang,
Sandrine Imbeaud,
Esther Graudens,
Eric Eveno,
Charles Auffray,
Saijuan Chen,
Zhu Chen, and
Ji Zhang
From the State Key Laboratory of Medical Genomics and Shanghai Institute of Hematology, Ruijin Hospital, School of Medicine of Shanghai Jiao Tong University (SM-SJTU; formerly Shanghai Second Medical University [SSMU]), Shanghai, China; Institute of Health Sciences, SM-SJTU, and Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China; Genexpress, Functional Genomics and Systems Biology for Health, CNRS and Pierre et Marie Curie University-Paris VI, Villejuif, France; and Samuel Waxman Cancer Research Foundation Laboratory in SM-SJTU, Shanghai, China.
A treatment strategy that combines arsenic trioxide (ATO) with the tyrosine kinase inhibitor imatinib mesylate (STI571, Gleevec) appears to induce markedly more cell apoptosis than imatinib mesylate alone in chronic myeloid leukemia (CML). To understand the mechanisms underlying the synergistic/additive action of these agents, we applied cDNA microarrays, component plane presentation integrated self-organizing map (CPP-SOM), and methods of protein biochemistry to study cell apoptosis induced by imatinib mesylate, ATO, and the combination of the 2 agents in the CML cell line K562. Numerous features with temporospatial relationships were revealed, indicating the coordinated regulation of molecular networks from various aspects of proapoptotic and apoptotic activities in CML. Imatinib mesylate appears to induce mainly the intrinsic pathway of cell apoptosis, whereas ATO induces the endoplasmic reticulum (ER) stress-mediated pathway of cell apoptosis, and the combination of the 2 agents seems to more effectively induce the intrinsic, extrinsic, and ER stress-mediated pathways of cell apoptosis, which results in a more effective and efficient induction of programmed cell death in K562 cells. This finding appears to be supported also by data derived from bone marrow cells of 2 patients with CML, one in chronic phase and the other in blast-crisis phase of the disease.
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