Imatinib mesylate resistance through BCR-ABL independence in chronic myelogenous leukemia

被引:190
作者
Donato, NJ
Wu, JY
Stapley, J
Lin, H
Arlinghaus, R
Aggarwal, B
Shishodin, S
Albitar, M
Hayes, K
Kantarjian, H
Talpaz, M
机构
[1] Univ Texas, MD Anderson Canc Ctr, Dept Bioimmunotherapy, Houston, TX 77030 USA
[2] Univ Texas, MD Anderson Canc Ctr, Dept Mol Pathol, Houston, TX 77030 USA
[3] Univ Texas, MD Anderson Canc Ctr, Dept Hematopathol, Houston, TX 77030 USA
[4] Univ Texas, MD Anderson Canc Ctr, Dept Cytogenet, Houston, TX 77030 USA
[5] Univ Texas, MD Anderson Canc Ctr, Dept Leukemia, Houston, TX 77030 USA
关键词
D O I
10.1158/0008-5472.CAN-03-1484
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Imatinib mesylate (IM) binds to the BCR-ABL protein, inhibiting its kinase activity and effectively controlling diseases driven by this kinase. IM resistance has been associated with kinase mutations or increased BCR-ABL expression. However, disease progression may be mediated by other mechanisms that render tumor cells independent of BCR-ABL. To demonstrate this potential, IM-resistant cells were found in chronic myelogenous leukemia patients with continuous BCR-ABL gene expression but undetectable BCR-ABL protein expression. These cells were unresponsive to IM and acquired BCR-ABL-independent signaling characteristics. IM resistance in some patients may be mediated through loss of kinase target dependence.
引用
收藏
页码:672 / 677
页数:6
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