Stem cell and kinase activity-independent pathway in resistance of leukaemia to BCR-ABL kinase inhibitors.
Stem cell and kinase activity-independent pathway in resistance of leukaemia to BCR-ABL kinase inhibitors.
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DOI：
10.1111/j.1582-4934.2007.00108.x
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发表时间：
2007-11
影响因子：
5.3
通讯作者：
Li D
中科院分区：
文献类型：
--
作者：
Li S;Li D
BCR-ABL tyrosine kinase inhibitors, such as imatinib (Gleevec) are highly effective in treating human Philadelphia chromosome-positive (Ph+) chronic myeloid leukaemia (CML) in chronic phase but not in terminal acute phase; acquired drug resistance caused mainly by the development of BCR-ABL kinase domain mutations prevents cure of the leukaemia. In addition, imatinib is ineffective in treating Ph+ B-cell acute lymphoblastic leukaemia (B-ALL) and CML blast crisis, even in the absence of the kinase domain mutations. This type of drug resistance that is unrelated to BCR-ABL kinase domain mutations is caused by the insensitivity of leukaemic stem cells to kinase inhibitors such as imatinib and dasatinib, and by activation of a newly-identified signalling pathway involving SRC kinases that are independent of BCR-ABL kinase activity for activation. This SRC pathway is essential for leukaemic cells to survive imatinib treatment and for CML transition to lymphoid blast crisis. Apart from BCR-ABL and SRC kinases, stem cell pathways must also be targeted for curative therapy of Ph+ leukaemia.
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影响因子：
50.3
作者：
Dierov, J;Dierova, R;Carroll, M
通讯作者：
Carroll, M
DOI：
10.1073/pnas.88.14.6293
发表时间：
1991-07-01
影响因子：
11.1
作者：
FEINSTEIN, E;CIMINO, G;CANAANI, E
通讯作者：
CANAANI, E
影响因子：
20.3
作者：
Holtz, MS;Slovak, ML;Bhatia, R
通讯作者：
Bhatia, R
影响因子：
20.3
作者：
Giles, Francis J.;Cortes, Jorge;Freedman, Steven J.
通讯作者：
Freedman, Steven J.
影响因子：
20.3
作者：
Elrick, LJ;Jorgensen, HG;Holyoake, TL
通讯作者：
Holyoake, TL