Title : Contribution of BCR-ABL-independent activation of ERK1/2 to acquired imatinib resistance in K562 chronic myeloid leukemia cells.

Pub. Date : 2010 Jan

PMID : 19843070






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1 Contribution of BCR-ABL-independent activation of ERK1/2 to acquired imatinib resistance in K562 chronic myeloid leukemia cells. Imatinib Mesylate mitogen-activated protein kinase 3 Homo sapiens
2 In both cell lines, imatinib effectively reduced the phosphorylation of all the above, except ERK1/2, whose phosphorylation was, interestingly, only inhibited in the wild-type cells. Imatinib Mesylate mitogen-activated protein kinase 3 Homo sapiens
3 However, using an ERK1/2 inhibitor, U0126, we found that we could reduce phospho-ERK1/2 levels in K562/R cells and restore their sensitivity to imatinib. Imatinib Mesylate mitogen-activated protein kinase 3 Homo sapiens
4 However, using an ERK1/2 inhibitor, U0126, we found that we could reduce phospho-ERK1/2 levels in K562/R cells and restore their sensitivity to imatinib. Imatinib Mesylate mitogen-activated protein kinase 3 Homo sapiens
5 Taken together, we conclude that the BCR-ABL-independent activation of ERK1/2 contributes to imatinib resistance in K562/R cells, and that ERK1/2 could be a target for the treatment of CML patients whose imatinib resistance is due to this mechanism. Imatinib Mesylate mitogen-activated protein kinase 3 Homo sapiens
6 Taken together, we conclude that the BCR-ABL-independent activation of ERK1/2 contributes to imatinib resistance in K562/R cells, and that ERK1/2 could be a target for the treatment of CML patients whose imatinib resistance is due to this mechanism. Imatinib Mesylate mitogen-activated protein kinase 3 Homo sapiens
7 Taken together, we conclude that the BCR-ABL-independent activation of ERK1/2 contributes to imatinib resistance in K562/R cells, and that ERK1/2 could be a target for the treatment of CML patients whose imatinib resistance is due to this mechanism. Imatinib Mesylate mitogen-activated protein kinase 3 Homo sapiens