Title : A novel mechanism for imatinib mesylate (STI571) resistance in CML cell line KT-1: role of TC-PTP in modulating signals downstream from the BCR-ABL fusion protein.

Pub. Date : 2004 Nov

PMID : 15539083






5 Functional Relationships(s)
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1 A novel mechanism for imatinib mesylate (STI571) resistance in CML cell line KT-1: role of TC-PTP in modulating signals downstream from the BCR-ABL fusion protein. Imatinib Mesylate protein tyrosine phosphatase, non-receptor type 2 Mus musculus
2 Importantly, reconstitution of TC-PTP in KTR cells to levels found in parental KT-1 cells restored their sensitivity to imatinib mesylate as monitored by reduced proliferation and increased apoptosis. Imatinib Mesylate protein tyrosine phosphatase, non-receptor type 2 Mus musculus
3 CONCLUSIONS: We have demonstrated that forced expression of TC-PTP in imatinib mesylate-resistant KTR cells can restore sensitivity to imatinib mesylate. Imatinib Mesylate protein tyrosine phosphatase, non-receptor type 2 Mus musculus
4 CONCLUSIONS: We have demonstrated that forced expression of TC-PTP in imatinib mesylate-resistant KTR cells can restore sensitivity to imatinib mesylate. Imatinib Mesylate protein tyrosine phosphatase, non-receptor type 2 Mus musculus
5 Our studies indicate that loss of TC-PTP may represent a novel mechanism by which CML cells can acquire imatinib mesylate-resistance. Imatinib Mesylate protein tyrosine phosphatase, non-receptor type 2 Mus musculus