BCR-ABL independence and LYN kinase overexpression in chronic myelogenous leukemia cells selected for resistance to STI571.
By N. Donato, J. Wu, J. Stapley, G. Gallick, Hui-Kuan Lin, R. Arlinghaus, M. Talpaz. Blood, 2003
699 citations recorded by the source corpus.
Subfields: Genetics, Hematology, Rheumatology
View Paper: https://www.semanticscholar.org/paper/d0056e062a8057ee6d42c2cc551c3c6b31e48ca7
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Citations in the corpus
- The Cdk inhibitor p27 in human cancer: prognostic potential and relevance to anticancer therapy (2008, background): “Interestingly, imatinib resistance can emerge due to overexpression of LY”
- Bcr-Abl kinase domain mutations, drug resistance, and the road to a cure for chronic myeloid leukemia. (2007, background): “4 allele does not always explain clinical resistance to imatinib.(13,14) Here we review Bcr-Abl mutations in the context of CML pathogenesis and speculate on future prospects in”
- Src kinases as therapeutic targets for cancer (2009, background): “These results suggest that SFKs are required for BCR-ABL-positive B-lymphoblastic leukemia but not for CML”
- Src family kinases in tumor progression and metastasis (2003, neutral): “, [171]).”
- The structure of Dasatinib (BMS-354825) bound to activated ABL kinase domain elucidates its inhibitory activity against imatinib-resistant ABL mutants. (2006, background): “ABL dependent and BCR-ABL independent, such as overexpression of other tyrosine kinases, may also occur (9, 10).”
- In vitro activity of Bcr-Abl inhibitors AMN107 and BMS-354825 against clinically relevant imatinib-resistant Abl kinase domain mutants. (2005, methodology): “Similar assays with the Src family kinases Src and Lyn (17, 18), which is expressed at high levels in primary CML blast crisis cells, showed that BMS-354825 is a potent inhibitor of these Src family kinases, whereas imatinib and AMN107 are inactive against these kinases (Table 1).”