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- W2046194647 abstract "A minority of patients treated with imatinib are either refractory to imatinib or eventually relapse. Relapse frequently depends on re-emergence of BCR-ABL kinase activity but may also indicate BCR-ABL-independent disease progression. Over 90 point mutations coding for single amino acid substitutions in the BCR-ABL kinase domain have been isolated from CML patients resistant to imatinib treatment. These mutations affect amino acids involved in imatinib binding or in regulatory regions of the BCR-ABL kinase domain, resulting in decreased sensitivity to imatinib while retaining aberrant kinase activity. The early detection of BCR-ABL mutants during therapy may aid in risk stratification as well as molecular-based treatment decisions. Therapeutic strategies of imatinib resistant disease include novel tyrosine kinase inhibitors with activity against imatinib-resistant mutations and/or with inhibition of alternative pathways, dose escalation to optimise imatinib levels, treatment interruption to stop selection of resistant cells and allogeneic stem cell transplantation in eligible patients." @default.
- W2046194647 created "2016-06-24" @default.
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- W2046194647 date "2009-09-01" @default.
- W2046194647 modified "2023-09-30" @default.
- W2046194647 title "Cause and management of therapy resistance" @default.
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- W2046194647 doi "https://doi.org/10.1016/j.beha.2009.05.004" @default.
- W2046194647 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19959087" @default.
- W2046194647 hasPublicationYear "2009" @default.
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