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Impact of BCR-ABL mutations on patients with chronic myeloid leukemia

Therapies that target BCR-ABL in chronic myeloid leukemia, including imatinib, dasatinib and nilotinib, have dramatically improved patient outcome. BCR-ABL mutations, however, contribute to treatment resistance by disrupting drug contact sites or causing conformational changes thus making contact si...

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Hauptverfasser: Hochhaus, Andreas (VerfasserIn) , La Rosée, Paul (VerfasserIn) , Müller, Martin Christian (VerfasserIn) , Ernst, Thomas (VerfasserIn) , Cross, Nicholas C.P. (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: 15 Jan 2011
In: Cell cycle
Year: 2011, Jahrgang: 10, Heft: 2, Pages: 250-260
ISSN:1551-4005
DOI:10.4161/cc.10.2.14537
Online-Zugang:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.4161/cc.10.2.14537
Volltext
Verfasserangaben:Andreas Hochhaus, Paul La Rosée, Martin C. Müller, Thomas Ernst, Nicholas C.P. Cross
Beschreibung
Zusammenfassung:Therapies that target BCR-ABL in chronic myeloid leukemia, including imatinib, dasatinib and nilotinib, have dramatically improved patient outcome. BCR-ABL mutations, however, contribute to treatment resistance by disrupting drug contact sites or causing conformational changes thus making contact sites inaccessible. Clinical data indicate that developing BCR-ABL mutations during imatinib treatment is predictive for shorter progression-free survival, and that outcomes may depend on mutation type or location. In vitro, dasatinib and nilotinib inhibit most imatinib-resistant BCR-ABL mutations, except for T315I. In clinical studies, other mutations associated with treatment resistance include V299L, T315A, and F317I/L for dasatinib and Y253F/H, E255K/V, and F359C/V for nilotinib. Evaluating patients with clinical signs of resistance for BCR-ABL mutations is an important component of disease monitoring, potentially facilitating selection of subsequent therapy. First-line treatment with dasatinib or nilotinib instead of imatinib may reduce emergence of resistance but novel agents are needed to overcome the problematic T315I mutation.
Beschreibung:Gesehen am 12.09.2022
Beschreibung:Online Resource
ISSN:1551-4005
DOI:10.4161/cc.10.2.14537

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