Current CML therapy: progress and dilemma
Rarely has progress in treatment of leukemia been as dramatic and convincing as with the BCR-ABL tyrosine kinase inhibitor imatinib.1 Imatinib induces remissions of CML as fast as hydroxyurea, achieves rates of cytogenetic remissions that by far exceed those induced by interferon α and has a toxicit...
Gespeichert in:
| 1. Verfasser: | |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
23 May 2003
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| In: |
Leukemia
Year: 2003, Jahrgang: 17, Heft: 6, Pages: 1010-1012 |
| ISSN: | 1476-5551 |
| DOI: | 10.1038/sj.leu.2402951 |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1038/sj.leu.2402951 Verlag, lizenzpflichtig, Volltext: https://www.nature.com/articles/2402951 
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| Verfasserangaben: | R. Hehlmann |
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| 520 | |a Rarely has progress in treatment of leukemia been as dramatic and convincing as with the BCR-ABL tyrosine kinase inhibitor imatinib.1 Imatinib induces remissions of CML as fast as hydroxyurea, achieves rates of cytogenetic remissions that by far exceed those induced by interferon α and has a toxicity profile as favourable as that of hydroxyurea and much superior to that of interferon α.2 In addition, the causal approach of this new drug, which may well serve as a model for new treatment modalities in other neoplasias is reassuring. | ||
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