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Interferon alpha for treatment of chronic myeloid leukemia

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  1. The α7 nicotinic acetylcholine receptor complex: one, two or multiple drug targets?

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  2. Interferon-α treatment in systemic mastocytosis

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  3. Interferon-alpha in the treatment of Philadelphia-negative chronic myeloproliferative neoplasms. Status and perspectives

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  4. Interferon treatment in patients with hypereosinophilia

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  5. Rational targeting of the urokinase receptor (uPAR): development of antagonists and non-invasive imaging probes

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  1. Genomic profiling of a randomized trial of interferon-α vs hydroxyurea in MPN reveals mutation-specific responses

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  2. Abnormal eosinophil count at CLL diagnosis correlates with shorter treatment free survival

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  3. Ruxolitinib and interferon-α2 combination therapy for patients with polycythemia vera or myelofibrosis: a phase II study

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  4. Association of the blood eosinophil count with end-organ symptoms

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Treatment of chronic myeloid leukemia (CML) with interferon-alpha (IFN-α) was introduced in the early 1980s. Several clinical trials showed a survival advantage for patients treated with IFN-α compared to conventional chemotherapy. Some patients achieved longstanding complete cytogenetic remissions (i.e. >2 log tumor mass reduction). IFN-α was then recommended as first line medical treatment until 2001. The mechanism of this anti-leukemic effect is not clear, although IFN-α has many effects of potential relevance on stem cells and immunology. There is no evidence of benefit for high dose (in practice a maximally tolerated dose) compared with lower dose IFN-α. When IFN-α is combined with other drugs, we advice lower dose IFN to minimize toxicity and increase treatment adherence and duration. IFN-α combined with Ara-C moderately improves treatment outcome. Imatinib, a tyrosine kinase inhibitor, is now first line treatment for CML, but two large randomized studies show improved outcome when pegylated IFN-α is added to the treatment with imatinib. One explanation for this might be that IFN-α, contrary to imatinib, stimulates the quiescent stem cells to proliferate and thereby potentially increases sensitivity to imatinib. Although imatinib and other tyrosine kinase inhibitors are very efficient, they are rarely curative. IFN-α could be included in curatively aimed combination treatment protocols and thus still be an important element in CML treatment.
Original languageEnglish
JournalCurrent Drug Targets
Volume12
Issue number3
Pages (from-to)420-8
Number of pages9
ISSN1389-4501
Publication statusPublished - 1 Mar 2011

ID: 32236770