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Blood, 15 September 2006, Vol. 108, No. 6, pp. 2037-2040.
Prepublished online as a Blood First Edition Paper on May 18, 2006; DOI 10.1182/blood-2006-03-009860.
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Submitted March 14, 2006
Accepted May 5, 2006
High molecular response rate of polycythemia vera patients treated with pegylated interferon alpha-2a
Jean-Jacques Kiladjian, Bruno Cassinat, Pascal Turlure, Nathalie Cambier, Murielle Roussel, Sylvia Bellucci, Marie-Laurence Menot, Gerald Massonnet, Jean-Luc Dutel, Kamel Ghomari, Philippe Rousselot, Marie-Jose Grange, Yasmina Chait, William Vainchenker, Nathalie Parquet, Lina Abdelkader-Aljassem, Jean-Francois Bernard, Jean-Didier Rain, Sylvie Chevret, Christine Chomienne, and Pierre Fenaux*
AP-HP, Hopital Avicenne
AP-HP, Hopital Saint-Louis
CHU Dupuytren, Service d'Hematologie
CHRU de Lille, Hopital Huriez
AP-HP, Hopital Lariboisiere
CH de Beauvais
CH de Versailles
AP-HP, Hopital Bichat
CH de Montfermeil
INSERM U.790
CH de Chartres
Hopital Avicenne/Paris 13 University
* Corresponding author; email: pierre.fenaux{at}avc.aphp.fr.
V617F JAK2 mutation is a reliable molecular marker of polycythemia vera (PV), potentially useful to monitor the effect of treatments in this disease. In a phase 2 study of peg-IFN -2a in PV, we performed prospective sequential quantitative evaluation of the percentage of mutated JAK2 allele (%V617F) by real-time PCR. %V617F decreased in 24 of 27 (89%) treated patients, from a mean of 49% to a mean of 27% (mean decrease of 44%; P<0.001), and no evidence for a plateau was observed. In one patient, mutant JAK2 was no longer detectable after 12 months. In 3 patients homozygous for the mutation, reappearance of 50% of wild type allele was observed during treatment. Those results seem to confirm the hypothesis that IFN preferentially targets the malignant clone in PV, and show that %V617F assessment using a quantitative method may provide the first tool to monitor minimal residual disease in PV.
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