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接受伊马替尼或α干扰素治疗的真性红细胞增多症患者的最小分子反应

Minimal molecular response in polycythemia vera patients treated with imatinib or interferon alpha.

作者信息

Jones Amy V, Silver Richard T, Waghorn Katherine, Curtis Claire, Kreil Sebastian, Zoi Katerina, Hochhaus Andreas, Oscier David, Metzgeroth Georgia, Lengfelder Eva, Reiter Andreas, Chase Andrew J, Cross Nicholas C P

机构信息

Wessex Regional Genetics Laboratory, Salisbury District Hospital, Salisbury SP2 8BJ, United Kingdom.

出版信息

Blood. 2006 Apr 15;107(8):3339-41. doi: 10.1182/blood-2005-09-3917. Epub 2005 Dec 13.

Abstract

Imatinib and recombinant interferon alpha (rIFNalpha) can induce remission in polycythemia vera (PV) patients, but gauging the depth of responses has not been possible due to lack of a specific disease marker. We found that patients undergoing imatinib (n = 14) or rIFNalpha (n = 7) therapy remained strongly positive for V617F JAK2, although there was a significant reduction in the median percentage of mutant alleles that correlated with hematologic response (P = .001). Furthermore, individuals who achieved complete hematologic remission had lower levels of V617F than those who did not (P = .001). Of 9 imatinib-treated cases for whom pretreatment samples were available, 7 with no or partial hematologic responses showed a marginal increase (median, 1.2-fold; range, 1.0-1.5) in the percentage of V617F alleles on treatment, whereas the 2 patients who achieved complete hematologic remission showed a 2- to 3-fold reduction. Our data indicate that, although PV patients may benefit from imatinib or rIFNalpha, molecular responses are relatively modest.

摘要

伊马替尼和重组干扰素α(rIFNα)可诱导真性红细胞增多症(PV)患者缓解,但由于缺乏特异性疾病标志物,一直无法评估缓解的深度。我们发现,接受伊马替尼治疗(n = 14)或rIFNα治疗(n = 7)的患者V617F JAK2仍呈强阳性,尽管突变等位基因的中位数百分比有显著降低,且这与血液学反应相关(P = .001)。此外,实现完全血液学缓解的个体的V617F水平低于未实现完全血液学缓解的个体(P = .001)。在9例有治疗前样本的伊马替尼治疗病例中,7例无血液学反应或部分血液学反应的患者在治疗时V617F等位基因百分比有小幅增加(中位数为1.2倍;范围为1.0 - 1.5),而2例实现完全血液学缓解的患者则有2至3倍的降低。我们的数据表明,尽管PV患者可能从伊马替尼或rIFNα中获益,但分子反应相对较小。

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