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干扰素在慢性粒细胞白血病治疗中的应用。

Use of interferon in the treatment of chronic myelogenous leukemia.

作者信息

Talpaz M

机构信息

Department of Medicine, University of Texas M.D. Anderson Cancer Center, Houston 77030.

出版信息

Semin Oncol. 1994 Dec;21(6 Suppl 14):3-7.

PMID:7992097
Abstract

In a series of studies spanning 14 years, investigators from M.D. Anderson Cancer Center (Houston, TX) documented the activity of interferon-alfa (IFN-alpha) in chronic myelogenous leukemia (CML). Beginning with partially purified IFN-alpha, we demonstrated that this biologic compound has clinical activity against CML, that some malignancies are resistant to IFN-alpha, and that the effect is selective whereby the malignant clone can be restored to normalcy. These observations were confirmed by us and others when larger quantities of IFN-alpha became available through recombinant DNA technology (rIFN-alpha). In contrast with our experience with chemotherapy, myelosuppression was not required for cytogenetic remission; this dissociation may be the basis for the selectivity of IFN-alpha against CML. Recently, another group demonstrated that patients randomized to receive rIFN-alpha 2a survived longer than those treated with standard hydroxyurea chemotherapy. New tests are needed to identify the subset of patients most likely to benefit from IFN-alpha therapy and to distinguish cytogenetic responders who are truly cured from those with minimal residual disease.

摘要

在一项历时14年的系列研究中,得克萨斯州休斯敦市MD安德森癌症中心的研究人员记录了干扰素-α(IFN-α)在慢性粒细胞白血病(CML)中的活性。从部分纯化的IFN-α开始,我们证明了这种生物化合物对CML具有临床活性,一些恶性肿瘤对IFN-α耐药,并且其作用具有选择性,恶性克隆可恢复正常。当通过重组DNA技术(rIFN-α)可获得大量IFN-α时,我们和其他研究人员证实了这些观察结果。与我们使用化疗的经验相比,细胞遗传学缓解并不需要骨髓抑制;这种分离可能是IFN-α对CML具有选择性的基础。最近,另一组研究表明,随机接受rIFN-α 2a治疗的患者比接受标准羟基脲化疗的患者存活时间更长。需要新的检测方法来识别最有可能从IFN-α治疗中获益的患者亚组,并区分真正治愈的细胞遗传学反应者和仅有微小残留疾病的患者。

相似文献

1
Use of interferon in the treatment of chronic myelogenous leukemia.干扰素在慢性粒细胞白血病治疗中的应用。
Semin Oncol. 1994 Dec;21(6 Suppl 14):3-7.
2
Multicenter prospective study of interferon-alpha and conventional chemotherapy versus bone marrow transplantation for newly diagnosed patients with chronic myelogenous leukemia. Kouseisho Leukemia Study Group.α干扰素与传统化疗对比骨髓移植治疗新诊断慢性粒细胞白血病患者的多中心前瞻性研究。厚生省白血病研究组
Int J Hematol. 2000 Aug;72(2):229-36.
3
Interferon alfa versus chemotherapy for chronic myeloid leukemia: a meta-analysis of seven randomized trials: Chronic Myeloid Leukemia Trialists' Collaborative Group.干扰素α与化疗治疗慢性髓性白血病的比较:七项随机试验的荟萃分析:慢性髓性白血病试验协作组
J Natl Cancer Inst. 1997 Nov 5;89(21):1616-20.
4
Chemotherapy and bone marrow transplantation in the treatment of chronic myelogenous leukemia.化疗和骨髓移植治疗慢性粒细胞白血病。
Semin Oncol. 1994 Dec;21(6 Suppl 14):8-13.
5
Biologic therapy of chronic myelogenous leukemia.
Oncology (Williston Park). 1987 Sep;1(7):35-40, 48-9, 52.
6
Interferon alpha in the treatment of chronic myelogenous leukemia.α干扰素治疗慢性粒细胞白血病
Arch Immunol Ther Exp (Warsz). 1998;46(6):347-53.
7
Prior treatment with alpha-interferon does not adversely affect the outcome of allogeneic BMT in chronic phase chronic myeloid leukemia.在慢性期慢性髓性白血病中,先前使用α-干扰素治疗不会对异基因骨髓移植的结果产生不利影响。
Haematologica. 1998 Mar;83(3):231-6.
8
A randomized study of intermediate as compared with high doses of interferon-alpha for chronic myeloid leukemia: no differences in cytogenetic responses.
Ann Hematol. 2003 Dec;82(12):750-8. doi: 10.1007/s00277-003-0724-z. Epub 2003 Sep 27.
9
[Interferon-alpha in chronic myeloid leukemia].[慢性髓性白血病中的干扰素-α]
Fortschr Med. 1997 Mar 30;115(9):30-4, 37-8.
10
[Treatment with lymphoblastoid alpha interferon in patients with chronic myeloid leukemia refractory to recombinant interferon alpha 2].用淋巴母细胞α干扰素治疗对重组α2干扰素难治的慢性髓性白血病患者
Sangre (Barc). 1998 Oct;43(5):443-6.

引用本文的文献

1
Expression of interferon consensus sequence binding protein (ICSBP) is downregulated in Bcr-Abl-induced murine chronic myelogenous leukemia-like disease, and forced coexpression of ICSBP inhibits Bcr-Abl-induced myeloproliferative disorder.干扰素共有序列结合蛋白(ICSBP)的表达在Bcr-Abl诱导的小鼠慢性粒细胞白血病样疾病中下调,并且ICSBP的强制共表达可抑制Bcr-Abl诱导的骨髓增殖性疾病。
Mol Cell Biol. 2000 Feb;20(4):1149-61. doi: 10.1128/MCB.20.4.1149-1161.2000.