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α干扰素恢复慢性粒细胞白血病中的非克隆性造血。

Restoration of nonclonal hematopoiesis in chronic myelogenous leukemia with interferon alpha.

作者信息

Egert G, Kanz L, Löhr G W, Fauser A A

机构信息

Department of Hematology, Medical School, Albert-Ludwigs-University, Freiburg, Federal Republic of Germany.

出版信息

Blut. 1990 May;60(5):282-6. doi: 10.1007/BF01736229.

DOI:10.1007/BF01736229
PMID:2350591
Abstract

Studies have shown that recombinant human alpha interferon (rIFN alpha) inhibits the growth of colonies of multipotential stem cells from human bone marrow. This report demonstrates that rIFN alpha inhibits the growth of such colonies from the bone marrow of patients with chronic myelogenous leukemia (CML) to a greater extent than from bone marrow of healthy individuals. It also shows that T lymphocyte colonies subcloned with interleukin 2 (IL-2) from CML mixed colonies were inhibited more by rIFN alpha than were similar colonies subcultured from normal mixed colonies. The report demonstrates that the Ph' chromosome is present in such T cell colonies subcultured from CML mixed colonies. When mixed colonies were grown from CML bone marrow in the presence of rIFN alpha, Ph' negative colonies were observed, whereas no such Ph' negative mixed colonies grew from a similar number of bone marrow cells incubated without rIFN alpha. These observations confirm that T lymphocytes derived from bone marrow stem cells are from the CML clone, and that the inhibition of growth of Ph' positive colonies, by rIFN alpha permits the growth of residual normal stem cells. The disappearance of the Ph-chromosome in subclones of T lymphocytes supports the notion of nonclonal hematopoiesis in patients with CML.

摘要

研究表明,重组人α干扰素(rIFNα)可抑制人骨髓多能干细胞集落的生长。本报告表明,rIFNα对慢性粒细胞白血病(CML)患者骨髓中此类集落生长的抑制作用比对健康个体骨髓的抑制作用更强。报告还显示,从CML混合集落中用白细胞介素2(IL-2)亚克隆的T淋巴细胞集落比从正常混合集落传代培养的类似集落更易被rIFNα抑制。该报告表明,从CML混合集落传代培养的此类T细胞集落中存在Ph'染色体。当在rIFNα存在的情况下从CML骨髓中培养混合集落时,观察到了Ph'阴性集落,而在没有rIFNα的情况下培养相同数量的骨髓细胞则未长出此类Ph'阴性混合集落。这些观察结果证实,源自骨髓干细胞的T淋巴细胞来自CML克隆,并且rIFNα对Ph'阳性集落生长的抑制作用使得残留的正常干细胞得以生长。T淋巴细胞亚克隆中Ph染色体的消失支持了CML患者非克隆性造血的观点。

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2
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引用本文的文献

1
Interferon in chronic myeloid leukemia. A workshop report.慢性粒细胞白血病中的干扰素。一份研讨会报告。
Ann Hematol. 1993 Aug;67(2):101-6. doi: 10.1007/BF01788134.

本文引用的文献

1
Chronic myelogenous leukemia--new concepts (first of two parts).慢性粒细胞白血病——新概念(两部分中的第一部分)
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Recloned colonies positive for T-cell-associated antigens derived from mixed hemopoietic colonies (CFU-GEMM)1.从混合造血集落(CFU-GEMM)1衍生而来的、对T细胞相关抗原有阳性反应的再克隆集落。
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A cellular oncogene is translocated to the Philadelphia chromosome in chronic myelocytic leukaemia.
在慢性粒细胞白血病中,一种细胞癌基因易位至费城染色体。
Nature. 1982 Dec 23;300(5894):765-7. doi: 10.1038/300765a0.
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A method for obtaining high quality chromosome preparations from single hemopoietic colonies on a routine basis.一种常规从单个造血集落获取高质量染色体标本的方法。
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Restoration of nonclonal hematopoiesis in chronic myelogenous leukemia (CML) following a chemotherapy-induced loss of the Ph1 chromosome.化疗诱导Ph1染色体缺失后慢性粒细胞白血病(CML)中非克隆性造血的恢复
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6
Cytogenetic studies of early myeloid progenitor compartments in Ph1-positive chronic myeloid leukemia. II. Long-term culture reveals the persistence of Ph1-negative progenitors in treated as well as newly diagnosed patients.Ph1阳性慢性髓性白血病早期髓系祖细胞区室的细胞遗传学研究。II. 长期培养显示,在接受治疗的患者以及新诊断的患者中均存在Ph1阴性祖细胞。
Blood. 1984 May;63(5):1172-7.
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Philadelphia chromosomal breakpoints are clustered within a limited region, bcr, on chromosome 22.费城染色体断点聚集在22号染色体上一个有限的区域——bcr内。
Cell. 1984 Jan;36(1):93-9. doi: 10.1016/0092-8674(84)90077-1.
8
An 8-kilobase abl RNA transcript in chronic myelogenous leukemia.慢性粒细胞白血病中的一种8千碱基abl RNA转录本。
Proc Natl Acad Sci U S A. 1984 Sep;81(18):5648-52. doi: 10.1073/pnas.81.18.5648.
9
Letter: A new consistent chromosomal abnormality in chronic myelogenous leukaemia identified by quinacrine fluorescence and Giemsa staining.信件:通过喹吖因荧光和吉姆萨染色鉴定出慢性粒细胞白血病中一种新的一致染色体异常。
Nature. 1973 Jun 1;243(5405):290-3. doi: 10.1038/243290a0.
10
T cells and probably B cells arise from the malignant clone in chronic myelogenous leukemia.T细胞以及可能的B细胞源自慢性粒细胞白血病中的恶性克隆。
J Clin Invest. 1985 Mar;75(3):1080-2. doi: 10.1172/JCI111771.