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13-顺式维甲酸和全反式维甲酸对慢性粒细胞白血病细胞具有抗增殖作用,并且在体外联合治疗后可增强α干扰素的抗增殖效力。

13cis- and all-trans retinoic acid have antiproliferative effects on CML cells and render IFN alpha antiproliferative potency after combined treatment in vitro.

作者信息

Benthin M, Dallmann I, Atzpodien J

机构信息

Medizinische Hochschule Hannover, Germany.

出版信息

Cancer Biother Radiopharm. 2001 Aug;16(4):323-31. doi: 10.1089/108497801753131408.

DOI:10.1089/108497801753131408
PMID:11603003
Abstract

The treatment of CML with IFN alpha is limited due to resistance against this substance. Recent studies with different cells than chronic myelogenous leukemic cells revealed a synergistic effect of a combined use of Retinoids (RA) and IFN alpha. The purpose of the study was to detect possible interactions of IFN alpha and RA in CML considering also the effect of the BCR-ABL gene-product. Therefore, we investigated three CML cell lines in their proliferation after incubation with IFN alpha and Retinoids alone and in combination. We measured low susceptibility to IFN alpha but a marked influence of the Retinoids. In combination, the growth inhibition was enhanced potentially in response to an increased efficacy of IFN alpha. Even solely, ineffective concentrations of both substances lead to decreased proliferation.

摘要

由于对α干扰素产生耐药性,用其治疗慢性粒细胞白血病(CML)受到限制。最近针对不同于慢性粒细胞白血病细胞的其他细胞进行的研究显示,维甲酸(RA)与α干扰素联合使用具有协同效应。本研究的目的是探讨α干扰素与RA在CML中可能存在的相互作用,同时考虑BCR-ABL基因产物的作用。因此,我们研究了三种CML细胞系在单独及联合使用α干扰素和维甲酸孵育后的增殖情况。我们发现这些细胞系对α干扰素敏感性较低,但维甲酸有显著影响。联合使用时,由于α干扰素疗效增加,潜在地增强了生长抑制作用。甚至单独使用时,两种物质的无效浓度也会导致增殖减少。

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引用本文的文献

1
[Effects of 13-cis-retinoic acid combined with interferon-α2b in mantle cell lymphoma cell lines (Jeko-1) ].13-顺式维甲酸联合干扰素-α2b对套细胞淋巴瘤细胞系(Jeko-1)的作用
Zhonghua Xue Ye Xue Za Zhi. 2017 Jan 14;38(1):50-54. doi: 10.3760/cma.j.issn.0253-2727.2017.01.011.
2
[Anti-tumor effects of 13-cis-retinoic acid combined with interferon α-2b in animal model of mantle cell lymphoma].13-顺式维甲酸联合干扰素α-2b在套细胞淋巴瘤动物模型中的抗肿瘤作用
Zhonghua Xue Ye Xue Za Zhi. 2016 Sep 14;37(9):784-789. doi: 10.3760/cma.j.issn.0253-2727.2016.09.011.