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细胞凋亡和细胞生长抑制作为干扰素的抗肿瘤效应功能。

Apoptosis and cell growth inhibition as antitumor effector functions of interferons.

作者信息

Strander H

机构信息

Research Laboratory of Radiumhemmet, Karolinska Hospital, Stockholm, Sweden.

出版信息

Med Oncol. 2001;18(1):3-14. doi: 10.1385/mo:18:1:3.

DOI:10.1385/mo:18:1:3
PMID:11778967
Abstract

Since their introduction to the clinic some 30 yr ago, interferons (IFNs) have become standard therapy for a range of disorders, including malignant and benign tumors as well as various viral diseases. Although IFNs will induce remissions in some patients with cancer, they are of no benefit or, at best, lead only to minor improvements in the great majority of patients with malignant disease. One of the great challenges of IFN research is to understand the multiple ways by which IFNs influence the behavior of tumor cells and to identify the factors that underlie the resistance of some tumors to IFNs. This review is written with a focus on two anticellular effects of IFN, inhibition of proliferation and induction of apoptosis, possible mechanisms underlying the antitumor action of IFN. In addition, possible reasons for IFN tumor cell resistance are also discussed.

摘要

大约30年前干扰素(IFNs)引入临床以来,已成为一系列疾病的标准治疗方法,包括恶性和良性肿瘤以及各种病毒性疾病。尽管干扰素能使一些癌症患者病情缓解,但对绝大多数恶性疾病患者并无益处,或至多只能带来轻微改善。干扰素研究的一大挑战是了解干扰素影响肿瘤细胞行为的多种方式,并确定某些肿瘤对干扰素耐药的潜在因素。本综述重点阐述干扰素的两种抗细胞效应,即抑制增殖和诱导凋亡,这可能是干扰素抗肿瘤作用的潜在机制。此外,还讨论了干扰素肿瘤细胞耐药的可能原因。

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Apoptosis and cell growth inhibition as antitumor effector functions of interferons.细胞凋亡和细胞生长抑制作为干扰素的抗肿瘤效应功能。
Med Oncol. 2001;18(1):3-14. doi: 10.1385/mo:18:1:3.
2
Interferon and malignant disease--how does it work and why doesn't it always?干扰素与恶性疾病——它是如何起作用的,为何并非总能起效?
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[Interferons in hemato-cancerology].[血液肿瘤学中的干扰素]
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Why do so many cancer patients fail to respond to interferon therapy?
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J Clin Oncol. 2006 Aug 10;24(23):3771-9. doi: 10.1200/JCO.2005.03.4074. Epub 2006 Jun 26.

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Comparative proteomics as a tool for identifying specific alterations within interferon response pathways in human glioblastoma multiforme cells.比较蛋白质组学作为一种工具,用于鉴定多形性胶质母细胞瘤细胞中干扰素反应途径内的特定改变。
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Type-I-interferons in infection and cancer: Unanticipated dynamics with therapeutic implications.

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10
Cell proliferation and survival induced by Toll-like receptors is antagonized by type I IFNs.Toll样受体诱导的细胞增殖和存活受到I型干扰素的拮抗。
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The genes of interferons and interferon-related factors: localization and relationships with chromosome aberrations in cancer.干扰素及干扰素相关因子的基因:定位及其与癌症中染色体畸变的关系
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Cytokines and JAK-STAT signaling.细胞因子与JAK-STAT信号传导
Exp Cell Res. 1999 Nov 25;253(1):7-14. doi: 10.1006/excr.1999.4670.
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Interferon-alpha inhibits proliferation in human T lymphocytes by abrogation of interleukin 2-induced changes in cell cycle-regulatory proteins.α干扰素通过消除白细胞介素2诱导的细胞周期调节蛋白变化来抑制人T淋巴细胞的增殖。
Cell Growth Differ. 1999 Aug;10(8):575-82.
8
Interferon gamma induces the expression of p21waf-1 and arrests macrophage cell cycle, preventing induction of apoptosis.γ干扰素可诱导p21waf-1的表达并使巨噬细胞的细胞周期停滞,从而防止细胞凋亡的诱导。
Immunity. 1999 Jul;11(1):103-13. doi: 10.1016/s1074-7613(00)80085-0.
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DAP-kinase participates in TNF-alpha- and Fas-induced apoptosis and its function requires the death domain.DAP激酶参与肿瘤坏死因子-α和Fas诱导的细胞凋亡,其功能需要死亡结构域。
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10
Molecular mechanisms underlying interferon-alpha-induced G0/G1 arrest: CKI-mediated regulation of G1 Cdk-complexes and activation of pocket proteins.α干扰素诱导G0/G1期阻滞的分子机制:细胞周期蛋白依赖性激酶抑制剂介导的G1期细胞周期蛋白依赖性激酶复合物调控及口袋蛋白激活。
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