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Mig,即由γ干扰素诱导产生的单核因子,可在体内促进肿瘤坏死。

Mig, the monokine induced by interferon-gamma, promotes tumor necrosis in vivo.

作者信息

Sgadari C, Farber J M, Angiolillo A L, Liao F, Teruya-Feldstein J, Burd P R, Yao L, Gupta G, Kanegane C, Tosato G

机构信息

Center for Biologics Evaluation and Research, Bethesda, MD 20892, USA.

出版信息

Blood. 1997 Apr 15;89(8):2635-43.

PMID:9108380
Abstract

Mig, the monokine induced by interferon-gamma, is a CXC chemokine active as a chemoattractant for activated T cells. Mig is related functionally to interferon-inducible protein 10 (IP-10), with which it shares a receptor, CXCR3. Previously, IP-10 was found to have antitumor activity in vivo. In the present study, murine Mig RNA was found to be expressed at higher levels in regressing Burkitt's lymphoma tumors established in nude mice compared with progressively growing tumors. Daily inoculations of purified recombinant human Mig into Burkitt's tumors growing subcutaneously in nude mice consistently caused tumor necrosis associated with extensive vascular damage. These effects were indistinguishable from those produced by intratumor inoculations of Burkitt's tumors with IP-10. These results support the notion that Mig, like IP-10, has antitumor activity in vivo.

摘要

Mig是由γ干扰素诱导产生的单核因子,是一种CXC趋化因子,对活化的T细胞具有趋化活性。Mig在功能上与干扰素诱导蛋白10(IP-10)相关,二者共享受体CXCR3。此前发现IP-10在体内具有抗肿瘤活性。在本研究中,与逐渐生长的肿瘤相比,在裸鼠中建立的正在消退的伯基特淋巴瘤肿瘤中,小鼠Mig RNA的表达水平更高。每天将纯化的重组人Mig接种到裸鼠皮下生长的伯基特肿瘤中,持续导致与广泛血管损伤相关的肿瘤坏死。这些效应与用IP-10对伯基特肿瘤进行瘤内接种所产生的效应没有区别。这些结果支持了Mig与IP-10一样在体内具有抗肿瘤活性这一观点。

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