Ablation of TNF or lymphotoxin signaling and the frequency of spontaneous tumors in p53-deficient mice

被引：14

作者：

Kuprash, Dmitry V. ^{[1
]}

Qin, Zhihai ^{[1
,7
]}

Ito, Daisuke ^{[3
,4
]}

Grivennikov, Sergei I. ^{[1
,3
,4
]}

Abe, Koichiro ^{[3
,4
]}

Drutskaya, Ludmila N. ^{[3
,4
]}

Blankenstein, Thomas ^{[2
,5
]}

Nedospasov, Sergel A. ^{[1
,6
]}

机构：

[1] Russian Acad Sci, VA Engelhardt Mol Biol Inst, Moscow 119991, Russia

[2] Charite, Inst Immunol, D-12200 Berlin, Germany

[3] NCI, Mol Immunoregulat Lab, Ctr Canc Res, Frederick, MD 21702 USA

[4] NCI, Basic Res Lab, Ctr Canc Res, Frederick, MD 21702 USA

[5] Max Delbruck Ctr Mol Med, D-13092 Berlin, Germany

[6] German Rheumatism Res Ctr DRFZ, D-10117 Berlin, Germany

[7] Chinese Acad Sci, Inst Biophys, Beijing 100101, Peoples R China

来源：

CANCER LETTERS | 2008年 / 268卷 / 01期

基金：

美国国家卫生研究院;

关键词：

cytokine and chemokine biology; p53/mdm2; tumor immunology; knockout mice;

D O I：

10.1016/j.canlet.2008.03.023

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

TNF plays diverse and contrasting roles in cancer, promoting skin carcinogenesis and metastasis, but also possessing potent antitumor effects in mice. TNF via TNFR1 axis induces NF kappa B, and may contribute to inflammation-facilitated neoplasia. On the other hand, lymphomas are cited as rare complications of anti-TNF therapy in humans. In order to address possible modulating role of TNF and of a related cytokine, LT alpha, in spontaneous tumorigenesis, we compared mice with p53-TNF, p53-LT alpha, p53-TNFR1 and p53-TNF-LT combined deficiencies. Unexpectedly, neither of these mice showed significant modulation of their survival or shift in the spectrum of emerging tumors, as compared to p53-deficient mice, arguing against direct link between TNF blockade and lymphoma development. (C) 2008 Elsevier Ireland Ltd. All rights reserved.

引用

页码：70 / 75

页数：6

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