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Inhibition of methylcholanthrene-induced carcinogenesis by an interferon gamma receptor-dependent foreign body reaction

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Official URL:https://doi.org/10.1084/jem.20011887
PubMed:View item in PubMed
Creators Name:Qin, Z. and Kim, H.J. and Hemme, J. and Blankenstein, T.
Journal Title:Journal of Experimental Medicine
Journal Abbreviation:J Exp Med
Volume:195
Number:11
Page Range:1479-1490
Date:3 June 2002
Keywords:Inflammation, Tissue Damage, Tissue Repair, Encapsulation, Immune Surveillance, Animals, Mice
Abstract:The foreign body reaction is one of the oldest host defense mechanisms against tissue damage which involves inflammation, scarring, and encapsulation. The chemical carcinogen methylcholanthrene (MCA) induces fibrosarcoma and tissue damage in parallel at the injection site. Tumor development induced by MCA but not due to p53-deficiency is increased in interferon-{gamma} receptor (IFN-{gamma}R)-deficient mice. In the absence of IFN-{gamma}R, MCA diffusion and DNA damage of surrounding cells is increased. Locally produced IFN-{gamma} induces the formation of a fibrotic capsule. Encapsulated MCA can persist virtually life-long in mice without inducing tumors. Together, the foreign body reaction against MCA prevents malignant transformation, probably by reducing DNA damage. This mechanism is more efficient in the presence of IFN-{gamma}R. Our results indicates that inflammation and scarring, both suspected to contribute to malignancy, prevent cancer in certain situations.
ISSN:0022-1007
Publisher:Rockefeller University Press (U.S.A.)
Item Type:Article

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