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Multhoff, G. ; Molls, M.* ; Radons, J.*

Chronic inflammation in cancer development.

Front. Immunol. 2:98 (2012)
Verlagsversion Volltext DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Chronic inflammatory mediators exert pleiotropic effects in the development of cancer. On the one hand, inflammation favors carcinogenesis, malignant transformation, tumor growth, invasion, and metastatic spread; on the other hand inflammation can stimulate immune effector mechanisms that might limit tumor growth. The link between cancer and inflammation depends on intrinsic and extrinsic pathways. Both pathways result in the activation of transcription factors such as NF-κB, STAT-3, and HIF-1 and in accumulation of tumorigenic factors in tumor and microenvironment. STAT-3 and NF-κB interact at multiple levels and thereby boost tumor-associated inflammation which can suppress anti-tumor immune responses. These factors also promote tumor growth, progression, and metastatic spread. IL-1, IL-6, TNF, and PGHS-2 are key mediators of an inflammatory milieu by modulating the expression of tumor-promoting factors. In this review we concentrate on the crucial role of pro-inflammatory mediators in inflammation-driven carcinogenesis and outline molecular mechanisms of IL-1 signaling in tumors. In addition, we elucidate the dual roles of stress proteins as danger signals in the development of anti-cancer immunity and anti-apoptotic functions.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter inflammation; carcinogenesis; tumorigenic factors; heat shock proteins; NF-κB,;STAT-3; IL-1
Sprache englisch
Veröffentlichungsjahr 2012
HGF-Berichtsjahr 0
ISSN (print) / ISBN 1664-3224
e-ISSN 1664-3224
Quellenangaben Band: 2, Heft: JAN, Seiten: , Artikelnummer: 98 Supplement: ,
Verlag Frontiers
Begutachtungsstatus Peer reviewed
POF Topic(s) 30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease
Forschungsfeld(er) Enabling and Novel Technologies
PSP-Element(e) G-521400-001
PubMed ID 22566887
Scopus ID 84863601838
Erfassungsdatum 2012-02-15