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Adv Cancer Res. 2015;128:173-96. doi: 10.1016/bs.acr.2015.04.014. Epub 2015 May 28.

Tumor-Elicited Inflammation and Colorectal Cancer.

Author information

1
Departments of Pharmacology and Pathology, Laboratory of Gene Regulation and Signal Transduction, School of Medicine, University of California, San Diego, California, USA.
2
Departments of Pharmacology and Pathology, Laboratory of Gene Regulation and Signal Transduction, School of Medicine, University of California, San Diego, California, USA. Electronic address: karinoffice@ucsd.edu.

Abstract

The link between chronic inflammation and cancer has long been suspected, due to the pioneering work of Rudolf Virchow over 150 years ago. Yet the causal relationship between inflammation and cancer was only deciphered in the past decade or so, using animal models of various cancers. Up to 20% of all human cancers result from chronic inflammation and persistent infections. Proinflammatory cytokines and tumor-infiltrating myeloid and immune cells play critical roles in almost every developmental stages of inflammation-induced cancers, from initiation, promotion, and progression to malignant metastasis. However, even in cancers with no preceding inflammation, inflammatory cells infiltrate tumor stroma and contribute to cancer development. Such "tumor-elicited inflammation" further emphasizes the importance of inflammation in different types of cancers, including that of the colon. In this review, we summarize our current knowledge of the function and induction mechanisms of inflammatory cytokines during colorectal cancer development, and hope to provide insight into the development of novel anticancer therapies by modulating tumor-elicited inflammation.

KEYWORDS:

Colorectal cancer; IL-10; IL-17; IL-21; IL-22; IL-23; IL-6; Inflammation; TGF-β; TNF

PMID:
26216633
DOI:
10.1016/bs.acr.2015.04.014
[Indexed for MEDLINE]

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