Editorial
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World J Gastroenterol. Sep 28, 2014; 20(36): 12713-12721
Published online Sep 28, 2014. doi: 10.3748/wjg.v20.i36.12713
Contribution of TLR signaling to the pathogenesis of colitis-associated cancer in inflammatory bowel disease
Ferenc Sipos, István Fűri, Miklós Constantinovits, Zsolt Tulassay, Györgyi Műzes
Ferenc Sipos, István Fűri, Miklós Constantinovits, Györgyi Műzes, 2nd Department of Internal Medicine, Semmelweis University, 1088 Budapest, Hungary
Zsolt Tulassay, Molecular Medicine Research Unit, Hungarian Academy of Sciences, 1088 Budapest, Hungary
Author contributions: Sipos F, Fűri I, Constantinovits M and Műzes G contributed to the writing and editing of this paper; Tulassay Z revised the manuscript.
Correspondence to: Györgyi Műzes, MD, CSc, PhD, 2nd Department of Internal Medicine, Semmelweis University, Szentkirályi Street 46, 1088 Budapest, Hungary. muzes.gyorgyi@med.semmelweis-univ.hu
Telephone: +36-1-2660926 Fax: +36-1-2660816
Received: February 28, 2014
Revised: April 28, 2014
Accepted: May 23, 2014
Published online: September 28, 2014
Core Tip

Core tip: Colorectal cancers arising in inflammatory bowel disease patients are considered typical examples of inflammation-associated cancers. The exact role of Toll-like receptor (TLR)-signaling in colitis-associated cancer initiation and development is conflicting. Here we aimed to summarize recent data on the contribution of TLR-mediated immune responses to inflamation-related colonic carcinogenesis.