Format

Send to

Choose Destination
Trends Immunol. 2013 Aug;34(8):379-89. doi: 10.1016/j.it.2013.03.008. Epub 2013 May 7.

MyD88 and its divergent toll in carcinogenesis.

Author information

1
Cancer and Inflammation Program, National Cancer Institute, Frederick, MD 217023, USA.

Abstract

Toll-like and interleukin-1 (IL-1) family receptors recognize microbial or endogenous ligands and inflammatory mediators, respectively, and with the exception of Toll-like receptor 3 (TLR3), signal via the adaptor molecule myeloid differentiation factor 88 (MyD88). MyD88 is involved in oncogene-induced cell intrinsic inflammation and in cancer-associated extrinsic inflammation, and as such MyD88 contributes to skin, liver, pancreatic, and colon carcinogenesis, as well as sarcomagenesis. MyD88 is also protective, for example in oncogenic virus carcinogenesis or, acting downstream of IL-18R to strengthen mucosal repair, in azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced colon carcinogenesis. Here, we discuss the mechanisms of the divergent effects of MyD88 and the balance of its protumor role in cancer-enhancing inflammation and immunity and its antitumor role in tissue homeostasis, repair, and immunity against the tumor or oncogenic pathogens.

KEYWORDS:

Toll-like receptors; cancer and inflammation; colon carcinogenesis; interleukin-1 family receptors; oncogene-induced inflammation; skin carcinogenesis

PMID:
23660392
PMCID:
PMC3847901
DOI:
10.1016/j.it.2013.03.008
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center