Activated toll-like receptor (TLR) signaling pathway has been reported in several endocrine neoplasms and has been found to be associated with the upregulation of proin-fiammatory cytokines. These cytokines are widely known as critical mediators of tumorigenesis. The stimulation of antitumor immunity through the activation of the TLR pathway can lead to the inhibition of the carcinogenesis process. However, TLRs have been considered as putative therapeutic target in various human cancers. A chronic inflammation in the absence of infection induces oxidative stress, DNA damage, and tissue damage promoting tumorigenesis. Thus, TLRs can be viewed as having a double-edged sword function.
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