| Literature DB >> 26153874 |
Yanhong Shi1, Zhenfeng Li2, Wei Zheng2, Xia Liu2, Chenyi Sun2, Jann-Birger Laugsand3, Zhanju Liu4, Guanglin Cui5.
Abstract
It is believed that chronic inflammation as seen in patients with ulcerative colitis significantly increases the colorectal cancer (CRC) risk and functions as the main driving force for the development of colitis associated CRC. Recently, increasing evidences suggest that inflammation is also involved in the processing of sporadic CRCs that mostly develop from the preformed adenomas through a long-term progression. Within the adenoma/CRC tumor microenvironment, high dense immunocytes with significant phenotypic and functional changes have been observed. These cells might produce high level of inflammatory mediators and then affect the adenoma-cancer transition. In this review, we summarize the update on altered phenotypes and inflammatory mediators within the tumor microenvironment from the adenomatous stage to the cancerous stage, and discuss the significance of inflammatory mediators as biomarkers in predicating the progression from the premalignant adenoma lesion to the sporadic CRC lesion and the potential as therapeutic targets.Entities:
Keywords: Adenoma; Carcinogenesis; Colorectum; Immunosuppressive; Immunosurveillance
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Year: 2015 PMID: 26153874 DOI: 10.1016/j.imbio.2015.06.003
Source DB: PubMed Journal: Immunobiology ISSN: 0171-2985 Impact factor: 3.144