Colitis-associated neoplasia: molecular basis and clinical translation

被引：51

作者：

Foersch, Sebastian ^{[1
]}

Neurath, Markus F. ^{[1
]}

机构：

[1] FAU Erlangen Nurnberg, Dept Med 1, D-91054 Erlangen, Germany

来源：

CELLULAR AND MOLECULAR LIFE SCIENCES | 2014年 / 71卷 / 18期

关键词：

Inflammatory bowel disease; Ulcerative colitis; Crohn's disease; Colitis-associated cancer; Colorectal carcinoma; Endoscopy; Chemoprevention; INFLAMMATORY-BOWEL-DISEASE; NF-KAPPA-B; COLORECTAL-CANCER PREVENTION; BETA-CATENIN ACTIVATION; BLOCKING TNF-ALPHA; REGULATORY T-CELLS; LONG-TERM SAFETY; K-RAS MUTATION; ULCERATIVE-COLITIS; COLON-CANCER;

D O I：

10.1007/s00018-014-1636-x

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

Crohn's disease and ulcerative colitis are both associated with an increased risk of inflammation-associated colorectal carcinoma. Colitis-associated cancer (CAC) is one of the most important causes for morbidity and mortality in patients with inflammatory bowel diseases (IBD). Colitis-associated neoplasia distinctly differs from sporadic colorectal cancer in its biology and the underlying mechanisms. This review discusses the molecular mechanisms of CAC and summarizes the most important genetic alterations and signaling pathways involved in inflammatory carcinogenesis. Then, clinical translation is evaluated by discussing new endoscopic techniques and their contribution to surveillance and early detection of CAC. Last, we briefly address different types of concepts for prevention (i.e., anti-inflammatory therapeutics) and treatment (i.e., surgical intervention) of CAC and give an outlook on this important aspect of IBD.

引用

页码：3523 / 3535

页数：13

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