i3S-Institute for Research and Innovation in Health, University of Porto, Porto, Portugal.
Department of Gastroenterology, Centro Hospitalar e Universitário do Porto, Porto, Portugal.
Inflamm Bowel Dis. 2022 Jun 3;28(6):947-962. doi: 10.1093/ibd/izab291.
Colitis-associated cancer is a major complication of inflammatory bowel disease remaining an important clinical challenge in terms of diagnosis, screening, and prognosis. Inflammation is a driving factor both in inflammatory bowel disease and cancer, but the mechanism underlying the transition from colon inflammation to cancer remains to be defined. Dysregulation of mucosal glycosylation has been described as a key regulatory mechanism associated both with colon inflammation and colorectal cancer development. In this review, we discuss the major molecular mechanisms of colitis-associated cancer pathogenesis, highlighting the role of glycans expressed at gut epithelial cells, at lamina propria T cells, and in serum proteins in the regulation of intestinal inflammation and its progression to colon cancer, further discussing its potential clinical and therapeutic applications.
结肠炎相关癌症是炎症性肠病的主要并发症，在诊断、筛查和预后方面仍然是一个重要的临床挑战。炎症是炎症性肠病和癌症的一个驱动因素，但从结肠炎症到癌症的转变的机制仍有待确定。黏膜糖基化失调已被描述为与结肠炎症和结直肠癌发展都相关的关键调控机制。在这篇综述中，我们讨论了结肠炎相关癌症发病机制的主要分子机制，强调了在肠道上皮细胞、固有层 T 细胞和血清蛋白中表达的聚糖在调节肠道炎症及其进展为结肠癌中的作用，并进一步讨论了其潜在的临床和治疗应用。
