Department of Internal Medicine, Cleveland Clinic, Cleveland, OH, USA.
Am J Gastroenterol. 2011 Apr;106(4):719-30. doi: 10.1038/ajg.2011.51. Epub 2011 Mar 8.
Chronic inflammatory diseases, depending upon the duration and severity, are frequently associated with an increased risk of developing cancer. A classic paradigm is the enhanced risk of colorectal cancer (CRC) in patients with inflammatory bowel disease (IBD). Carcinogenesis is a multifactorial process that involves accumulation of genetic defects, protein modification, and cell-matrix interaction. In this review, we discuss aspects of chronic inflammation in IBD that influence the development of CRC and highlight the key molecular mediators involved in this process. Also, we identify potential targets that could facilitate earlier detection of dysplasia. The targeted manipulation of specific molecules or pathways could provide opportunities for the development of therapeutic and chemopreventive interventions, which may prove effective in arresting the progression of colitis-associated cancer (CAC), with clinical implications.
慢性炎症性疾病，根据其持续时间和严重程度，常与癌症发生风险增加相关。一个典型的范例是炎症性肠病（IBD）患者结直肠癌（CRC）风险增加。癌变是一个多因素过程，涉及遗传缺陷的积累、蛋白质修饰和细胞基质相互作用。在这篇综述中，我们讨论了 IBD 中的慢性炎症如何影响 CRC 的发生，并强调了涉及这一过程的关键分子介质。此外，我们确定了一些潜在的靶点，这些靶点可以促进对异型增生的早期检测。对特定分子或途径的靶向操作可以为治疗和化学预防干预的发展提供机会，这可能有助于阻止结肠炎相关癌症（CAC）的进展，具有临床意义。
