Dan Wan-Yue, Zhou Guan-Zhou, Peng Li-Hua, Pan Fei
Department of Gastroenterology and Hepatology, The First Medical Center, Chinese PLA General Hospital, Beijing 100853, China.
Medical School, Nankai University, Tianjin 300071, China.
World J Gastrointest Oncol. 2023 Aug 15;15(8):1317-1331. doi: 10.4251/wjgo.v15.i8.1317.
Colitis-associated colorectal cancer (CAC) is defined as a specific cluster of colorectal cancers that develop as a result of prolonged colitis in patients with inflammatory bowel disease (IBD). Patients with IBD, including ulcerative colitis and Crohn's disease, are known to have an increased risk of developing CAC. Although the incidence of CAC has significantly decreased over the past few decades, individuals with CAC have increased mortality compared to individuals with sporadic colorectal cancer, and the incidence of CAC increases with duration. Chronic inflammation is generally recognized as a major contributor to the pathogenesis of CAC. CAC has been shown to progress from colitis to dysplasia and finally to carcinoma. Accumulating evidence suggests that multiple immune-mediated pathways, DNA damage pathways, and pathogens are involved in the pathogenesis of CAC. Over the past decade, there has been an increasing effort to develop clinical approaches that could help improve outcomes for CAC patients. Colonoscopic surveillance plays an important role in reducing the risk of advanced and interval cancers. It is generally recommended that CAC patients undergo endoscopic removal or colectomy. This review summarizes the current understanding of CAC, particularly its epidemiology, mechanisms, and management. It focuses on the mechanisms that contribute to the development of CAC, covering advances in genomics, immunology, and the microbiome; presents evidence for management strategies, including endoscopy and colectomy; and discusses new strategies to interfere with the process and development of CAC. These scientific findings will pave the way for the management of CAC in the near future.
结肠炎相关结直肠癌(CAC)被定义为炎症性肠病(IBD)患者因长期结肠炎而发生的一组特定的结直肠癌。已知患有IBD(包括溃疡性结肠炎和克罗恩病)的患者发生CAC的风险增加。尽管在过去几十年中CAC的发病率显著下降,但与散发性结直肠癌患者相比,CAC患者的死亡率更高,且CAC的发病率随病程延长而增加。慢性炎症通常被认为是CAC发病机制的主要促成因素。已证明CAC从结肠炎发展为发育异常,最终发展为癌。越来越多的证据表明,多种免疫介导途径、DNA损伤途径和病原体参与了CAC的发病机制。在过去十年中,人们越来越努力开发有助于改善CAC患者预后的临床方法。结肠镜监测在降低晚期癌和间期癌风险方面发挥着重要作用。通常建议CAC患者接受内镜下切除或结肠切除术。本综述总结了目前对CAC的认识,特别是其流行病学、发病机制和管理。它重点关注促成CAC发生发展的机制,涵盖基因组学、免疫学和微生物组学方面的进展;提供管理策略(包括内镜检查和结肠切除术)的证据;并讨论干扰CAC进程和发展的新策略。这些科学发现将为不久的将来CAC的管理铺平道路。