Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh, UK.
NHS Lothian Edinburgh IBD Unit, Western General Hospital, UK.
J Crohns Colitis. 2021 Dec 18;15(12):2131-2141. doi: 10.1093/ecco-jcc/jjab102.
The cumulative impact of chronic inflammation in patients with inflammatory bowel diseases predisposes to the development of inflammatory bowel disease-associated colorectal cancer [IBD-CRC]. Inflammation can induce mutagenesis, and the relapsing-remitting nature of this inflammation, together with epithelial regeneration, may exert selective pressure accelerating carcinogenesis. The molecular pathogenesis of IBD-CRC, termed the 'inflammation-dysplasia-carcinoma' sequence, is well described. However, the immunopathogenesis of IBD-CRC is less well understood. The impact of novel immunosuppressive therapies, which aim to achieve deep remission, is mostly unknown. Therefore, this timely review summarizes the clinical context of IBD-CRC, outlines the molecular and immunological basis of disease pathogenesis, and considers the impact of novel biological therapies.
慢性炎症对炎症性肠病患者的累积影响易导致炎症性肠病相关结直肠癌(IBD-CRC)的发生。炎症可诱导突变,这种炎症的反复发作性与上皮细胞再生一起,可能产生选择性压力,加速癌变。IBD-CRC 的分子发病机制,即“炎症-异型增生-癌”序列,已有很好的描述。然而,IBD-CRC 的免疫发病机制还不太清楚。旨在实现深度缓解的新型免疫抑制疗法的影响大多未知。因此,本及时综述总结了 IBD-CRC 的临床背景,概述了疾病发病机制的分子和免疫学基础,并考虑了新型生物疗法的影响。