The risk of developing colorectal cancer (CRC) is increased in ulcerative colitis patients compared to the general population. This increased risk results from the state of chronic inflammation, a well-known tumour-promoting condition. This review explores the pathologic and molecular characteristics of colitis-associated colon cancer (CAC), emphasizing the distinct features from sporadic CRC. We focus on the key signalling pathways involved in the transition to CAC, highlighting the emerging role of alternative splicing in these processes, namely on how inflammation-induced alternative splicing can significantly contribute to the increased CRC risk observed among UC patients. This review calls for more transcriptomic studies to elucidate the molecular mechanisms through which inflammation-induced alternative splicing drives CAC pathogenesis. A better understanding of these splicing events is crucial as they may reveal novel biomarkers for disease progression and have the potential to target changes in alternative splicing as a therapeutic strategy.
与普通人群相比，溃疡性结肠炎患者罹患结直肠癌的风险显著增高。这种风险增加源于慢性炎症状态——一种已知的肿瘤促进条件。本综述探讨了结肠炎相关结肠癌的病理学与分子特征，重点阐述其与散发性结直肠癌的差异特征。我们聚焦于参与结肠炎相关结肠癌转化的关键信号通路，特别关注可变剪接在这些过程中的新兴作用，即炎症诱导的可变剪接如何显著增加溃疡性结肠炎患者的结直肠癌风险。本综述呼吁开展更多转录组学研究，以阐明炎症诱导的可变剪接驱动结肠炎相关结肠癌发病的分子机制。深入理解这些剪接事件至关重要，因为它们可能揭示疾病进展的新型生物标志物，并有望成为靶向可变剪接变化的治疗策略。
肿瘤(癌症)患者之家