Yamamoto-Furusho Jesus K, Gutierrez-Herrera Fausto D
Inflammatory Bowel Disease Clinic, Department of Gastroenterology, Instituto Nacional de Ciencias Medicas y Nutricion Salvador Zubiran, Ciudad de México 14080, Mexico.
Cells. 2025 Jan 22;14(3):162. doi: 10.3390/cells14030162.
Inflammatory bowel diseases have long been recognized as entities with a higher risk of colorectal cancer. An increasing amount of information has been published regarding ulcerative colitis-associated colorectal cancer and its unique mechanisms in recent decades, as ulcerative colitis constitutes a chronic process characterized by cycles of activity and remission of unpredictable durations and intensities; cumulative genomic alterations occur during active disease and mucosal healing, resulting in a special sequence of events different to the events associated with sporadic colorectal cancer. The recognition of the core differences between sporadic colorectal cancer and colitis-associated cancer is of great importance to understand and guide the directions in which new research could be performed, and how it could be applied to current clinical scenarios. A DSS/AOM murine model has allowed for a better understanding of the pathogenic mechanisms in colitis-associated cancer, as it is currently the closest model to this unique scenario. In this review, we provide a summary of the main molecular mechanisms and the clinical aspects of colitis-associated cancer in ulcerative colitis.
炎症性肠病长期以来一直被认为是患结直肠癌风险较高的疾病。近几十年来,关于溃疡性结肠炎相关结直肠癌及其独特机制的信息越来越多,因为溃疡性结肠炎是一个慢性过程,其特点是活动期和缓解期的持续时间和强度不可预测;在疾病活动期和黏膜愈合过程中会发生累积的基因组改变,从而导致一系列与散发性结直肠癌不同的特殊事件。认识散发性结直肠癌和结肠炎相关癌之间的核心差异对于理解和指导新研究的开展方向以及如何将其应用于当前临床情况非常重要。DSS/AOM小鼠模型有助于更好地理解结肠炎相关癌的致病机制,因为它是目前最接近这种独特情况的模型。在本综述中,我们总结了溃疡性结肠炎中结肠炎相关癌的主要分子机制和临床方面。