现在已经得到确认，癌症的生物学不仅受到恶性细胞的影响，也受到肿瘤微环境中其他成分的影响。长期以来，人们一直推测慢性炎症和纤维化参与了癌变过程。慢性炎症可以通过生长因子/细胞因子介导的细胞增殖、凋亡抵抗、免疫抑制以及自由基引起的氧化DNA损伤来促进肿瘤发生。纤维化可能会扰乱肿瘤微环境的动态，潜在地对正常上皮细胞的基因监控机制造成损害。在本综述中，我们将对与炎症和纤维化相关的多种疾病进行深入讨论，这些疾病与恶性肿瘤的风险增加有关。特别是，我们将全面概述由于炎症和/或纤维化引起的基质组成改变对肿瘤发生的影响。此外，我们还将讨论包括应用具有基质调控潜力的各种治疗药物以及针对某些炎症性疾病的靶向癌症筛查在减少癌症风险方面的策略。©2023作者。白师灯出版集团版权所有。

It is now well established that the biology of cancer is influenced by not only malignant cells but also other components of the tumour microenvironment. Chronic inflammation and fibrosis have long been postulated to be involved in carcinogenesis. Chronic inflammation can promote tumorigenesis via growth factor/cytokine-mediated cellular proliferation, apoptotic resistance, immunosuppression; and free-radical-induced oxidative deoxyribonucleic acid damage. Fibrosis could cause a perturbation in the dynamics of the tumour microenvironment, potentially damaging the genome surveillance machinery of normal epithelial cells. In this review, we will provide an in-depth discussion of various diseases characterised by inflammation and fibrosis that have been associated with an increased risk of malignancy. In particular, we will present a comprehensive overview of the impact of alterations in stromal composition on tumorigenesis, induced as a consequence of inflammation and/or fibrosis. Strategies including the application of various therapeutic agents with stromal manipulation potential and targeted cancer screening for certain inflammatory diseases which can reduce the risk of cancer will also be discussed.©The Author(s) 2023. Published by Baishideng Publishing Group Inc. All rights reserved.