Delgado-Gonzalez P, Quiroz-Reyes AG, Simental-Mendía MA, Loaiza-Gutiérrez VL, Garza-Treviño EN. Inflammation-driven carcinogenesis in ulcerative colitis: Molecular and immunological pathways. World J Gastrointest Oncol 2026; 18(11): 125273 [DOI: 10.4251/wjgo.125273]
Corresponding Author of This Article
Paulina Delgado-Gonzalez, Research Assistant Professor, Department of Biochemistry and Molecular Medicine, School of Medicine, Universidad Autonoma de Nuevo Leon, s/n, Monterrey 64460, Nuevo León, Mexico. paulina.delgadogn@uanl.edu.mx
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
review-article
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastrointest Oncol. Nov 15, 2026; 18(11): 125273 Published online Nov 15, 2026. doi: 10.4251/wjgo.125273
Inflammation-driven carcinogenesis in ulcerative colitis: Molecular and immunological pathways
Paulina Delgado-Gonzalez, Adriana G Quiroz-Reyes, Mario A Simental-Mendía, Verónica L Loaiza-Gutiérrez, Elsa N Garza-Treviño
Paulina Delgado-Gonzalez, Adriana G Quiroz-Reyes, Verónica L Loaiza-Gutiérrez, Elsa N Garza-Treviño, Department of Biochemistry and Molecular Medicine, School of Medicine, Universidad Autonoma de Nuevo Leon, Monterrey 64460, Nuevo León, Mexico
Mario A Simental-Mendía, Orthopedic Trauma Service, University Hospital Dr. José Eleuterio González, School of Medicine, Universidad Autonoma de Nuevo Leon, Monterrey 64460, Nuevo León, Mexico
Co-corresponding authors: Paulina Delgado-Gonzalez and Elsa N Garza-Treviño.
Author contributions: Delgado-González P supervised and directed the development of the manuscript; Quiroz-Reyes AG designed the tables and figures, conducted the literature analysis, and contributed to manuscript writing; Simental-Mendía MA analyzed the literature and contributed to manuscript writing Loaiza-Gutiérrez VL drafted the manuscript and designed the tables; Garza-Treviño EN critically reviewed, edited, and revised the manuscript; Delgado-González P and Garza-Treviño EN they contributed equally to this article, they are the co-corresponding authors of this manuscript; and all authors read and approved the final version of the manuscript
AI contribution statement: Portions of this manuscript were edited using AI tools solely for language refinement. The authors carefully reviewed and verified all AI-assisted outputs and take full responsibility for the scientific content of the manuscript.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Corresponding author: Paulina Delgado-Gonzalez, Research Assistant Professor, Department of Biochemistry and Molecular Medicine, School of Medicine, Universidad Autonoma de Nuevo Leon, s/n, Monterrey 64460, Nuevo León, Mexico. paulina.delgadogn@uanl.edu.mx
Received: July 3, 2026 Revised: July 21, 2026 Accepted: August 18, 2026 Published online: November 15, 2026 Processing time: 117 Days and 4.3 Hours
Abstract
Ulcerative colitis (UC) is a chronic inflammatory bowel disorder resulting from a genetic predisposition, environmental factors, and immune system dysfunction. Chronic mucosal inflammation is an established precursor of colitis-associated colorectal cancer; however, the molecular transition from persistent inflammation to neoplasia remains unclear. The pathogenesis of UC involves disruption of the intestinal barrier, resulting in dysregulated innate immune responses mediated by toll-like receptor signaling and NOD-like receptor family pyrin domain containing 3 inflammasome activation, followed by polarized adaptive responses mediated by T helper 2 and T helper 17 cells. Intestinal dysbiosis further influences immunity by facilitating DNA damage through oxidative stress and metabolic alterations. Mechanisms of immune evasion, including regulatory T-cell dysfunction and the activation of anti-apoptotic pathways such as Janus kinase/signal transducer and activator of transcription and nuclear factor kappa-light-chain-enhancer of activated B cells, perpetuate chronic inflammation. This pro-inflammatory environment, characterized by interleukin-6 and tumor necrosis factor alpha signaling, promotes genomic instability and establishes oncogenic conditions favorable for gastrointestinal malignancies. The transition from UC to cancer is sustained by microbe-induced inflammation and immune evasion. This review aims to synthesize current knowledge of the immunological and inflammatory mechanisms in UC, highlighting the functions of innate and adaptive immunity, dysbiosis, oxidative stress, and immune evasion, while also addressing how these findings contribute to biomarker identification and personalized therapeutic approaches in gastrointestinal oncology.
Core Tip: Chronic inflammation in ulcerative colitis disrupts immune balance and gut microbiota, leading to reactive oxygen species production and driving molecular changes that foster colorectal cancer like cell growth, anti-apoptosis. This article synthesizes immunological, inflammatory, and molecular mechanisms in ulcerative colitis-associated carcinogenesis highlights risk factors such dysbiosis, biomarker identification, genomic instability, immune evasion and therapeutic implications for cancer prevention, while outlining future research directions to improve diagnostics and treatment.
