Cure8 research brief
People with ulcerative colitis face a higher colorectal cancer risk driven in part by chronic inflammation; this review explains the molecular and immune mechanisms behind that risk and highlights biomarkers and microbiome factors that could affect prevention and surveillance.
Patients with long-standing UC, gastroenterologists, colorectal surgeons, and researchers focused on IBD-related cancer risk and biomarkers.
This review article summarizes molecular and immunological mechanisms that link chronic inflammation in ulcerative colitis (UC) to colorectal cancer development, highlighting roles for dysbiosis, oxidative stress, genomic instability, immune evasion, and biomarker identification.
The authors synthesize current research on how persistent mucosal inflammation promotes reactive oxygen species, DNA damage, altered cell survival pathways, and changes in the tumor microenvironment that can favor carcinogenesis in UC.
The paper also discusses the potential for microbial shifts (bowel dysbiosis) and immune pathway alterations to contribute to risk, and the implications for surveillance and prevention strategies. The review is presented as an invited, peer-reviewed manuscript in World Journal of Gastrointestinal Oncology and is available open access.
Article is a peer-reviewed review in press; it synthesizes published research rather than presenting new clinical trial data. Use it for background and research insight, not as a source of practice-changing evidence.
Review the original publication for the complete reporting, methods, and context.
This Cure8 brief is based on source text from the linked article. Cure8 is informational only and is not a substitute for professional medical advice, diagnosis, or treatment.
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