Molecular Pathogenesis of Cancer Induced by Inflammatory Bowel Disease
A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Biological Factors".
Deadline for manuscript submissions: 31 August 2026 | Viewed by 2
Special Issue Editor
Special Issue Information
Dear Colleagues,
This Special Issue focuses on cancer risk and the distinct genomic landscapes of inflammatory bowel disease-associated cancer (IBD-AC), highlighting mechanisms that diverge from conventional sporadic colorectal carcinogenesis. Chronic inflammation, epithelial injury and aberrant DNA damage responses shape a unique evolutionary trajectory in IBD-AC, with early genomic instability and non-canonical driver events.
A central theme of this issue is the oncogenic role of missense mutant p53, which is frequently acquired early in IBD-associated neoplasia. Rather than acting solely as a loss-of-function tumor suppressor, mutant p53 exhibits gain-of-function activities that reprogram transcriptional networks, promote epithelial survival under inflammatory stress, and facilitate malignant progression. Particular emphasis is placed on the mutant p53–FOSL1–MCL1 axis, a signaling pathway that enhances cell survival, resistance to apoptosis and clonal expansion in inflamed mucosa.
Collectively, the contributions in this issue integrate genomic, molecular and pathological insights to advance our understanding of IBD-associated carcinogenesis and to identify potential biomarkers and therapeutic vulnerabilities driven by mutant p53 signaling. This work underscores the need for disease-specific models of cancer-risk assessment and targeted intervention in patients with chronic inflammatory bowel disease.
Prof. Dr. Guang-Yu Yang
Guest Editor
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Keywords
- cancer
- inflammatory bowel disease
- genomic
- pathogenesis
- biomarkers
- pathway
- therapeutic strategies
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