ArticleGastroenterology2016
Whole-Exome Sequencing Analyses of Inflammatory Bowel Disease-Associated Colorectal Cancers.
Article in Gastroenterology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 160 papers, 3 of them syntheses that pooled it.
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Who cites it
160 citing papers in PubMed, 3 syntheses or guidelines pooled it, 263 citations in OpenAlex.
- Long-Term Outcomes After Colorectal Surgery in Patients with Ulcerative Colitis-Associated Colorectal Cancer Versus Sporadic Colorectal Cancer.Annals of surgical oncology · 2022Pooled it
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- Integrated clinicogenomic analysis reveals the evolution and metastatic tropisms of advanced colorectal cancer.Cancer cell · 2026Article
- Loss of SATB2 is associated with MUC16 upregulation in the invasive component of colitis-associated colorectal carcinoma.Virchows Archiv : an international journal of pathology · 2026Article
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- Pathophysiology of colitis-associated colorectal cancer.Nature reviews. Gastroenterology & hepatology · 2026Review
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- Dendritic cell-liposome conjugates reverse immunosuppressive tumor microenvironment for inhibiting colitis-associated colorectal cancer.Acta pharmacologica Sinica · 2026Article
- RHOA at the intersection of inflammation-driven and sporadic colorectal cancer.Frontiers in immunology · 2026Review
- Lactylation-Related Genes in Ulcerative Colitis: A Multiomics Mendelian Randomization Study for Therapeutic Target Discovery.Human mutation · 2026Article
- Japanese Society for Cancer of the Colon and Rectum (JSCCR) Guidelines 2024 for the Clinical Practice of Inflammatory Bowel Disease-Associated Intestinal Neoplasia (English Version).Journal of the anus, rectum and colon · 2026Review
- Sessile Serrated Lesions in Inflammatory Bowel Disease: Hidden Players in Colitis-Associated Colorectal Cancer?Journal of clinical medicine · 2025Review
- Nutrition, Environment, and Genetics in Colorectal Cancer. Epigenetics and Possible Future Perspective.Current nutrition reports · 2025Review
- Navigating Neoplasm Risk in Inflammatory Bowel Disease and Primary Sclerosing Cholangitis.Cancers · 2025Review
- Interface integrity in septin protofilaments is maintained by an arginine residue conserved from yeast to man.Molecular biology of the cell · 2025Article
- Article
- Article
- Review
- Article
100 more citing papers are in PubMed but not listed here.
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Authors and funding
17 authors at 4 institutions in 1 country.
Funding
Abstract
BACKGROUND &
aimsA long duration of inflammatory bowel disease (IBD) increases the risk for colorectal cancer. Mutation analysis of limited numbers of genes has indicated that colorectal tumors that develop in patients with IBD differ from those of patients without IBD. We performed whole-exome sequencing analyses to characterize the genetic landscape of these tumors.
methodsWe collected colorectal tumor and non-neoplastic tissues from 31 patients with IBD and colorectal cancer (15 with ulcerative colitis, 14 with Crohn's disease, and 2 with indeterminate colitis) and performed whole-exome sequencing analyses of the microdissected tumor and matched nontumor tissues. We identified somatic alterations by comparing matched specimens. The prevalence of mutations in sporadic colorectal tumors was obtained from previously published exome-sequencing studies.
resultsTwo specimens had somatic mutations in the DNA proofreading or mismatch repair genes POLE, MLH1, and MSH6 and the tumor cells had a hypermutable phenotype. The remaining tumors had, on average, 71 alterations per sample. TP53 was the most commonly mutated gene, with prevalence similar to that of sporadic colorectal tumors (63% of cases). However, tumors from the patients with IBD had a different mutation spectrum. APC and KRAS were mutated at significantly lower rates in tumors from patients with IBD than in sporadic colorectal tumors (13% and 20% of cases, respectively). Several genes were mutated more frequently or uniquely in tumors from patients with IBD, including SOX9 and EP300 (which encode proteins in the WNT pathway), NRG1 (which encodes an ERBB ligand), and IL16 (which encodes a cytokine). Our study also revealed recurrent mutations in components of the Rho and Rac GTPase network, indicating a role for noncanonical WNT signaling in development of colorectal tumors in patients with IBD.
conclusionsColorectal tumors that develop in patients with IBD have distinct genetic features from sporadic colorectal tumors. These findings could be used to develop disease-specific markers for diagnosis and treatment of patients with IBD and colorectal cancer.
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