ArticleInflammatory bowel diseases2012
Unique patterns of CpG island methylation in inflammatory bowel disease-associated colorectal cancers.
Article in Inflammatory bowel diseases, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- KRAS and TP53 mutations in inflammatory bowel disease-associated colorectal cancer: a meta-analysis.Oncotarget · 2017Pooled it
- Trial
- Colonic Mucosal Gene Expression Profile in Patients with Neoplastic Progression in Longstanding Ulcerative Colitis.Clinical and experimental gastroenterology · 2025Article
- Genetic Profiling of Colorectal Carcinomas of Patients with Primary Sclerosing Cholangitis and Inflammatory Bowel Disease.Inflammatory bowel diseases · 2022Article
- Effect of TLR2 on the proliferation of inflammation-related colorectal cancer and sporadic colorectal cancer.Cancer cell international · 2020Article
- Interval Colorectal Cancer in Inflammatory Bowel Disease: The Role of Guideline Adherence.Digestive diseases and sciences · 2020Article
- IBD-associated Colon Cancers Differ in DNA Methylation and Gene Expression Profiles Compared With Sporadic Colon Cancers.Journal of Crohn's & colitis · 2019Article
- Impact of Global DNA Methylation in Treatment Outcome of Colorectal Cancer Patients.Frontiers in pharmacology · 2018Article
- Inflammation-associated DNA methylation patterns in epithelium of ulcerative colitis.Epigenetics · 2017Article
- High CpG island methylation of p16 gene and loss of p16 protein expression associate with the development and progression of tetralogy of Fallot.Journal of genetics · 2016Article
- Whole-Exome Sequencing Analyses of Inflammatory Bowel Disease-Associated Colorectal Cancers.Gastroenterology · 2016Article
- miRNA-26b Overexpression in Ulcerative Colitis-associated Carcinogenesis.Inflammatory bowel diseases · 2015Article
- Relationship between methylation and colonic inflammation in inflammatory bowel disease.World journal of gastroenterology · 2014Observational
- How does genotype influence disease phenotype in inflammatory bowel disease?Inflammatory bowel diseases · 2013Review
- Epigenetics and colorectal cancer pathogenesis.Cancers · 2013Article
- The CpG island methylator phenotype (CIMP) in colorectal cancer.Gastroenterology and hepatology from bed to bench · 2013Review
- CpG Island Methylation, Microsatellite Instability, and BRAF Mutations and Their Clinical Application in the Treatment of Colon Cancer.Chemotherapy research and practice · 2012Article
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundCpG island (CGI) hypermethylation at discrete loci is a prevalent cancer-promoting abnormality in sporadic colorectal carcinomas (S-CRCs). We investigated genome-wide CGI methylation in inflammatory bowel disease (IBD)-associated CRCs (IBD-CRCs).
methodsMethylation microarray analyses were conducted on seven IBD-CRCs, 17 S-CRCs, and eight normal control colonic tissues from patients without CRC or IBD. CGI methylator phenotype (CIMP), a surrogate marker for widespread cancer-specific CGI hypermethylation, was examined in 30 IBD-CRCs and 43 S-CRCs.
resultsThe genome-wide CGI methylation pattern of IBD-CRCs was CIMP status-dependent. Based on methylation array data profiling of all autosomal loci, CIMP(+) IBD-CRCs grouped together with S-CRCs, while CIMP(-) IBD-CRCs grouped together with control tissues. CIMP(-) IBD-CRCs demonstrated less methylation than did age-matched CIMP(-) S-CRCs at autosomal CGIs (z-score -0.17 vs. 0.09, P = 3 × 10(-3)) and CRC-associated hypermethylation target CGIs (z-score -0.43 vs. 0.68, P = 1 × 10(-4)). Age-associated hypermethylation target CGIs were significantly overrepresented in CGIs that were hypermethylated in S-CRCs (P = 1 × 10(-192)), but not in CGIs that were hypermethylated in IBD-CRCs (P = 0.11). In contrast, KRAS mutation prevalence was similar between IBD-CRCs and S-CRCs. Notably, CIMP(+) prevalence was significantly higher in older than in younger IBD-CRC cases (50.0 vs. 4.2, P = 0.02), but not in S-CRC cases (9.7 vs. 16.7, P = 0.92).
conclusionsCancer-specific CGI hypermethylation and age-associated CGI hypermethylation are diminished in IBD-CRCs relative to S-CRCs, while the KRAS mutation rate is comparable between these cancers. CGI hypermethylation appears to play only a minor role in IBD-associated carcinogenesis. We speculate that aging, rather than inflammation per se, promotes CIMP(+) CRCs in IBD patients.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.