ArticleCancer research2011
Ulcerative colitis-associated colorectal cancer arises in a field of short telomeres, senescence, and inflammation.
Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07341282 (Investigation of Vancomycin Efficacy in Patients With Ulcerative Colitis and Primary Sclerosing Cholangitis), which is not on this map. Cited by 88 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Investigation of Vancomycin Efficacy in Patients With Ulcerative Colitis and Primary Sclerosing Cholangitis
Who cites it
88 citing papers in PubMed, 1 synthesis or guideline pooled it, 143 citations in OpenAlex.
- A meta-analysis of the clinicopathological characteristics and survival outcomes of inflammatory bowel disease associated colorectal cancer.International journal of colorectal disease · 2017Pooled it
- The ageing holobiont: crosstalk between telomere dynamics, oxidative stress and the gut microbiome.Biological reviews of the Cambridge Philosophical Society · 2026Review
- Multivariable genome-wide analysis elucidates the shared genetic architecture, immunosenescence features, and gut-origin therapeutic targets of ulcerative colitis-associated multisystem inflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Colitis-Associated Carcinoma: The Quintessential Epithelial Neoplasia Driven by Chronic Inflammation.Cells · 2026Review
- The Molecular Landscape of Inflammation in Inflammatory Bowel Disease (IBD): Targets for Precision Medicine.Biomedicines · 2025Review
- Network pharmacology and experimental validation reveal clotrimazole alleviates dextran sulfate sodium-induced ulcerative colitis by inhibiting intestinal senescence.The Journal of pharmacology and experimental therapeutics · 2025Article
- Obesity impact on leukocyte telomere shortening and immune aging assessed by Mendelian randomization and transcriptomics analysis.Scientific reports · 2025Article
- Article
- Integrative machine learning and bioinformatics analysis to identify cellular senescence-related genes and potential therapeutic targets in ulcerative colitis and colorectal cancer.Frontiers in bioinformatics · 2025Article
- Management of Colorectal Neoplasia in IBD Patients: Current Practice and Future Perspectives.Journal of Crohn's & colitis · 2024Review
- Prognostic significance of a signature based on senescence-related genes in colorectal cancer.GeroScience · 2024Article
- Low coverage whole genome sequencing of low-grade dysplasia strongly predicts colorectal cancer risk in ulcerative colitis.medRxiv : the preprint server for health sciences · 2024Article
- Article
- Non-coding RNA-related FCGBP downregulation in head and neck squamous cell carcinoma: a novel biomarker for predicting paclitaxel resistance and immunosuppressive microenvironment.Scientific reports · 2024Article
- The impact of ageing mechanisms on musculoskeletal system diseases in the elderly.Frontiers in immunology · 2024Review
- ERCC4: a potential regulatory factor in inflammatory bowel disease and inflammation-associated colorectal cancer.Frontiers in endocrinology · 2024Review
- Telomeres: Dysfunction, Maintenance, Aging and Cancer.Aging and disease · 2023Review
- Cellular Senescence, Inflammation, and Cancer in the Gastrointestinal Tract.International journal of molecular sciences · 2023Review
- Review
- Intestinal Epithelial Cells Adapt to Chronic Inflammation through Partial Genetic Reprogramming.Cancers · 2023Article
28 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 7 institutions in 2 countries.
Funding
Abstract
Inflammation plays a role in the progression to cancer and it is linked to the presence of senescent cells. Ulcerative colitis (UC) is a chronic inflammatory disease that predisposes to colorectal cancer. Tumorigenesis in this setting is associated with telomere shortening that can be observed in the nondysplastic epithelium of UC patients with high-grade dysplasia (HGD) or cancer (UC progressors). We hypothesized that a preneoplastic field of inflammation, telomere shortening, and senescence underlies tumor progression in UC progressors. Multiple biopsies of varying histologic grade were collected along the colon of nine UC progressors and analyzed for telomere length, DNA damage, senescence, p53, p16, and chronic and acute inflammation. Twenty biopsies from four UC nonprogressors and twenty-one biopsies from control individuals without UC were also analyzed. Short telomeres and increased DNA damage, senescence, and infiltrating leukocytes were observed in biopsies located less than 10 cm from HGD or cancer. Low-grade dysplasia (LGD) had the shortest telomeres along with the highest levels of senescence and infiltrating leukocytes, whereas HGD biopsies showed the opposite pattern. The expression of p16 and p53 was low in nondysplastic biopsies but progressively increased in LGD and HGD. In addition, high levels of infiltrating leukocytes were associated with telomere shortening, senescence, and reduced p53 expression. These results suggest that dysplasia arises in a preneoplastic field of chronic inflammation, which leads to telomere shortening, DNA damage, and senescence. Our findings argue that senescence acts as a tumor suppressor mechanism that is abrogated during the transition from LGD to HGD in UC.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.