Evidence map›Paper›PMID 18519043›Full record

ArticleGastroenterology2008

Ulcerative colitis is a disease of accelerated colon aging: evidence from telomere attrition and DNA damage.

Rosa Ana Risques, Lisa A Lai, Teresa A Brentnall, Lin Li, Ziding Feng, Jasmine Gallaher, Margaret T Mandelson, John D Potter, Mary P Bronner, Peter S Rabinovitch

Open access · bronzeAbstract read
In one paragraph

Article in Gastroenterology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
6.9field-weighted citation impact, top 2% of its field
1 · What the graph read from 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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

96 citing papers in PubMed, 180 citations in OpenAlex.

  1. Review
  2. Aging and cancer: current understandings and future perspectives.Signal transduction and targeted therapy · 2026
    Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. A Clinical Trial to Evaluate the Safety and Efficacy ofJGH open : an open access journal of gastroenterology and hepatology · 2025
    Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

36 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 2 countries.

Rosa Ana RisquesDepartment of Pathology, University of Washington, Seattle, Washington, USA.
Lisa A Lai
Teresa A Brentnall
Lin Li
Ziding Feng
Jasmine Gallaher
Margaret T Mandelson
John D Potter
Mary P Bronner
Peter S Rabinovitch
Fred Hutch Cancer Center · USUniversity of Washington · USCape Town HVTN Immunology Laboratory / Hutchinson Centre Research Institute of South Africa · ZACleveland Clinic · US

Funding

SPECIFICITY OF OXYGEN DNA DAMAGE AND MUTAGENESISP01AG001751 · NIA · UNIVERSITY OF WASHINGTON · PI RABINOVITCH, PETER S · 1985 to 2021
$29.6M
University of Washington Nathan Shock Center of Excellence in the Basic Biology of AgingP30AG013280 · NIA · UNIVERSITY OF WASHINGTON · PI David J. Marcinek, Jessica E Young · 1995 to 2026
$27.1M
HISTOLOGIC AND MOLECULAR CHANGES IN UC TUMORIGENESISR01CA068124 · NCI · UNIVERSITY OF WASHINGTON · PI BRENTNALL, TERESA A · 1995 to 2010
$3.5M
Seattle Cancer and Aging ProgramP20CA103728 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI RABINOVITCH, PETER S · 2003 to 2007
$3.4M
NCI NIH HHS P20 CA103728NCI NIH HHS R01 CA068124NIA NIH HHS P01 AG001751NIA NIH HHS P30 AG013280NIA NIH HHS P30 AG13280
6 · The paper itself

Abstract

BACKGROUND &

aimsTelomere shortening is implicated in cancer and aging and might link these 2 biologic events. We explored this hypothesis in ulcerative colitis (UC), a chronic inflammatory disease that predisposes to colorectal cancer and in which shorter telomeres have been associated with chromosomal instability and tumor progression.

methodsTelomere length was measured by quantitative polymerase chain reaction in colonocytes and leukocytes of 2 different sets of UC patients and compared with normal controls across a wide range of ages. For a subset of patients, telomere length was measured in epithelium and stroma of right and left colon biopsy specimens. A third set of biopsy specimens was analyzed for phosphorylation of histone H2AX (gammaH2AX), a DNA damage signal, by immunofluorescence and for telomere length by quantitative fluorescence in situ hybridization. Relationships between telomere length, gammaH2AX intensity, age, disease duration, and age of disease onset were explored.

resultsColonocyte telomeres shorten with age almost twice as rapidly in UC patients as in normal controls. This extensive shortening occurs within approximately 8 years of disease duration. Leukocyte telomeres are slightly shorter in UC patients than in controls, but telomeres of colon stromal cells are unaffected. gammaH2AX intensity is higher in colonocytes of UC patients than in controls and is not dependent on age or telomere length.

conclusionsColonocytes of UC patients show premature shortening of telomeres, which might explain the increased and earlier risk of cancer in this disease. Shorter leukocyte telomeres and increased gammaH2AX in colonocytes might reflect oxidative damage secondary to inflammation.

Indexed as

DNA DamageAdolescentAdultAgedAge DistributionAge FactorsAgingChildChild, PreschoolColitis, UlcerativeColonColorectal NeoplasmsCross-Sectional StudiesFemaleFluorescent Antibody TechniqueHistonesH2AX protein, humanHistones

Identifiers

PMID18519043
PMCPMC2574910
OpenAlexW2105558383

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.