Evidence map›Paper›PMID 18948225›Full record

ArticleMutation research2009

Accumulation of oxidatively induced clustered DNA lesions in human tumor tissues.

Somaira Nowsheen, Rebecca L Wukovich, Khaled Aziz, Peter T Kalogerinis, Christopher C Richardson, Mihalis I Panayiotidis, William M Bonner, Olga A Sedelnikova, Alexandros G Georgakilas

Abstract read
In one paragraph

Article in Mutation research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

33 citing papers in PubMed, 83 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Regulation of Selective B Cell Autophagy by the Pro-oxidant Adaptor p66SHC.Frontiers in cell and developmental biology · 2020
    Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Single Molecule Analysis of Laser Localized Psoralen Adducts.Journal of visualized experiments : JoVE · 2017
    Article
  13. Progression of Hepatic Adenoma to Carcinoma inOxidative medicine and cellular longevity · 2017
    Article
  14. Article
  15. Article
  16. Observational
  17. Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Somaira NowsheenDepartment of Biology, Thomas Harriot College of Arts and Sciences, East Carolina University, Greenville, NC 27858, USA.
Rebecca L Wukovich
Khaled Aziz
Peter T Kalogerinis
Christopher C Richardson
Mihalis I Panayiotidis
William M Bonner
Olga A Sedelnikova
Alexandros G Georgakilas
East Carolina University · USCenter for Cancer Research · USUniversity of Nevada, Reno · US

Funding

Studies of Histone Functions in Chromatin; H2AX and DNA DSBsZIABC006140 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI BONNER, WILLIAM · 2009 to 2015
$7.8M
Studies of Histone Functions in Chromatin; H2AX and DNA DSBsZ01BC006140 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI BONNER, WILLIAM · 1996 to 2008
$2.1M
Intramural NIH HHS Z01 BC006140
6 · The paper itself

Abstract

Increased levels of oxidatively induced DNA damage have been reported in various cases of human pathogenesis like age-related and chronic diseases. Advances in experimental carcinogenesis associate high oxidative stress with genome instability and oncogenic transformation. Cancer biomarkers are helpful for early tumor diagnostics, prediction of tumor development, and analysis of individual tumors' response to therapy as well as recurrence. The repair resistant oxidatively induced clustered DNA lesions (OCDLs) could serve as a common indicator of oxidative stress in human malignant cells or tissues. To test this hypothesis, we assessed the levels of endogenous OCDLs in several human tumor and adjacent normal tissues from patients with liver, ovary, kidney, breast and colon cancer. These tumor tissues have already been shown to accumulate higher endogenous levels of gamma-H2AX foci. For the detection of clustered DNA lesions we used the human repair enzymes APE1, OGG1 and NTH1 as well as the Escherichia coli homologue Endonuclease III. In the majority of cases we detected higher levels of OCDLs in tumor vs. normal tissues but not always with a statistically significant difference and not with uniform tissue dependence. These data suggest for the first time the importance of endogenous non-DSB clusters in human cancer and their potential use as cancer biomarkers.

Indexed as

DNA DamageAdolescentAgedAged, 80 and overCell Transformation, NeoplasticChildDNA Breaks, Single-StrandedFemaleHumansInfantMaleMiddle AgedMultigene FamilyNeoplasmsOxidative StressYoung Adult

Identifiers

PMID18948225
PMCPMC6944316
OpenAlexW2106664352

What OpenQuestion holds

Textmetadata
LicenceTDM
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.