Evidence map›Paper›PMID 30498558›Full record

ArticleJournal of cancer research updates2018

Aberrant DNA damage response and DNA repair pathway in high glucose conditions.

Amy Zhong, Melissa Chang, Theresa Yu, Raymond Gau, Daniel J Riley, Yumay Chen, Phang-Lang Chen

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research updates, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

24 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
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  5. Article
  6. Review
  7. Epigenetic Regulation of Pancreas Development and Function.Advances in anatomy, embryology, and cell biology · 2024
    Review
  8. Article
  9. DNA Damage and Repair in Eye Diseases.International journal of molecular sciences · 2023
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
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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

7 authors at 2 institutions in 1 country.

Amy ZhongDepartment of Medicine, Division of Endocrinology, University of California at Irvine.
Melissa ChangDepartment of Medicine, Division of Endocrinology, University of California at Irvine.
Theresa YuDepartment of Medicine, Division of Endocrinology, University of California at Irvine.
Raymond GauDepartment of Medicine, Division of Endocrinology, University of California at Irvine.
Daniel J RileyDepartment of Medicine, Division of Nephrology, University of Texas Health San Antonio.
Yumay ChenDepartment of Medicine, Division of Endocrinology, University of California at Irvine.
Phang-Lang ChenDepartment of Biological Chemistry, University of California at Irvine.
University of California, Irvine · USThe University of Texas at San Antonio · US

Funding

Pathogenic Mechanism of Polycystic Kidney DiseaseR01DK067339 · NIDDK · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI CHEN, YUMAY · 2006 to 2010
$1.2M
Cell Cycle Dependent Mechanisms of Renal HypertrophyR01DK061626 · NIDDK · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI RILEY, DANIEL J · 2002 to 2006
$1.0M
NIDDK NIH HHS R01 DK061626NIDDK NIH HHS R01 DK067339
6 · The paper itself

Abstract

backgroundHigher cancer rates and more aggressive behavior of certain cancers have been reported in populations with diabetes mellitus. This association has been attributed in part to the excessive reactive oxygen species generated in diabetic conditions and to the resulting oxidative DNA damage. It is not known, however, whether oxidative stress is the only contributing factor to genomic instability in patients with diabetes or whether high glucose directly also affects DNA damage and repair pathways.

resultsNormal renal epithelial cells and renal cell carcinoma cells are more chemo- and radiation resistant when cultured in high concentrations of glucose. In high glucose conditions, the CHK1-mediated DNA damage response is not activated properly. Cells in high glucose also have slower DNA repair rates and accumulate more mutations than cells grown in normal glucose concentrations. Ultimately, these cells develop a transforming phenotype.

conclusionsIn high glucose conditions, defective DNA damage responses most likely contribute to the higher mutation rate in renal epithelial cells, in addition to oxidative DNA damage. The DNA damage and repair are normal enzyme dependent mechanisms requiring euglycemic environments. Aberrant DNA damage response and repair in cells grown in high glucose conditions underscore the importance of maintaining good glycemic control in patients with diabetes mellitus and cancer.

Indexed as

ATRcheckpoint kinase 1Chemo resistantDiabetesDNA damage response

Identifiers

PMID30498558
PMCPMC6258084
OpenAlexW2810690831

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.