Evidence map›Paper›PMID 20028875›Full record

ArticleCancer prevention research (Philadelphia, Pa.)2010

DNA damage drives an activin a-dependent induction of cyclooxygenase-2 in premalignant cells and lesions.

Colleen Fordyce, Tim Fessenden, Curtis Pickering, Jason Jung, Veena Singla, Hal Berman, Thea Tlsty

Open access · bronzeAbstract read
In one paragraph

Article in Cancer prevention research (Philadelphia, Pa.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

29 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
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  3. Review
  4. Review
  5. Unlocking antitumor immunity with adenosine receptor blockers.Cancer drug resistance (Alhambra, Calif.) · 2023
    Review
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  7. Review
  8. Review
  9. Article
  10. Article
  11. CD36 and CD97 in Pancreatic Cancer versus Other Malignancies.International journal of molecular sciences · 2020
    Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. 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 1 institution in 1 country.

Colleen FordyceDepartment of Pathology, University of California, San Francisco, 94143, USA.
Tim Fessenden
Curtis Pickering
Jason Jung
Veena Singla
Hal Berman
Thea Tlsty
University of California, San Francisco · US

Funding

Tissue CoreP01CA107584 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SHEPHERD, JOHN ALAN · 2006 to 2010
$6.9M
Regulation of Genomic Instability in Early Breast CancerR01CA097214 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI TLSTY, THEA D · 2003 to 2014
$3.0M
Regulation of DNA hypermethylation in human mammary cellsR01CA122024 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI TLSTY, THEA D · 2006 to 2008
$637k
NCI NIH HHS P01 CA107584NCI NIH HHS R01 CA097214NCI NIH HHS R01 CA122024
6 · The paper itself

Abstract

Cyclooxygenase-2 (COX-2) catalyzes the rate-limiting step in the synthesis of prostaglandins. Its overexpression induces numerous tumor-promoting phenotypes and is associated with cancer metastasis and poor clinical outcome. Although COX-2 inhibitors are promising chemotherapeutic and chemopreventative agents for cancer, the risk of significant cardiovascular and gastrointestinal complications currently outweighs their potential benefits. Systemic complications of COX-2 inhibition could be avoided by specifically decreasing COX-2 expression in epithelial cells. To that end, we have investigated the signal transduction pathway regulating the COX-2 expression in response to DNA damage in breast epithelial cells. In variant human mammary epithelial cells that have silenced p16 (vHMEC), double-strand DNA damage or telomere malfunction results in a p53- and activin A-dependent induction of COX-2 and continued proliferation. In contrast, telomere malfunction in HMEC with an intact p16/Rb pathway induces cell cycle arrest. Importantly, in ductal carcinoma in situ lesions, high COX-2 expression is associated with high gammaH2AX, TRF2, activin A, and telomere malfunction. These data show that DNA damage and telomere malfunction can have both cell-autonomous and cell-nonautonomous consequences and can provide a novel mechanism for the propagation of tumorigenesis.

Indexed as

ActivinsAtaxia Telangiectasia Mutated ProteinsBlotting, WesternBreast NeoplasmsCarcinoma, Ductal, BreastCarcinoma in SituCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p16Cyclooxygenase 2DNA-Binding ProteinsDNA DamageEnzyme-Linked Immunosorbent AssayFemaleGene ExpressionGene Expression ProfilingHumansactivin AActivinsAtaxia Telangiectasia Mutated ProteinsATM protein, humanCDKN2A protein, humanCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p16Cyclooxygenase 2DNA-Binding ProteinsNeoplasm ProteinsProtein Serine-Threonine KinasesRetinoblastoma ProteinTelomeric Repeat Binding Protein 2Tumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID20028875
PMCPMC2954106
OpenAlexW2097968887

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.