Evidence map›Paper›PMID 18632607›Full record

ArticleCancer research2008

Targeted deletion of Rad9 in mouse skin keratinocytes enhances genotoxin-induced tumor development.

Zhishang Hu, Yuheng Liu, Chunbo Zhang, Yun Zhao, Wei He, Lu Han, Leilei Yang, Kevin M Hopkins, Xiao Yang, Howard B Lieberman and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

19 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Role of survivin re-expression in the development and progression of non-small cell lung cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  8. Article
  9. Clamping down on mammalian meiosis.Cell cycle (Georgetown, Tex.) · 2013
    Article
  10. Article
  11. Contributions of Rad9 to tumorigenesis.Journal of cellular biochemistry · 2012
    Review
  12. Article
  13. Article
  14. The role of RAD9 in tumorigenesis.Journal of molecular cell biology · 2011
    Review
  15. Article
  16. Article
  17. Mouse Rad9b is essential for embryonic development and promotes resistance to DNA damage.Developmental dynamics : an official publication of the American Association of Anatomists · 2010
    Article
  18. Article
  19. 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

11 authors at 4 institutions in 4 countries.

Zhishang HuNational Laboratory of Biomacromolecules, Chinese Academy of Sciences, Beijing, China.
Yuheng Liu
Chunbo Zhang
Yun Zhao
Wei He
Lu Han
Leilei Yang
Kevin M Hopkins
Xiao Yang
Howard B Lieberman
Haiying Hang
Laboratoire des Biomolécules · FRChinese Academy of Sciences · CNRoyal College of Physicians · GBCapital Normal University · CN

Funding

Mechanisms of Radioresistance and Cell Cycle ProgressionR01CA130536 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI LIEBERMAN, HOWARD B. · 2007 to 2016
$3.5M
The MRAD9 Radioresistance GeneR01GM079107 · NIGMS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI LIEBERMAN, HOWARD B. · 2006 to 2013
$2.6M
NCI NIH HHS CA130536NCI NIH HHS R01 CA130536NIGMS NIH HHS GM079107NIGMS NIH HHS R01 GM079107
6 · The paper itself

Abstract

The Rad9 gene is evolutionarily conserved from yeast to humans and plays crucial roles in genomic maintenance, DNA repair, and cell cycle checkpoint controls. However, the function of this gene with respect to tumorigenesis is not well-understood. A Rad9-null mutation in mice causes embryonic lethality. In this study, we created mice in which mouse Rad9, Mrad9, was deleted only in keratinocytes to permit examination of the potential function of the gene in tumor development. Mice with Mrad9(+/-) or Mrad9(-/-) keratinocytes showed no overt, spontaneous morphologic defects and seemed similar to wild-type controls. Painting the carcinogen 7,12-dimethylbenzanthracene (DMBA) onto the skin of the animals caused earlier onset and more frequent formation of tumors and senile skin plaques in Mrad9(-/-) mice, compared with Mrad9(+/-) and Mrad9(+/+) littermates. DNA damage response genes p21, p53, and Mrad9B were expressed at higher levels in Mrad9(-/-) relative to Mrad9(+/+) skin. Keratinocytes isolated from Mrad9(-/-) skin had more spontaneous and DMBA-induced DNA double strand breaks than Mrad9(+/+) keratinocytes, and the levels were reduced by incubation with the antioxidant epigallocatechin gallate. These data suggest that Mrad9 plays an important role in maintaining genomic stability and preventing tumor development in keratinocytes.

Indexed as

Gene DeletionGene Expression Regulation, Neoplastic9,10-Dimethyl-1,2-benzanthraceneAnimalsCarcinogensCell CycleCell Cycle ProteinsCell ProliferationCell Transformation, NeoplasticDNA DamageGenetic Predisposition to DiseaseKeratinocytesMiceMutagensSkin9,10-Dimethyl-1,2-benzanthraceneCarcinogensCell Cycle ProteinsMutagensrad9 protein

Identifiers

PMID18632607
PMCPMC4331354
OpenAlexW2164562578

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.