Evidence map›Paper›PMID 22034047›Full record

ReviewJournal of cellular biochemistry2012

Contributions of Rad9 to tumorigenesis.

Constantinos G Broustas, Howard B Lieberman

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

23 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Knockdown of Rad9A enhanced DNA damage induced by trichostatin A in esophageal cancer cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Clamping down on mammalian meiosis.Cell cycle (Georgetown, Tex.) · 2013
    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

2 authors at 1 institution in 1 country.

Constantinos G BroustasCenter for Radiological Research, Columbia University College of Physicians and Surgeons, New York, New York 10032, USA.
Howard B Lieberman
Columbia University · US

Funding

THE FUNCTIONAL GENOMICS OF BYSTANDER RESPONSESP01CA049062 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI HEI, TOM K. · 1990 to 2014
$21.9M
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 5P01CA49062-20NCI NIH HHS 5R01CA130536-17NCI NIH HHS P01 CA049062NCI NIH HHS R01 CA130536NIGMS NIH HHS 5R01GM079107-10NIGMS NIH HHS R01 GM079107
6 · The paper itself

Abstract

Rad9 plays a crucial role in maintaining genomic stability by regulating cell cycle checkpoints, DNA repair, telomere stability, and apoptosis. Rad9 controls these processes mainly as part of the heterotrimeric 9-1-1 (Rad9-Hus1-Rad1) complex. However, in recent years it has been demonstrated that Rad9 can also act independently of the 9-1-1 complex as a transcriptional factor, participate in immunoglobulin class switch recombination, and show 3'-5' exonuclease activity. Aberrant Rad9 expression has been associated with prostate, breast, lung, skin, thyroid, and gastric cancers. High expression of Rad9 is causally related to, at least, human prostate cancer growth. On the other hand, deletion of Mrad9, the mouse homolog, is responsible for increased skin cancer incidence. These results reveal that Rad9 can act as an oncogene or tumor suppressor. Which of the many functions of Rad9 are causally related to initiation and progression of tumorigenesis and the mechanistic details by which Rad9 induces or suppresses tumorigenesis are presently not known, but are crucial for the development of targeted therapeutic interventions.

Indexed as

Cell Transformation, NeoplasticAnimalsApoptosisCell Cycle CheckpointsCell Cycle ProteinsDNA RepairHumansMiceTranscription FactorsCell Cycle Proteinsrad9 proteinTranscription Factors

Identifiers

PMID22034047
PMCPMC3264844
OpenAlexW2061223718

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.