Evidence map›Paper›PMID 21272329›Full record

ArticleCell division2011

The G1 phase Cdks regulate the centrosome cycle and mediate oncogene-dependent centrosome amplification.

Mary K Harrison, Arsene M Adon, Harold I Saavedra

Open access · goldAbstract read
In one paragraph

Article in Cell division, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

21 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Centrosome - a promising anti-cancer target.Biologics : targets & therapy · 2016
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. The expression of Nek7, FoxM1, and Plk1 in gallbladder cancer and their relationships to clinicopathologic features and survival.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2013
    Article
  18. Article
  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

3 authors at 2 institutions in 1 country.

Mary K HarrisonEmory University, Department of Radiation Oncology, Winship Cancer Institute, 1701 Uppergate Drive, Atlanta, Georgia, 30322, USA. hsaaved@emory.edu.
Arsene M Adon
Harold I Saavedra
Winship Cancer InstituteEmory University · US

Funding

PREDOCTORAL TRAINING PROGRAM IN GENETICST32GM008490 · NIGMS · EMORY UNIVERSITY · PI BOSS, JEREMY M. · 1993 to 2022
$8.0M
Nek2 and NPM in centrosome amplificationR01CA151521 · NCI · EMORY UNIVERSITY · PI SAAVEDRA, HAROLD I · 2010 to 2014
$1.5M
NCI NIH HHS R01 CA151521NIGMS NIH HHS T32 GM008490
6 · The paper itself

Abstract

Because centrosome amplification generates aneuploidy and since centrosome amplification is ubiquitous in human tumors, a strong case is made for centrosome amplification being a major force in tumor biogenesis. Various evidence showing that oncogenes and altered tumor suppressors lead to centrosome amplification and aneuploidy suggests that oncogenes and altered tumor suppressors are a major source of genomic instability in tumors, and that they generate those abnormal processes to initiate and sustain tumorigenesis. We discuss how altered tumor suppressors and oncogenes utilize the cell cycle regulatory machinery to signal centrosome amplification and aneuploidy.

Identifiers

PMID21272329
PMCPMC3038874
OpenAlexW2123203474

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.