Evidence map›Paper›PMID 18490919›Full record

ArticleOncogene2008

Roles of cyclins A and E in induction of centrosome amplification in p53-compromised cells.

K Hanashiro, M Kanai, Y Geng, P Sicinski, K Fukasawa

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

30 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Cell cycle regulation and hematologic malignancies.Blood science (Baltimore, Md.) · 2019
    Review
  6. Article
  7. Review
  8. CRKL protein overexpression enhances cell proliferation and invasion in pancreatic cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    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

5 authors at 4 institutions in 1 country.

K HanashiroMolecular Oncology Program, H Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA.
M Kanai
Y Geng
P Sicinski
K Fukasawa
Moffitt Cancer Center · USDana-Farber Cancer Institute · USHarvard University · USMolecular Oncology (United States) · US

Funding

E-Cyclins in normal and oncogenic proliferationR01CA108950 · NCI · DANA-FARBER CANCER INSTITUTE · PI SICINSKI, PETER · 2004 to 2013
$3.7M
P53 Mediated Regulation of Centrosome DuplicationR01CA090522 · NCI · UNIVERSITY OF CINCINNATI · PI FUKASAWA, KENJI · 2001 to 2010
$2.6M
NCI NIH HHS CA108950NCI NIH HHS CA90522NCI NIH HHS R01 CA090522NCI NIH HHS R01 CA108950
6 · The paper itself

Abstract

Abnormal amplification of centrosomes, which occurs frequently in cancers, leads to high frequencies of mitotic defect and chromosome segregation error, profoundly affecting the rate of tumor progression. Centrosome amplification results primarily from overduplication of centrosomes, and p53 is involved in the regulation of centrosome duplication partly through controlling the activity of cyclin-dependent kinase (CDK) 2-cyclin E, a kinase complex critical for the initiation of centrosome duplication. Thus, loss or mutational inactivation of p53 leads to an increased frequency of centrosome amplification. Moreover, the status of cyclin E greatly influences the frequency of centrosome amplification in cells lacking functional p53. Here, we dissected the roles of CDK2-associating cyclins, namely cyclins E and A, in centrosome amplification in the p53-negative cells. We found that loss of cyclin E was readily compensated by cyclin A for triggering the initiation of centrosome duplication, and thus the centrosome duplication kinetics was not significantly altered in cyclin E-deficient cells. It has been shown that cells lacking functional p53, when arrested in either early S-phase or late G(2) phase, continue to reduplicate centrosomes, resulting in centrosome amplification. In cells arrested in early S phase, cyclin E, but not cyclin A, is important in centrosome amplification, whereas in the absence of cyclin E, cyclin A is important for centrosome amplification. In late G(2)-arrested cells, cyclin A is important in centrosome amplification irrespective of the cyclin E status. These findings advance our understandings of the mechanisms underlying the numeral abnormality of centrosomes and consequential genomic instability associated with loss of p53 function and aberrant expression of cyclins E and A in cancer cells.

Indexed as

AnimalsAntibiotics, AntineoplasticAntiviral AgentsAphidicolinCentrosomeCyclin ACyclin EDoxorubicinEmbryo, MammalianFibroblastsFlow CytometryFluorescent Antibody Technique, IndirectG2 PhaseGene Expression Regulation, NeoplasticGenes, DominantHumansAntibiotics, AntineoplasticAntiviral AgentsAphidicolinCyclin ACyclin EDoxorubicinTumor Suppressor Protein p53

Identifiers

PMID18490919
PMCPMC2574884
OpenAlexW2090406070

What OpenQuestion holds

Textmetadata
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.