Evidence map›Paper›PMID 10815808›Full record

ArticleOncogene2000

p21Waf1/Cip1/Sdi1-induced growth arrest is associated with depletion of mitosis-control proteins and leads to abnormal mitosis and endoreduplication in recovering cells.

B D Chang, E V Broude, J Fang, T V Kalinichenko, R Abdryashitov, J C Poole, I B Roninson

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 8% 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

73 citing papers in PubMed, 1 synthesis or guideline pooled it, 171 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Role of p27Oncotarget · 2018
    Review
  12. Article
  13. Article
  14. Cellular Model of p21-Induced Senescence.Methods in molecular biology (Clifton, N.J.) · 2017
    Article
  15. The Immortal Senescence.Methods in molecular biology (Clifton, N.J.) · 2017
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

13 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

B D ChangDepartment of Molecular Genetics (M/C 669), University of Illinois at Chicago, 60607-7170, USA.
E V Broude
J Fang
T V Kalinichenko
R Abdryashitov
J C Poole
I B Roninson
Ashland (United States) · USUniversity of Illinois Chicago · US

Funding

TARGETING TUMOR CELLS WITH GENETIC SUPPRESSOR ELEMENTSR01CA062099 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI RONINSON, IGOR B · 1994 to 2000
$215k
HUMAN MULTIDRUG RESISTANCE (P-GLYCOPROTEIN) GENESR37CA040333 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI RONINSON, IGOR B · 1993 to 1999
–
NCI NIH HHS R01CA62099NCI NIH HHS R37CA40333
6 · The paper itself

Abstract

Induction of a cyclin-dependent kinase inhibitor p21Waf1/ Cip1/Sdi1 is an integral part of cell growth arrest associated with senescence and damage response. p21 overexpression from an inducible promoter resulted in senescence-like growth arrest in a human fibrosarcoma cell line. After release from p21-induced growth arrest, cells re-entered the cell cycle but displayed growth retardation, cell death and decreased clonogenicity. The failure to form colonies was associated with abnormal mitosis and endoreduplication in the recovering cells and was correlated with the induced level of p21 and the duration of p21 induction. p21 induction was found to inhibit the expression of multiple proteins involved in the execution and control of mitosis. p21-induced depletion of the cellular pools of mitosis-control proteins was followed by asynchronous resynthesis of such proteins after release from p21, which explains the observed mitotic abnormalities. Genetic destabilization in cells recovering from p21-induced growth arrest may conceivably play a role in carcinogenesis and tumor progression.

Indexed as

AutoantigensCarrier ProteinsMitosisCalcium-Binding ProteinsCDC2 Protein KinaseCell Cycle ProteinsCell DivisionCentromere Protein AChromosomal Proteins, Non-HistoneCyclin BCyclin B1Cyclin-Dependent Kinase Inhibitor p21CyclinsDNADose-Response Relationship, DrugFibrosarcomaAutoantigensCalcium-Binding ProteinsCarrier ProteinsCCNB1 protein, humanCDC2 Protein KinaseCDKN1A protein, humanCell Cycle ProteinsCentromere Protein Acentromere protein FChromosomal Proteins, Non-HistoneCyclin BCyclin B1Cyclin-Dependent Kinase Inhibitor p21CyclinsDNAFluorescent DyesFungal ProteinsIsopropyl ThiogalactosideMicrofilament ProteinsNuclear ProteinsOrganic ChemicalsPKH2-GLPolo-Like Kinase 1Protein KinasesProtein Serine-Threonine KinasesProto-Oncogene Proteins

Identifiers

PMID10815808
OpenAlexW2327372357

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.