Evidence map›Paper›PMID 12665584›Full record

ArticleMolecular and cellular biology2003

Abolition of cyclin-dependent kinase inhibitor p16Ink4a and p21Cip1/Waf1 functions permits Ras-induced anchorage-independent growth in telomerase-immortalized human fibroblasts.

Wenyi Wei, Wendy A Jobling, Wen Chen, William C Hahn, John M Sedivy

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

33 citing papers in PubMed, 69 citations in OpenAlex.

  1. Review
  2. Immortalization of primary sheep embryo kidney cells.In vitro cellular & developmental biology. Animal · 2021
    Article
  3. eLife · 2017
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Proteomic profiling of Myc-associated proteins.Cell cycle (Georgetown, Tex.) · 2010
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Ras oncogenes: split personalities.Nature reviews. Molecular cell biology · 2008
    Review
  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

5 authors at 2 institutions in 1 country.

Wenyi WeiDepartment of Molecular Biology, Cell Biology and Biochemistry, Brown University, Providence, Rhode Island 02912, USA.
Wendy A Jobling
Wen Chen
William C Hahn
John M Sedivy
John Brown University · USBrigham and Women's Hospital · US

Funding

MECHANISMS OF REPLICATIVE SENESCENCE IN CELLSR01AG016694 · NIA · BROWN UNIVERSITY · PI SEDIVY, JOHN M · 1999 to 2024
$5.7M
GENETIC STUDIES OF C-MYC GENE FUNTION IN THE CELL CYCLER01GM041690 · NIGMS · YALE UNIVERSITY · PI SEDIVY, JOHN M. · 1990 to 2006
$2.6M
New Models of Human CancerK01CA094223 · NCI · DANA-FARBER CANCER INSTITUTE · PI HAHN, WILLIAM C · 2001 to 2005
$765k
NCI NIH HHS K01 CA094223NCI NIH HHS K01CA94223NIA NIH HHS R01 AG016694NIA NIH HHS R01AG16694NIGMS NIH HHS R01 GM041690NIGMS NIH HHS R01GM41690
6 · The paper itself

Abstract

Human cells are more resistant to both immortalization and malignant transformation than rodent cells. Recent studies have established the basic genetic requirements for the transformation of human cells, but much of this work relied on the expression of transforming proteins derived from DNA tumor viruses. We constructed an isogenic panel of human fibroblast cell lines using a combination of gene targeting and ectopic expression of dominantly acting mutants of cellular genes. Abolition of p21(Cip1/Waf1) and p16(Ink4a) functions prevented oncogenically activated Ras from inducing growth arrest and was sufficient for limited anchorage-independent growth but not tumorigenesis. Deletion of the tumor suppressor p53 combined with abolition of p16(Ink4a) function failed to mimic the introduction of simian virus 40 large T antigen, indicating that large T antigen may target additional cellular functions. Ha-Ras and Myc cooperated only to a limited extent, but in the absence of Ras, Myc cooperated strongly with the simian virus 40 small t antigen to elicit aggressive anchorage-independent growth. The experiments reported here further define specific components of human transformation pathways.

Indexed as

Antigens, Polyomavirus TransformingCell AdhesionCell DivisionCell Line, TransformedCell Transformation, NeoplasticCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p21CyclinsGenes, mycGenes, p16Gene TargetingHumansras ProteinsTelomeraseAntigens, Polyomavirus TransformingCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p21Cyclinsras ProteinsTelomerase

Identifiers

PMID12665584
PMCPMC152557
OpenAlexW2081570461

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.