Evidence map›Paper›PMID 22989750›Full record

ArticleBiochemical and biophysical research communications2012

Allele specific gain-of-function activity of p53 mutants in lung cancer cells.

Catherine A Vaughan, Rebecca Frum, Isabella Pearsall, Shilpa Singh, Brad Windle, Andrew Yeudall, Swati P Deb, Sumitra Deb

Open access · greenAbstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Association ofmedRxiv : the preprint server for health sciences · 2023
    Article
  4. Review
  5. Functional Precision Medicine Identifies Novel Druggable Targets and Therapeutic Options in Head and Neck Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. [P53 family proteins provide new insights into lung carcinogenesis and clinical treatment].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2013
    Review
  17. 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

8 authors at 1 institution in 1 country.

Catherine A VaughanDepartment of Biochemistry & Molecular Biology, Virginia Commonwealth University, Richmond, VA 23298, USA.
Rebecca Frum
Isabella Pearsall
Shilpa Singh
Brad Windle
Andrew Yeudall
Swati P Deb
Sumitra Deb
Virginia Commonwealth University · US

Funding

Chemoresistance and Motility: Role of Mutant p53 and NF-kB2 in CancerR01CA121144 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI DEB, SUMITRA · 2008 to 2011
$1.0M
OVEREXPRESSION OF MDM2 IN THE ETIOLOGY OF BREAST CANCERR01CA074172 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI DEB, SWATI P · 1998 to 2001
$448k
BREAST CANCER ETIOLOGY--P53 GAIN OF FUNCTION MUTATIONSR01CA070712 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI DEB, SUMITRA · 1996 to 2000
$223k
NCI NIH HHS CA121144NCI NIH HHS CA70712NCI NIH HHS CA74172NCI NIH HHS R01 CA121144
6 · The paper itself

Abstract

p53 mutations are mostly single amino acid changes resulting in expression of a stable mutant protein with "gain of function" (GOF) activity having a dominant oncogenic role rather than simple loss of function of wild-type p53. Knock-down of mutant p53 in human lung cancer cell lines with different endogenous p53 mutants results in loss of GOF activity as shown by lowering of cell growth rate. Two lung cancer cell lines, ABC1 and H1437, carrying endogenous mutants p53-P278S and -R267P, show reduction in growth rate on knock-down on p53 levels. However, whereas reduction of the p53 level induces loss of tumorigenicity in nude mice for ABC1 cells, it escalates tumorigenicity for H1437 cells. We have tested their transactivation potential on p53 target gene promoters by performing transient transcriptional assays in the p53-null H1299 lung cancer cell line. Interestingly, while the mutant p53 target promoter Axl was activated by both the mutants, the p21 promoter was activated by p53-R267P and wild-type p53 but not by p53-P278S; showing a clear difference in transcriptional activity between the two mutants. Our results demonstrate allele specificity between GOF p53 mutants and attempt to show that the specificity is dependent on the transactivation property of GOF p53; it also suggests importance of p21 activation in tumor suppression by p53.

Indexed as

AdenocarcinomaAnimalsAxl Receptor Tyrosine KinaseCell Line, TumorCell Transformation, NeoplasticGene Expression Regulation, NeoplasticGene Knockdown TechniquesGenes, p53HumansLung NeoplasmsMiceMice, NudeMutationPromoter Regions, GeneticProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)Axl Receptor Tyrosine KinaseProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)Receptor Protein-Tyrosine KinasesTumor Suppressor Protein p53

Identifiers

PMID22989750
PMCPMC4731231
OpenAlexW2043291943

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.