Evidence map›Paper›PMID 12934108›Full record

ArticleOncogene2003

p73 can suppress the proliferation of cells that express mutant p53.

Amy C Willis, Tara Pipes, Jianhui Zhu, Xinbin Chen

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.7field-weighted citation impact, top 33% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Propagation of aggregated p53: Cross-reaction and coaggregation vs. seeding.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
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  12. Article
  13. Review
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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

4 authors at 1 institution in 1 country.

Amy C WillisDepartment of Cell Biology and UAB Comprehensive Cancer Center, The University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Tara Pipes
Jianhui Zhu
Xinbin Chen
University of Alabama at Birmingham · US

Funding

MECHANISM OF P73 DEPENDENT TUMOR SUPPRESSIONR01CA081237 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHEN, XINBIN · 1999 to 2022
$6.8M
NCI NIH HHS R01CA81237
6 · The paper itself

Abstract

Mutation of the p53 tumor suppressor gene is the most common genetic alteration in human cancer. p73, a member of the p53 family, has been found to exhibit activity similar to that of p53, including the ability to induce growth arrest and apoptosis. p53 and p73 have a high percentage of similarity at several domains, including the DNA binding domain. This domain in p53 is the location of missense mutations in many human cancers. Mutant p53, which cannot suppress cell proliferation, has been found to have a dominant-negative activity that inactivates wild-type p53. To determine the effects of mutant p53 on wild-type p73, we have established cell lines expressing both mutant p53 and wild-type p73 in a dual-inducible system. This system expresses mutant p53 in a tetracycline-repressible system and p73beta in an ecdysone-inducible system in a p53-null lung carcinoma parental cell line. We have found that wild-type p73beta, in the presence of mutant p53, retains the ability to transactivate p21 and suppresses cell growth through induction of both cell cycle arrest and apoptosis. In addition, in cell lines expressing wild-type p53 and wild-type p73beta, we have found that these proteins cooperate to additively transactivate p21 and suppress cell proliferation.

Indexed as

ApoptosisCell DivisionCyclin-Dependent Kinase Inhibitor p21CyclinsDNA-Binding ProteinsGenes, Tumor SuppressorHumansNuclear ProteinsTumor Protein p73Tumor Suppressor Protein p53Tumor Suppressor ProteinsCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21CyclinsDNA-Binding ProteinsNuclear ProteinsTP73 protein, humanTumor Protein p73Tumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID12934108
OpenAlexW1980364516

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.