Evidence map›Paper›PMID 23318424›Full record

ReviewOncogene2013

The mutant p53 mouse as a pre-clinical model.

J G Jackson, G Lozano

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
–field-weighted citation impact
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

38 citing papers in PubMed.

  1. Review
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  18. Article
  19. New therapeutic strategies to treat human cancers expressing mutant p53 proteins.Journal of experimental & clinical cancer research : CR · 2018
    Review
  20. Review
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

2 authors.

J G JacksonDepartment of Genetics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
G Lozano

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
6 · The paper itself

Abstract

The p53 tumor-suppressor pathway is dismantled in the development of most cancers. Mice with various p53 mutant alleles either singly or in combination with other genetic alterations are predisposed to tumor development. Here, we review studies utilizing p53 mutant mice that have recapitulated and informed clinical observations. These studies have demonstrated the p53 contribution, sometimes beneficial and sometimes detrimental, to treatment response in lymphomas, and lung and breast cancers. Further, we examine how p53 mutant mouse models have been used to test the efficacy of p53 reactivation as a therapeutic strategy.

Indexed as

MutationAnimalsDisease Models, AnimalDrug Evaluation, PreclinicalDrug Screening Assays, AntitumorHumansMiceMice, TransgenicNeoplasmsTumor Suppressor Protein p53Tumor Suppressor Protein p53

Identifiers

PMID23318424

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.