Evidence map›Paper›PMID 24374933›Full record

ArticleThe Journal of pathology2014

Effects of TP53 mutational status on gene expression patterns across 10 human cancer types.

Neha Parikh, Susan Hilsenbeck, Chad J Creighton, Tajhal Dayaram, Ryan Shuck, Eve Shinbrot, Liu Xi, Richard A Gibbs, David A Wheeler, Lawrence A Donehower

Open access · greenAbstract readComparative Study
In one paragraph

Article in The Journal of pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

61 citing papers in PubMed, 79 citations in OpenAlex.

  1. Journal of enzyme inhibition and medicinal chemistry · 2026
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  5. Review
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  7. Article
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  14. The Pathology according to p53 Pathway.Pathobiology : journal of immunopathology, molecular and cellular biology · 2024
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. [High expression of MYBL2 promotes progression and predicts a poor survival outcome of prostate cancer].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022
    Article

1 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

10 authors at 3 institutions in 1 country.

Neha ParikhDepartment of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX, USA.
Susan Hilsenbeck
Chad J Creighton
Tajhal Dayaram
Ryan Shuck
Eve Shinbrot
Liu Xi
Richard A Gibbs
David A Wheeler
Lawrence A Donehower
Baylor College of Medicine · USChildren's Cancer Center · USBaylor Genetics · US

Funding

The Human Genome Sequencing CenterU54HG003273 · NHGRI · BAYLOR COLLEGE OF MEDICINE · PI GIBBS, RICHARD A · 2004 to 2015
$341.3M
Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI DAVID R ROWLEY · 2007 to 2026
$73.9M
NCI NIH HHS P30 CA125123NHGRI NIH HHS U54 HG003273
6 · The paper itself

Abstract

Mutations in the TP53 tumour suppressor gene occur in half of all human cancers, indicating its critical importance in inhibiting cancer development. Despite extensive studies, the mechanisms by which mutant p53 enhances tumour progression remain only partially understood. Here, using data from the Cancer Genome Atlas (TCGA), genomic and transcriptomic analyses were performed on 2256 tumours from 10 human cancer types. We show that tumours with TP53 mutations have altered gene expression profiles compared to tumours retaining two wild-type TP53 alleles. Among 113 known p53-up-regulated target genes identified from cell culture assays, 10 were consistently up-regulated in at least eight of 10 cancer types that retain both copies of wild-type TP53. RPS27L, CDKN1A (p21(CIP1)) and ZMAT3 were significantly up-regulated in all 10 cancer types retaining wild-type TP53. Using this p53-based expression analysis as a discovery tool, we used cell-based assays to identify five novel p53 target genes from genes consistently up-regulated in wild-type p53 cancers. Global gene expression analyses revealed that cell cycle regulatory genes and transcription factors E2F1, MYBL2 and FOXM1 were disproportionately up-regulated in many TP53 mutant cancer types. Finally, > 93% of tumours with a TP53 mutation exhibited greatly reduced wild-type p53 messenger expression, due to loss of heterozygosity or copy neutral loss of heterozygosity, supporting the concept of p53 as a recessive tumour suppressor. The data indicate that tumours with wild-type TP53 retain some aspects of p53-mediated growth inhibitory signalling through activation of p53 target genes and suppression of cell cycle regulatory genes.

Indexed as

Gene Expression ProfilingGene Expression Regulation, NeoplasticGenes, Tumor SuppressorMutationBiomarkers, TumorCell Cycle ProteinsHumansLoss of HeterozygosityNeoplasmsRNA, MessengerSignal TransductionTranscription FactorsTumor Suppressor Protein p53Biomarkers, TumorCell Cycle ProteinsRNA, MessengerTP53 protein, humanTranscription FactorsTumor Suppressor Protein p53CDKN1AE2F1FOXM1MYBL2nonsense-mediated mRNA decayp53RPS27LiTCGATP53ZMAT3

Identifiers

PMID24374933
PMCPMC4362779
OpenAlexW1517872057

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.