Evidence map›Paper›PMID 31152665›Full record

ReviewJournal of molecular cell biology2019

Common genetic variants in the TP53 pathway and their impact on cancer.

Thibaut Barnoud, Joshua L D Parris, Maureen E Murphy

Open access · goldAbstract readReview
In one paragraph

Review in Journal of molecular cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

39 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. TP53: the unluckiest of genes?Cell death and differentiation · 2025
    Review
  8. Generation of Monosomy 21q Human iPS Cells by CRISPR/Cas9-Mediated Interstitial Megabase Deletion.Genes to cells : devoted to molecular & cellular mechanisms · 2025
    Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Emerging insights into ethnic-specific TP53 germline variants.Journal of the National Cancer Institute · 2023
    Review
  18. Article
  19. Article
  20. Association ofBiomedicines · 2023
    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

3 authors at 1 institution in 1 country.

Thibaut BarnoudProgram in Molecular and Cellular Oncogenesis, The Wistar Institute, Philadelphia, PA, USA.
Joshua L D ParrisProgram in Molecular and Cellular Oncogenesis, The Wistar Institute, Philadelphia, PA, USA.
Maureen E MurphyProgram in Molecular and Cellular Oncogenesis, The Wistar Institute, Philadelphia, PA, USA.
The Wistar Institute · US

Funding

Tumor Microenvironment and MetastasisP30CA010815 · NCI · WISTAR INSTITUTE · PI Luis J Montaner · 1985 to 2026
$75.9M
TRAINING PROGRAM IN BASIC CANCER RESEARCHT32CA009171 · NCI · WISTAR INSTITUTE · PI Alessandro Gardini · 1985 to 2026
$15.3M
Functional Analysis of p53 Polymorphic Variants - Diversity SupplementR01CA102184 · NCI · WISTAR INSTITUTE · PI Maureen E. Murphy · 2005 to 2026
$7.4M
p53 Variants in Cancer Risk and TherapyR01CA201430 · NCI · WISTAR INSTITUTE · PI MURPHY, MAUREEN E. · 2016 to 2020
$2.2M
Tumor Suppression by an African Specific Variant of p53F32CA220972 · NCI · WISTAR INSTITUTE · PI BARNOUD, THIBAUT · 2018 to 2019
$114k
NCI NIH HHS F32 CA220972NCI NIH HHS P30 CA010815NCI NIH HHS R01 CA102184NCI NIH HHS R01 CA201430NCI NIH HHS T32 CA009171
6 · The paper itself

Abstract

The TP53 gene is well known to be the most frequently mutated gene in human cancer. In addition to mutations, there are > 20 different coding region single-nucleotide polymorphisms (SNPs) in the TP53 gene, as well as SNPs in MDM2, the negative regulator of p53. Several of these SNPs are known to alter p53 pathway function. This makes p53 rather unique among cancer-critical genes, e.g. the coding regions of other cancer-critical genes like Ha-Ras, RB, and PI3KCA do not have non-synonymous coding region SNPs that alter their function in cancer. The next frontier in p53 biology will consist of probing which of these coding region SNPs are moderately or strongly pathogenic and whether they influence cancer risk and the efficacy of cancer therapy. The challenge after that will consist of determining whether we can tailor chemotherapy to correct the defects for each of these variants. Here we review the SNPs in TP53 and MDM2 that show the most significant impact on cancer and other diseases. We also propose avenues for how this information can be used to better inform personalized medicine approaches to cancer and other diseases.

Indexed as

NeoplasmsPolymorphism, Single NucleotideProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53AnimalsGenes, rasHumansRetinoblastoma ProteinSignal TransductionTranscription FactorsMDM2 protein, humanPI3KCA protein, humanProto-Oncogene Proteins c-mdm2Retinoblastoma ProteinTP53 protein, humanTranscription FactorsTumor Suppressor Protein p53MDM2p53PASPro47SerPro72ArgSNP309

Identifiers

PMID31152665
PMCPMC6736421
OpenAlexW2947789668

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.