Evidence map›Paper›PMID 17998932›Full record

ArticleOncogene2008

Common tumour p53 mutations in immortalized cells from Hupki mice heterozygous at codon 72.

M Reinbold, J-L Luo, T Nedelko, B Jerchow, M E Murphy, C Whibley, Q Wei, M Hollstein

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

29 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Evaluation of in vivo mutagenesis for assessing the health risk of air pollutants.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2017
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Comparison of the metabolic activation of environmental carcinogens in mouse embryonic stem cells and mouse embryonic fibroblasts.Toxicology in vitro : an international journal published in association with BIBRA · 2015
    Article
  14. Article
  15. Article
  16. Article
  17. Regulation of female reproduction by p53 and its family members.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2011
    Article
  18. Article
  19. Article
  20. 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 6 institutions in 3 countries.

M ReinboldDepartment of Genetic Alterations in Carcinogenesis, German Cancer Research Center, Heidelberg, Germany.
J-L Luo
T Nedelko
B Jerchow
M E Murphy
C Whibley
Q Wei
M Hollstein
German Cancer Research Center · DEFox Chase Cancer Center · USHeidelberg University · DEMax Delbrück Center · DEUniversity of California, San Diego · USUniversity of Leeds · GB

Funding

Functional Analysis of p53 Polymorphic Variants - Diversity SupplementR01CA102184 · NCI · WISTAR INSTITUTE · PI Maureen E. Murphy · 2005 to 2026
$7.4M
Cancer Research UKNCI NIH HHS R01 CA102184
6 · The paper itself

Abstract

Codon 72 of human p53 gene is polymorphic, encoding arginine or proline. Here we report construction of a human p53 knock-in (Hupki) mouse encoding the codon 72(pro) variant. The new strain was crossed with the original Hupki mice (codon 72(arg/arg)) to obtain primary embryonic fibroblasts polymorphic at codon 72 or homozygous for codon 72(pro). The fibroblasts, cultured under standard conditions, immortalized within 12 weeks and acquired p53 mutations similarly to Hupki codon 72(arg/arg) cells investigated previously. Sequencing of human p53 exons 4-9 in immortalized cultures revealed missense mutations found repeatedly in human tumours. In cell lines ensuing from benzo(a)pyrene-treated cultures the combined p53 mutation pattern from experiments with the 3 codon 72 genotypes showed a predominance of strand-biased G to T transversions (18 of 36 mutations), and mutations recurring at smokers' lung tumour hotspot codons 157 and 273, supporting involvement of tobacco carcinogens in shaping the mutation signature in lung cancers of smokers. Mutations in cell lines from unexposed cultures did not cluster at these codons and G to T transversions were uncommon (2 of 52 mutations) (Fisher's exact test P<0.0001). Most mutations (13/16) in cell lines derived from cells polymorphic at codon 72 were found on the proline allele, with loss of the arginine allele.

Indexed as

Genes, p53HeterozygoteAmino Acid SubstitutionAnimalsCell Line, TransformedCodonHumansMiceMice, TransgenicMutagenesis, Site-DirectedPolymorphism, GeneticTumor Suppressor Protein p53CodonTumor Suppressor Protein p53

Identifiers

PMID17998932
PMCPMC6813802
OpenAlexW2080431351

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.