Evidence map›Paper›PMID 16462765›Full record

ArticleOncogene2006

Trp53-dependent DNA-repair is affected by the codon 72 polymorphism.

M Siddique, K Sabapathy

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 4 pooled it
5.7field-weighted citation impact, top 3% 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, 4 syntheses or guidelines pooled it, 129 citations in OpenAlex.

  1. Pooled it
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  11. IntronicCancers · 2020
    Article
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  18. Journal of Cancer · 2019
    Article
  19. Article
  20. Oncology letters · 2018
    Review

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

2 authors at 2 institutions in 1 country.

M SiddiqueLaboratory of Molecular Carcinogenesis, National Cancer Centre, Singapore.
K Sabapathy
National Cancer Centre Singapore · SGNational University of Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Trp53 is arguably the most critical tumour suppressor gene product that inhibits malignant transformation. Besides mutations that inactivate Trp53 functions, genetic polymorphisms have been suggested to be risk factors for cancer. A polymorphic site at codon 72 in exon 4 encodes either an arginine amino acid (Trp53(72R)) or a proline residue (Trp53(72P)). Previous studies have shown that the Trp53(72R) form is more efficient in apoptosis induction, whereas the Trp53(72P) form was suggested to induce G1 arrest better. Here we report that Trp53(72P) is more efficient than Trp53(72R) in specifically activating several Trp53-dependent DNA-repair target genes in several cellular systems. Moreover, using isogenic cell lines and several DNA-repair assays, we show that Trp53(72P) cells have a significantly higher DNA-repair capacity than the Trp53(72R) cells. Furthermore, Trp53(72P)-expressing cells exhibit reduced micronuclei formation compared to Trp53(72R)-expressing cells, suggesting that genomic instability is reduced in these cells. Together, the data highlight the functional differences between the Trp53 polymorphic variants, and suggest that their expression status may influence cancer risk.

Indexed as

Polymorphism, GeneticAnimalsApoptosisBlotting, WesternCell LineCell Transformation, NeoplasticCodonDNA RepairHumansReverse Transcriptase Polymerase Chain ReactionRisk FactorsTumor Suppressor Protein p53CodonTumor Suppressor Protein p53

Identifiers

PMID16462765
OpenAlexW2078222310

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.