Evidence map›Paper›PMID 23715779›Full record

SynthesisTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2013

P53 codon 72 polymorphism and lung cancer risk: evidence from 27,958 subjects.

Chao Zhou, Hao Chen, An Wang

Abstract readMeta-Analysis
PubMed Publisher
In one paragraph

Synthesis in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 30% 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

3 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Lung cancer risk in relation to TP53 codon 47 and codon 72 polymorphism in Bangladeshi population.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    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.

Chao ZhouDepartment of Respiratory Medicine, Zhou Pu Hospital, 135 Guanyue Road, Pudong new District, Shanghai, 201318, China, zhou2000sh@163.com.
Hao Chen
An Wang
Pudong Medical Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The role of p53 codon 72 polymorphism in the development of lung cancer remains obscure due to inconsistent findings of individual case-control studies published to date. A meta-analysis was conducted to better estimate the association between the p53 codon 72 variant and lung cancer risk. All relevant publications from the PubMed, Embase, Web of Science, and Wanfang databases were retrieved. Based on the inclusion criteria, 39 publications involving 44 independent case-control studies were finally included into this meta-analysis. Data were extracted and the pooled odds ratio (OR) with the corresponding 95 % confidence interval (95 % CI) was calculated. The overall pooled ORs showed no significant relationship of the p53 codon 72 polymorphism with increased or decreased risk of lung cancer in all gene contrast models (OR Pro vs. Arg = 1.04, 95 % CI = 0.96-1.13, P OR < 0.001; OR Pro/Pro vs. Arg/Arg = 1.07, 95 % CI = 0.91-1.25, P OR < 0.001; OR Arg/Pro vs. Arg/Arg =1.04, 95 % CI = 0.94-1.15, P OR < 0.001; OR Pro/Pro + Arg/Pro vs. Arg/Arg = 1.04, 95 % CI = 0.94-1.16, P OR < 0.001; OR Pro/Pro vs. Arg/Arg + Arg/Pro = 1.07, 95 % CI = 0.93-1.23, P OR < 0.001). According to the ethnicity, no significant association was observed in subgroup analyses of the Asians, Caucasians, Africans and the mixed population. Similar finding was found in subgroup analyses of hospital-based and population-based studies. Concerning the histological types of lung cancer, the p53 codon 72 variant exerts risk effect on the lung carcinogenesis in patients with adenocarcinoma (OR Arg/Pro vs. Arg/Arg = 1.10, 95 % CI = 1.00-1.22, P OR = 0.048). Additionally, subgroup analysis by the smoking status demonstrated that the p53 codon 72 variant seemed to play a protective role in lung carcinogenesis among the non-smokers but not the smokers in the contrast model of Arg/Pro vs. Arg/Arg (OR Arg/Pro vs. Arg/Arg = 0.71, 95 % CI = 0.50-1.00, P OR = 0.049). The present meta-analysis suggests the p53 codon 72 polymorphism may weakly modify the risk for lung cancer among the adenocarcinoma patients and non-smokers. Nevertheless, this association needs further confirmation in future studies with high quality.

Indexed as

AdenocarcinomaCase-Control StudiesCodonGene FrequencyGenetic Association StudiesGenetic Predisposition to DiseaseHumansLung NeoplasmsOdds RatioPolymorphism, Single NucleotideRisk FactorsTumor Suppressor Protein p53CodonTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID23715779
OpenAlexW2009040797

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.