Evidence map›Paper›PMID 22200742›Full record

ArticleOncology reports2012

Genetic polymorphisms and cervical cancer development: ATM G5557A and p53bp1 C1236G.

S Oliveira, J Ribeiro, H Sousa, D Pinto, I Baldaque, R Medeiros

Open access · bronzeAbstract read
In one paragraph

Article in Oncology reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 4 pooled it
1.2field-weighted citation impact, top 21% 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

17 citing papers in PubMed, 4 syntheses or guidelines pooled it, 21 citations in OpenAlex.

  1. Polymorphism rs1801516 (G > A) in theThe Journal of international medical research · 2020
    Pooled it
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  5. Article
  6. Review
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  10. Article
  11. Ataxia Telangiectasia-Mutated (Frontiers in public health · 2017
    Article
  12. Article
  13. Article
  14. Article
  15. Defective antioxidant systems in cervical cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    Review
  16. Article
  17. 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

6 authors at 2 institutions in 2 countries.

S OliveiraMolecular Oncology Group, Portuguese Institute of Oncology of Porto, Rua Dr António Bernardino Almeida, 4200-072 Porto, Portugal.
J Ribeiro
H Sousa
D Pinto
I Baldaque
R Medeiros
Instituto Português de Oncologia Francisco Gentil · PTMolecular Oncology (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Persistent infections by high-risk types of human papillomavirus (HPV) have been established as the etiological agent of cervical cancer. The integration of the HPV genome into the host genome is a crucial step in cervical carcinogenesis, although, correct activation of DNA damage repair pathways will avoid the development of cancer. Recent data indicate that several polymorphisms of key regulators from the DNA damage repair pathway (i.e. 53BP1 and ATM) are associated with cancer development susceptibility. We have developed a hospital-based retrospective study considering 429 cervical specimens from women with different cervical lesions including invasive carcinoma. This study aimed to evaluate the role of the ATM D1853N (5557G>A) and 53bp1 D353E (1236C>G) polymorphisms in the development of cervical cancer, using TaqMan SNP Genotyping Assays. Statistical analysis revealed that ATM 5557GG homozygous individuals (OR=1.94; p=0.044) are at increased risk of developing LSIL, while for the 53BP1 1236C>G polymorphism no association was found. Nevertheless, we observed a tendency for an increased risk of LSIL in 53BP1 1236C allele carriers (OR=1.63; p=0.069). Logistic regression adjusted for age revealed no significant differences from the non-adjusted analysis. This is the first study to evaluate the role of ATM G5557A and P53BP1 C1236G polymorphisms in cervical cancer susceptibility. This study reveals a possible trend of both polymorphisms for a genetic susceptibility pattern of cervical cancer development. Hence, our results may be of interest for future understanding of the progression of cervical cancer.

Indexed as

Polymorphism, GeneticAdultAgedAtaxia Telangiectasia Mutated ProteinsBiomarkers, TumorCarcinomaCell Cycle ProteinsChi-Square DistributionDNA-Binding ProteinsFemaleGene FrequencyGenetic Predisposition to DiseaseHomozygoteHumansLogistic ModelsMiddle AgedAtaxia Telangiectasia Mutated ProteinsATM protein, humanBiomarkers, TumorCell Cycle ProteinsDNA-Binding ProteinsProtein Serine-Threonine KinasesTP53 protein, humanTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID22200742
PMCPMC3583604
OpenAlexW2042076105

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.