Evidence map›Paper›PMID 24955348›Full record

ArticleBioMed research international2014

Polymorphism of XRCC1, XRCC3, and XPD genes and risk of chronic myeloid leukemia.

Claudia Bănescu, Adrian P Trifa, Smaranda Demian, Erzsebeth Benedek Lazar, Delia Dima, Carmen Duicu, Minodora Dobreanu

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 2 pooled it
5.1field-weighted citation impact, top 5% 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

16 citing papers in PubMed, 2 syntheses or guidelines pooled it, 36 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  13. Polymorphisms in DNA repair genes in gastrointestinal stromal tumours: susceptibility and correlation with tumour characteristics and clinical outcome.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
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  14. Analysis ofBiomedical reports · 2016
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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

7 authors at 3 institutions in 1 country.

Claudia BănescuDepartment of Medical Genetics, University of Medicine and Pharmacy Tirgu Mures, 38 Gh, Marinescu Street, Romania.
Adrian P TrifaDepartment of Medical Genetics, "Iuliu Hatieganu" University of Medicine and Pharmacy, Cluj-Napoca, Romania.
Smaranda DemianHematology Clinic 1, University of Medicine and Pharmacy Tirgu Mures, Romania.
Erzsebeth Benedek LazarHematology Clinic 2, University of Medicine and Pharmacy Tirgu Mures, Romania.
Delia DimaDepartment of Hematology, "Ion Chiricuta" Cancer Institute, Cluj-Napoca, Romania.
Carmen DuicuPediatric Clinic, University of Medicine and Pharmacy Tirgu Mures, Romania.
Minodora DobreanuLaboratory Medicine, University of Medicine and Pharmacy Tirgu Mures, Romania.
Universitatea de Medicină, Farmacie, Științe și Tehnologie „George Emil Palade” din Târgu Mureș · ROInstitute of Oncology Prof. Dr. Ion Chiricuta · ROIuliu Hațieganu University of Medicine and Pharmacy · RO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The genetic polymorphisms of X-ray repair cross complementing group 1 (XRCC1), X-ray repair cross complementing group 3 (XRCC3), and xeroderma pigmentosum complementation group D (XPD) repair genes may lead to genetic instability and leukemogenesis. The purpose of the study was to evaluate the association between XRCC1 Arg399Gln, Arg280His and Arg194Trp, XRCC3 Thr241Met, and XPD Lys751Gln polymorphisms and the risk of developing CML in Romanian patients. A total of 156 patients diagnosed with CML and 180 healthy controls were included in this study. We found no association between CML and XRCC1 or XRCC3 variant genotypes in any of the investigated cases. A significant difference was observed in the variant genotype frequencies of the XPD Lys751Gln polymorphism between the patients with CML and control group (for variant homozygous genotypes, OR = 2.37; 95% CI = 1.20-4.67; P value = 0.016 and for combined heterozygous and variant homozygous genotypes, OR = 1.72; 95% CI = 1.10-2.69; P value = 0.019). This was also observed when analyzing the variant 751Gln allele (OR = 1.54; 95% CI = 1.13-2.11; P value = 0.008). Our results suggest that the XPD Lys751Gln variant genotype increases the risk of CML.

Indexed as

AdultAgedAllelesDNA-Binding ProteinsFemaleGenetic Association StudiesGenetic Predisposition to DiseaseHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMaleMiddle AgedPolymorphism, Single NucleotideRisk FactorsXeroderma Pigmentosum Group D ProteinX-ray Repair Cross Complementing Protein 1DNA-Binding ProteinsERCC2 protein, humanXeroderma Pigmentosum Group D ProteinX-ray Repair Cross Complementing Protein 1X-ray repair cross complementing protein 3XRCC1 protein, human

Identifiers

PMID24955348
PMCPMC4052066
OpenAlexW2073051813

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Registered trials

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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.