Evidence map›Paper›PMID 20358297›Full record

ArticleMolecular biology reports2011

ARLTS1, MDM2 and RAD51 gene variations are associated with familial breast cancer.

Elif Akisik, Hulya Yazici, Nejat Dalay

Abstract read
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In one paragraph

Article in Molecular biology reports, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 4 pooled it
1.8field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 4 syntheses or guidelines pooled it, 33 citations in OpenAlex.

  1. Pooled it
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  11. Lack of an Association between a Functional Polymorphism in theReports of biochemistry & molecular biology · 2017
    Article
  12. Hereditary cancer in clinical practice · 2017
    Review
  13. Article
  14. Association between RAD51 polymorphism and breast cancer susceptibility: a meta analysis.International journal of clinical and experimental medicine · 2015
    Article
  15. Article
  16. Article
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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

3 authors at 1 institution in 1 country.

Elif AkisikDepartment of Basic Oncology, I. U. Oncology Institute, Istanbul University, Istanbul, Capa, 34093, Turkey.
Hulya Yazici
Nejat Dalay
Istanbul University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genetic factors that contribute to the risk of breast cancer are largely not known and association studies have revealed several genes with low penetrance risk alleles for breast cancer. Analysis of these genes may provide important information on the risk factors affecting carcinogenesis. Variations in the ARLTS1, RAD51 and MDM2 genes have been associated with increased risk of different cancer types but for breast cancer the results are not consistent. In this study we investigated the role of the allelic variants in candidate genes acting in the tumor suppressor, DNA repair and p53 pathways as risk factors for familial breast cancer in 147 patients displaying characteristics of familial disease. Presence of the polymorphic variants were investigated by amplification of the corresponding regions and restriction fragment length polymorphism analysis. Genotype and allele frequencies in the patients were significantly different for all three variants. Our results indicate that the polymorphic variants might affect individual susceptibility towards breast cancer.

Indexed as

Genetic Association StudiesGenetic Predisposition to DiseasePolymorphism, GeneticADP-Ribosylation FactorsAdultBreast NeoplasmsCase-Control StudiesFamilyFemaleGene FrequencyHumansProto-Oncogene Proteins c-mdm2Rad51 RecombinaseADP-Ribosylation FactorsARL11 protein, humanMDM2 protein, humanProto-Oncogene Proteins c-mdm2RAD51 protein, humanRad51 Recombinase

Identifiers

PMID20358297
OpenAlexW1981092366

What OpenQuestion holds

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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.