Evidence map›Paper›PMID 36835215›Full record

ArticleInternational journal of molecular sciences2023

Polymorphisms in DNA Repair Genes and Association with Rheumatoid Arthritis in a Pilot Study on a Central European Population.

Grzegorz Galita, Joanna Sarnik, Olga Brzezinska, Tomasz Budlewski, Grzegorz Dragan, Marta Poplawska, Ireneusz Majsterek, Tomasz Poplawski, Joanna S Makowska

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.7field-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

5 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. Article
  3. (Chemical) Roles of HOCl in Rheumatic Diseases.Antioxidants (Basel, Switzerland) · 2024
    Review
  4. Article
  5. 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

9 authors at 2 institutions in 1 country.

Grzegorz GalitaDepartment of Clinical Chemistry and Biochemistry, Medical University of Lodz, 92-215 Lodz, Poland.ORCID 0000-0002-1559-2796
Joanna SarnikDepartment of Rheumatology, Medical University of Lodz, 92-115 Lodz, Poland.
Olga BrzezinskaDepartment of Rheumatology, Medical University of Lodz, 92-115 Lodz, Poland.ORCID 0000-0002-3885-8497
Tomasz BudlewskiDepartment of Rheumatology, Medical University of Lodz, 92-115 Lodz, Poland.
Grzegorz DraganDepartment of Clinical Chemistry and Biochemistry, Medical University of Lodz, 92-215 Lodz, Poland.
Marta PoplawskaBiobank, Department of Immunology and Allergy, Medical University of Lodz, 92-213 Lodz, Poland.
Ireneusz MajsterekDepartment of Clinical Chemistry and Biochemistry, Medical University of Lodz, 92-215 Lodz, Poland.
Tomasz PoplawskiDepartment of Pharmaceutical Microbiology and Biochemistry, Medical University of Lodz, 92-215 Lodz, Poland.ORCID 0000-0003-2300-7339
Joanna S MakowskaDepartment of Rheumatology, Medical University of Lodz, 92-115 Lodz, Poland.
Medical University of Lodz · PLUniversity of Łódź · PL

Funding

National Center Science (NCN), Poland UMO-2017/25/B/NZ6/01358
6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is a chronic, multifactorial autoimmune disease characterized by chronic arthritis, a tendency to develop joint deformities, and involvement of extra-articular tissues. The risk of malignant neoplasms among patients with RA is the subject of ongoing research due to the autoimmune pathogenesis that underlies RA, the common etiology of rheumatic disease and malignancies, and the use of immunomodulatory therapy, which can alter immune system function and thus increase the risk of malignant neoplasms. This risk can also be increased by impaired DNA repair efficiency in individuals with RA, as reported in our recent study. Impaired DNA repair may reflect the variability in the genes that encode DNA repair proteins. The aim of our study was to evaluate the genetic variation in RA within the genes of the DNA damage repair system through base excision repair (BER), nucleotide excision repair (NER), and the double strand break repair system by homologous recombination (HR) and non-homologous end joining (NHEJ). We genotyped a total of 28 polymorphisms in 19 genes encoding DNA repair-related proteins in 100 age- and sex-matched RA patients and healthy subjects from Central Europe (Poland). Polymorphism genotypes were determined using the Taq-man SNP Genotyping Assay. We found an association between the RA occurrence and

Indexed as

Arthritis, RheumatoidDNA RepairGenetic Predisposition to DiseaseCase-Control StudiesGenotypeHumansPilot ProjectsPolymorphism, GeneticX-ray Repair Cross Complementing Protein 1X-ray Repair Cross Complementing Protein 1XRCC1 protein, humanDNA damage responseDNA repair genespolymorphismsrheumatoid arthritisSNP

Identifiers

PMID36835215
PMCPMC9964492
OpenAlexW4320920532

What OpenQuestion holds

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LicenceCC BY
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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.