Evidence map›Paper›PMID 37605254›Full record

ArticleAdvances in rheumatology (London, England)2023

TP53 and p21 (CDKN1A) polymorphisms and the risk of systemic lupus erythematosus.

Jacyara Maria Brito Macedo, Amanda Lima Silva, Amanda Chaves Pinto, Leandro Ferreira Lopes Landeira, Elyzabeth Avvad Portari, Cintia Barros Santos-Rebouças, Evandro Mendes Klumb

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Article in Advances in rheumatology (London, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.9field-weighted citation impact, top 20% 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

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. 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

7 authors at 2 institutions in 1 country.

Jacyara Maria Brito MacedoDepartment of Biochemistry, State University of Rio de Janeiro - UERJ, Rio de Janeiro, Brazil.ORCID http://orcid.org/0000-0002-4976-9318
Amanda Lima SilvaDepartment of Biochemistry, State University of Rio de Janeiro - UERJ, Rio de Janeiro, Brazil.ORCID http://orcid.org/0000-0002-2143-4719
Amanda Chaves PintoDepartment of Biochemistry, State University of Rio de Janeiro - UERJ, Rio de Janeiro, Brazil.ORCID http://orcid.org/0000-0002-4372-096X
Leandro Ferreira Lopes LandeiraDepartment of Biochemistry, State University of Rio de Janeiro - UERJ, Rio de Janeiro, Brazil.ORCID http://orcid.org/0000-0001-5121-8139
Elyzabeth Avvad PortariDepartment of Pathological Anatomy, State University of Rio de Janeiro - UERJ, Rio de Janeiro, Brazil.ORCID http://orcid.org/0000-0003-2372-0898
Cintia Barros Santos-RebouçasDepartment of Pathological Anatomy, State University of Rio de Janeiro - UERJ, Rio de Janeiro, Brazil.ORCID http://orcid.org/0000-0003-4729-2373
Evandro Mendes KlumbDepartment of Rheumatology, Pedro Ernesto University Hospital, State University of Rio de Janeiro - UERJ, Boulevard 28 de Setembro, 87, Vila Isabel, Rio de Janeiro, RJ, CEP 20551-030, Brazil. klumb@uol.com.br.ORCID http://orcid.org/0000-0001-9546-3144
Universidade do Estado do Rio de Janeiro · BRHospital Universitário Pedro Ernesto · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe p53 and p21 proteins are important regulators of cell cycle and apoptosis and may contribute to autoimmune diseases, such as systemic lupus erythematosus (SLE). As genetic polymorphisms may cause changes in protein levels and functions, we investigated associations of TP53 and p21 (CDKN1A) polymorphisms (p53 72 G > C-rs1042522; p53 PIN3-rs17878362; p21 31 C > A-rs1801270; p21 70 C > T-rs1059234) with the development of systemic lupus erythematosus (SLE) in a Southeastern Brazilian population.

methodsGenotyping of 353 female volunteers (cases, n = 145; controls, n = 208) was performed by polymerase chain reaction, restriction fragment length polymorphism and/or DNA sequencing. Associations between TP53 and p21 polymorphisms and SLE susceptibility and clinical manifestations of SLE patients were assessed by logistic regression analysis.

resultsProtective effect was observed for the genotype combinations p53 PIN3 A1/A1-p21 31 C/A, in the total study population (OR 0.45), and p53 PIN3 A1/A2-p21 31 C/C, in non-white women (OR 0.28). In Whites, p53 72 C-containing (OR 3.06) and p53 PIN3 A2-containing (OR 6.93) genotypes were associated with SLE risk, and higher OR value was observed for the combined genotype p53 72 G/C-p53 PIN3 A1/A2 (OR 9.00). Further, p53 PIN3 A1/A2 genotype was associated with serositis (OR 2.82), while p53 PIN3 A2/A2 and p53 72 C/C genotypes were associated with neurological disorders (OR 4.69 and OR 3.34, respectively).

conclusionsOur findings showed that the TP53 and p21 polymorphisms included in this study may have potential to emerge as SLE susceptibility markers for specific groups of patients. Significant interactions of the TP53 polymorphisms with serositis and neurological disorders were also observed in SLE patients.

Indexed as

Cyclin-Dependent Kinase Inhibitor p21Lupus Erythematosus, SystemicTumor Suppressor Protein p53FemaleHumansPolymorphism, GeneticSerositisCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21TP53 protein, humanTumor Suppressor Protein p53Genetic polymorphismsp21Systemic lupus erythematosusTP53

Identifiers

PMID37605254
OpenAlexW4386027582

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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.