Lack of replication of interactions between polymorphisms in rheumatoid arthritis susceptibility: case-control study. (Registro nro. 16381)
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| 000 -CABECERA | |
|---|---|
| Campo de control de longitud fija | nab a22 7a 4500 |
| 003 - IDENTIFICADOR DEL NÚMERO DE CONTROL | |
| Campo de control | PC16381 |
| 005 - FECHA Y HORA DE LA ÚLTIMA TRANSACCIÓN | |
| Campo de control | 20210625062821.0 |
| 008 - CÓDIGOS DE INFORMACIÓN DE LONGITUD FIJA | |
| Campo de control de longitud fija | 210504b xxu||||| |||| 00| 0 eng d |
| 040 ## - FUENTE DE LA CATALOGACIÓN | |
| Centro transcriptor | H12O |
| 041 ## - CÓDIGO DE LENGUA | |
| Código de lengua del texto/banda sonora o título independiente | eng |
| 100 ## - PUNTO DE ACCESO PRINCIPAL - NOMBRE DE PERSONA | |
| 9 (RLIN) | 1010 |
| Nombre de persona | Pablos Álvarez, José Luis |
| Término indicativo de función | Reumatología |
| 245 00 - MENCIÓN DE TÍTULO | |
| Título | Lack of replication of interactions between polymorphisms in rheumatoid arthritis susceptibility: case-control study. |
| Tipo de material | [artículo] |
| 260 ## - PUBLICATION, DISTRIBUTION, ETC. (IMPRINT) | |
| Nombre del editor distribuidor etc. | Arthritis research & therapy, |
| Fecha de publicación distribución etc. | 2014 |
| 300 ## - DESCRIPCIÓN FÍSICA | |
| Extensión | 16(5):436. |
| 500 ## - NOTA GENERAL | |
| Nota general | Formato Vancouver: Ferreiro-Iglesias A, Calaza M, Pérez-Pampin E, López Longo FJ, Marenco JL, Blanco FJ et al. Lack of replication of interactions between polymorphisms in rheumatoid arthritis susceptibility: case-control study. Arthritis Res Ther. 2014 Sep 27;16(5):436. |
| 501 ## - NOTA DE “CON” | |
| Nota de "Con" | PMID: 25260880 PMC4207328 |
| 504 ## - NOTA DE BIBLIOGRAFÍA; ETC. | |
| Nota de bibliografía etc. | Contiene 50 referencias |
| 520 ## - NOTA DE SUMARIO; ETC. | |
| Sumario etc. | Introduction: Approximately 100 loci have been definitively associated with rheumatoid arthritis (RA) susceptibility. However, they explain only a fraction of RA heritability. Interactions between polymorphisms could explain part of the remaining heritability. Multiple interactions have been reported, but only the shared epitope (SE) × protein tyrosine phosphatase nonreceptor type 22 (PTPN22) interaction has been replicated convincingly. Two recent studies deserve attention because of their quality, including their replication in a second sample collection. In one of them, researchers identified interactions between PTPN22 and seven single-nucleotide polymorphisms (SNPs). The other showed interactions between the SE and the null genotype of glutathione S-transferase Mu 1 (GSTM1) in the anti-cyclic citrullinated peptide-positive (anti-CCP+) patients. In the present study, we aimed to replicate association with RA susceptibility of interactions described in these two high-quality studies. Methods: A total of 1,744 patients with RA and 1,650 healthy controls of Spanish ancestry were studied. Polymorphisms were genotyped by single-base extension. SE genotypes of 736 patients were available from previous studies. Interaction analysis was done using multiple methods, including those originally reported and the most powerful methods described. Results: Genotypes of one of the SNPs (rs4695888) failed quality control tests. The call rate for the other eight polymorphisms was 99.9%. The frequencies of the polymorphisms were similar in RA patients and controls, except for PTPN22 SNP. None of the interactions between PTPN22 SNPs and the six SNPs that met quality control tests was replicated as a significant interaction term--the originally reported finding--or with any of the other methods. Nor was the interaction between GSTM1 and the SE replicated as a departure from additivity in anti-CCP+ patients or with any of the other methods. Conclusions: None of the interactions tested were replicated in spite of sufficient power and assessment with different assays. These negative results indicate that whether interactions are significant contributors to RA susceptibility remains unknown and that strict standards need to be applied to claim that an interaction exists. |
| 710 ## - PUNTO DE ACCESO ADICIONAL - NOMBRE DE ENTIDAD | |
| 9 (RLIN) | 123 |
| Nombre de entidad o nombre de jurisdicción como elemento inicial | Servicio de Reumatología |
| 710 ## - PUNTO DE ACCESO ADICIONAL - NOMBRE DE ENTIDAD | |
| 9 (RLIN) | 625 |
| Nombre de entidad o nombre de jurisdicción como elemento inicial | Instituto de Investigación imas12 |
| 856 ## - LOCALIZACIÓN Y ACCESO ELECTRÓNICOS | |
| Identificador Uniforme del Recurso (URI) | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4207328/ |
| Acceso | Acceso l ibre |
| 942 ## - ENTRADA PARA ELEMENTOS AGREGADOS (KOHA) | |
| Fuente de clasificación o esquema de ordenación en estanterías | |
| Koha [por defecto] tipo de item | Artículo |
| Suprimido en OPAC | Público |
| Suprimido | Estado de pérdida | Fuente de clasificación o esquema de ordenación en estanterías | Estropeado | No para préstamo | Localización permanente | Localización actual | Fecha de adquisición | Signatura completa | Fecha última consulta | Fecha del precio de reemplazo | Tipo de item de Koha |
|---|---|---|---|---|---|---|---|---|---|---|---|
| Hospital Universitario 12 de Octubre | Hospital Universitario 12 de Octubre | 2021-05-04 | PC16381 | 2021-05-04 | 2021-05-04 | Artículo |
