B Torres

Publications (8)44.92 Total impact

• Article: Caspase 7 influences susceptibility to rheumatoid arthritis.

  J R García-Lozano, B Torres, O Fernández, G Orozco, A Alvarez-Márquez, A García, M A González-Gay, A Núñez-Roldán, J Martín, M F González-Escribano
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  ABSTRACT: The aim of this study was to investigate the possible role of the caspase 7 (CASP7) in susceptibility to rheumatoid arthritis (RA). Genotyping of three single nucleotide polymorphisms (SNPs) of the CASP7 gene: rs11593766 (G/ T), rs2227310 (C/G) and rs2227309 (G/A) was performed in a total of 906 RA patients and 528 matched healthy controls using TaqMan assays. All the subjects were of Spanish Caucasian origin. A relative quantification of mRNA encoding the non-functional variant of procaspase 7 (isoform beta) vs functional isoforms was performed in total RNA from 32 healthy individuals using real-time PCR. Only the rs2227309 SNP was found to be associated with susceptibility to RA. Frequency of the G allele was significantly higher among RA patients [overall frequency of the G allele 74.0% in cases vs 68.4% in controls, P = 0.001, Odds ratio (OR) = 1.32, 95% Confidence intervals (95% CI) 1.11-1.56] and a higher frequency of GG homozygous individuals was found in the RA patient group (overall frequency of GG genotype 56.0% in cases and 46.4% in controls, P = 0.0005, OR = 1.47, 95%CI 1.18-1.83). A statistically significant deviation was observed to compare the relative expression of the procaspase 7 isoform beta in samples from individuals stratified according their rs2227309 genotypes (AA + AG: 1.36 +/- 0.55, n = 19, vs GG: 2.35 +/- 0.74, n = 13; P = 0.0002). Our results support involvement of the CASP7 gene in the susceptibility to RA. The higher production of the no functional variant of CASP7 by individuals with a particular genotype could be the basis of this association.
  Rheumatology 09/2007; 46(8):1243-7. · 4.06 Impact Factor
• Article: Asporin repeat polymorphism in rheumatoid arthritis.

  B Torres, G Orozco, J R García-Lozano, J Oliver, O Fernández, M A González-Gay, A Balsa, A García, D Pascual-Salcedo, M A López-Nevot, A Núñez-Roldán, J Martín, M F González-Escribano
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  ABSTRACT: Asporin belongs to a family of proteins associated with the cartilage matrix. To investigate the role of the functional polymorphism consisting of an aspartic acid (D) repeat polymorphism located in the ASPN gene in the susceptibility to and clinical outcome of rheumatoid arthritis. A total of 803 Spanish Caucasian patients with rheumatoid arthritis and 904 controls of the same ethnic origin and matched for age and sex were included in the study. The asporin D repeat polymorphism was genotyped using polymerase chain reaction with a fluorescent primer. No significant differences were detected in the distribution of the 10 alleles found in our population on comparing patients with rheumatoid arthritis with control groups. Nevertheless, individuals bearing D14 produced rheumatoid factor more often than the rest (85.7% v 72.1%, p = 0.006, odds ratio (OR) = 2.35, 95% confidence interval 1.21 to 4.50), and the mean (SD) onset age was higher in the group of individuals bearing D13 (50.09 (13.94)) compared with the rest (47.21 (14.31)), although the difference did not reach significance (p = 0.06). The results do not support a major role for asporin D repeat polymorphism in the susceptibility to rheumatoid arthritis. Nevertheless, they support the influence of this gene on the outcome of the disease.
  Annals of the Rheumatic Diseases 02/2007; 66(1):118-20. · 8.73 Impact Factor
• Article: No primary association of MICA polymorphism with systemic lupus erythematosus.

  E Sánchez, B Torres, J R Vilches, M A López-Nevot, N Ortego-Centeno, J Jiménez-Alonso, M A González-Gay, E de Ramón, J Sánchez-Román, A Núñez-Roldán, J Martín, M F González-Escribano
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  ABSTRACT: To replicate the described association between MHC class I chain-related A (MICA) gene polymorphism and susceptibility to systemic lupus erythematosus (SLE). MICA transmembrane microsatellite polymorphism was genotyped using a polymerase chain reaction (PCR)-based method. Genotyping of HLA-B* and DRB1* was performed using PCR and detection with a reverse sequence-specific oligonucleotide (SSO) probe system. Combined data for these three loci (HLA-B*, DRB1* and MICA) were obtained from a total of 333 patients and 361 healthy controls. Significant association with B*08 [P < 10(-7), odds ratio (OR) 3.17, 95% confidence interval (CI) 2.02-5.00], DRB1*0301 (P < 10(-7), OR 2.07, 95% CI 1.59-2.68) and MICA5.1 (P = 0.01, OR 1.23, 95% CI 1.04-1.46) was observed. The combinations DRB1*0301-MICA5.1-B8 and HLA-DRB1*0301-B*08-positive and MICA5-1-negative were more frequent among SLE patients (11.4 vs 3.3% in healthy controls, P = 3.9 x 10(-5), OR 3.76, 95% CI 1.85-7.73, and 6.9 vs 1.7%, P = 0.0007, OR 4.32, 95% CI 1.68-13.10, respectively). Additionally, individuals who were HLA-DRB1*0301-B*08-negative and MICA5-1-positive were less frequent among patients (22.2 vs 31.3% in healthy controls, P = 0.007, OR 0.63, 95% CI 0.44-0.89) and the magnitude of the OR was similar to that obtained in individuals negative for all the three factors (OR 0.69, 95% CI 050-0.94). Further analysis performed to detect independent association strongly suggested that the association between MICA5.1 and SLE is secondary to the linkage disequilibrium of this allele with B*08. Our results do not support an independent association of MICA gene polymorphism with susceptibility to SLE.
  Rheumatology 10/2006; 45(9):1096-100. · 4.06 Impact Factor
• Article: Study of the role of functional variants of SLC22A4, RUNX1 and SUMO4 in systemic lupus erythematosus.

  G Orozco, E Sánchez, L M Gómez, M A González-Gay, M A López-Nevot, B Torres, N Ortego-Centeno, J Jiménez-Alonso, E de Ramón, J Sánchez Román, J M Anaya, G Sturfelt, I Gunnarsson, E Svennungsson, M Alarcón-Riquelme, M F González-Escribano, J Martín
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  ABSTRACT: Functional polymorphisms of the solute carrier family 22, member 4 (SLC22A4), runt related transcription factor 1 (RUNX1) and small ubiquitin-like modifier 4 (SUMO4) genes have been shown to be associated with several autoimmune diseases. To test the possible role of these variants in susceptibility to or severity of systemic lupus erythematosus (SLE), on the basis that common genetic bases are shared by autoimmune disorders. 597 SLE patients and 987 healthy controls of white Spanish origin were studied. Two additional cohorts of 228 SLE patients from Sweden and 122 SLE patients from Colombia were included. A case-control association study was carried out with six single nucleotide polymorphisms (SNP) spanning the SLC22A4 gene, one SNP in RUNX1 gene, and one additional SNP in SUM04 gene. No significant differences were observed between SLE patients and healthy controls when comparing the distribution of the genotypes or alleles of any of the SLC22A4, RUNX1, or SUMO4 polymorphisms tested. Significant differences were found in the distribution of the SUMO4 genotypes and alleles among SLE patients with and without nephritis, but after multiple testing correction, the significance of the association was lost. The association of SUMO4 with nephritis could not be verified in two independent SLE cohorts from Sweden and Colombia. These results suggest that the SLC22A4, RUNX1, and SUMO4 polymorphisms analysed do not play a role in the susceptibility to or severity of SLE.
  Annals of the Rheumatic Diseases 07/2006; 65(6):791-5. · 8.73 Impact Factor
• Article: Interleukin 12 (IL12B), interleukin 12 receptor (IL12RB1) and interleukin 23 (IL23A) gene polymorphism in systemic lupus erythematosus.

  E Sánchez, S Morales, L Paco, M A López-Nevot, C Hidalgo, J Jiménez-Alonso, B Torres, M A González-Gay, J L Callejas, N Ortego-Centeno, J Sánchez-Roman, M F González-Escribano, J Martín
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  ABSTRACT: The aim of this study was to assess the possible association between the interleukin-12B (IL12B) and interleukin-12 receptor beta 1 (IL12RB1) gene polymorphisms with systemic lupus erythematosus (SLE). In addition, we have undertaken a systematic search for genetic variants of interleukin 23 (IL23A). The study was conducted on 559 SLE patients and 603 ethnically matched healthy controls. Genotyping of the IL12B [IL12Bpro and IL12B 3' untranslated region (UTR)] and IL12RB1 (641A-->G, 1094T-->C and 1132G-->C) polymorphisms was performed with polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and PCR-fluorescent methods, whereas IL23A genetic variants were realized with direct sequencing. No statistically significant differences in the distribution of the IL12B and the IL12RB1 genotypes and alleles were observed when comparing SLE patients and control subjects. Additionally, no differences in the genotype and allele distribution were found when SLE patients were stratified according to the presence or absence of lupus nephritis. Despite an extensive analysis in 30 individuals, variations located in the exons and in the 5' and 3' UTR regions of IL23A gene were not found in any case. These results suggest that polymorphisms located in IL12B, IL12RB1 and IL23A genes may not play a relevant role in the susceptibility or severity of SLE in the Spanish population.
  Rheumatology 10/2005; 44(9):1136-9. · 4.06 Impact Factor
• Article: Cytotoxic T-lymphocyte antigen-4-CT60 polymorphism in rheumatoid arthritis.

  G Orozco, B Torres, A Núñez-Roldán, M F González-Escribano, J Martín
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  ABSTRACT: Cytotoxic T-lymphocyte antigen-4 (CTLA-4) is a functional candidate gene with susceptibility to rheumatoid arthritis (RA). The aim of this work was to investigate the possible influence of the recently described CT60A/G dimorphism of the CTLA-4 gene in the susceptibility to RA in Spanish patients. A total of 433 RA patients and 398 control subjects were included in the study. Genotyping of CTLA-4 CT60 was performed using two different methods: polymerase chain reaction restriction fragment length polymorphism system using an amplification-created restriction site and a TaqMan 5'-allelic discrimination assay. In order to validate results obtained by different methods, a quality-control exercise was performed. No significant deviation in the distribution of the alleles or genotypes of the CT60 was found when we compared RA patient and control groups. In addition, no differences in CTLA-4 CT60 genotypic distribution was found when RA patients and controls were stratified by the presence or absence of the shared epitope. In conclusion, our results do not support an association between CT60A/G polymorphism and susceptibility to RA in the Spanish population, although the contribution of other positions located within the 3' region of the CTLA-4 gene to RA susceptibility cannot be discarded.
  Tissue Antigens 01/2005; 64(6):667-70. · 2.59 Impact Factor
• Article: Cytotoxic T‐lymphocyte antigen‐4‐CT60 polymorphism in rheumatoid arthritis

  G. Orozco, B. Torres, A. Núñez-Roldán, M.F. González-Escribano, J. Martín
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  ABSTRACT:   Cytotoxic T-lymphocyte antigen-4 (CTLA-4) is a functional candidate gene with susceptibility to rheumatoid arthritis (RA). The aim of this work was to investigate the possible influence of the recently described CT60A/G dimorphism of the CTLA-4 gene in the susceptibility to RA in Spanish patients. A total of 433 RA patients and 398 control subjects were included in the study. Genotyping of CTLA-4 CT60 was performed using two different methods: polymerase chain reaction restriction fragment length polymorphism system using an amplification-created restriction site and a TaqMan 5′-allelic discrimination assay. In order to validate results obtained by different methods, a quality-control exercise was performed. No significant deviation in the distribution of the alleles or genotypes of the CT60 was found when we compared RA patient and control groups. In addition, no differences in CTLA-4 CT60 genotypic distribution was found when RA patients and controls were stratified by the presence or absence of the shared epitope. In conclusion, our results do not support an association between CT60A/G polymorphism and susceptibility to RA in the Spanish population, although the contribution of other positions located within the 3′ region of the CTLA-4 gene to RA susceptibility cannot be discarded.
  Tissue Antigens 11/2004; 64(6):667 - 670. · 2.59 Impact Factor
• Article: SLC11A1 promoter gene polymorphisms and fibrosis progression in chronic hepatitis C.

  M Romero-Gómez, M A Montes-Cano, M A Otero-Fernández, B Torres, D Sánchez-Muñoz, F Aguilar, N Barroso, L Gómez-Izquierdo, V M Castellano-Megias, A Núñez-Roldán, J Aguilar-Reina, M F González-Escribano
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  ABSTRACT: The solute carrier family 11 member 1 (SLC11A1) gene (formerly Nramp1) encodes for the protein solute carrier family 11, member 1. It affects susceptibility and clinical outcome of autoimmune and infectious diseases. We investigated the possible role of the functional polymorphism located in the promoter region of SLC11A1 and tumour necrosis factor (TNF) genes in the progression of fibrosis in chronic hepatitis C. A total of 242 Caucasian Spanish patients with biopsy proven chronic hepatitis C and 194 healthy control subjects were genotyped for SLC11A1 and TNF promoter polymorphisms. No significant differences in the distribution of frequencies among patient and control groups were observed. The SCL11A1 homozygous 2/2 genotype was rarely detected among patients showing advanced fibrosis (2/82; 2.4%) but was highly represented in those with mild fibrosis (29/160; 18.1%; odds ratio (OR) 8.85 (95% confidence interval (CI) 1.9-55.2, p(c) = 0.002). In patients carrying allele 3 of SLC11A1, the presence of -238 TNF A/G was associated with advanced fibrosis (14/26 (53.8%) v 68/216 (31.4%); OR 2.53 (95% CI 1.03-6.23); p = 0.02). SLC11A1 gene promoter polymorphism could influence fibrosis progression in chronic hepatitis C in that the homozygous genotype 2/2 exerts a protective effect against cirrhosis development. Also, the combination of TNF -238 A/G and the presence of allele 3 is conducive to progression to pre-cirrhotic or cirrhotic stages of the disease.
  Gut 04/2004; 53(3):446-50. · 10.11 Impact Factor