Skip to main content

Lund University Publications

LUND UNIVERSITY LIBRARIES

A large multicentre analysis of CTGF - 2945 promoter polymorphism does not confirm association with systemic sclerosis susceptibility or phenotype

Rueda, B. ; Simeon, C. ; Hesselstrand, Roger LU ; Herrick, A. ; Worthington, J. ; Ortego-Centeno, N. ; Riemekasten, G. ; Fonollosa, V. ; Vonk, M. C. and van den Hoogen, F. H. J. , et al. (2009) In Annals of the Rheumatic Diseases 68(10). p.1618-1620
Abstract
Objective: To conduct a replication study to investigate whether the 2945 CTGF genetic variant is associated with systemic sclerosis (SSc) susceptibility or specific SSc phenotype. Methods: The study population comprised 1180 patients with SSc and 1784 healthy controls from seven independent case-control sets of European ancestry (Spanish, French, Dutch, German, British, Swedish and North American). The 2945 CTGF genetic variant was genotyped using a Taqman 59 allelic discrimination assay. Results: An independent association study showed in all the case-control cohorts no association of the CTGF 2945 polymorphism with SSc susceptibility. These findings were confirmed by a meta-analysis giving a pooled OR=1.12 (95% CI 0.99 to 1.25), p=0.06.... (More)
Objective: To conduct a replication study to investigate whether the 2945 CTGF genetic variant is associated with systemic sclerosis (SSc) susceptibility or specific SSc phenotype. Methods: The study population comprised 1180 patients with SSc and 1784 healthy controls from seven independent case-control sets of European ancestry (Spanish, French, Dutch, German, British, Swedish and North American). The 2945 CTGF genetic variant was genotyped using a Taqman 59 allelic discrimination assay. Results: An independent association study showed in all the case-control cohorts no association of the CTGF 2945 polymorphism with SSc susceptibility. These findings were confirmed by a meta-analysis giving a pooled OR=1.12 (95% CI 0.99 to 1.25), p=0.06. Investigation of the possible contribution of the 2945 CTGF genetic variant to SSc phenotype showed that stratification according to SSc subtypes (limited or diffuse), selective autoantibodies (anti-topoisomerase I or anticentromere) or pulmonary involvement reached no statistically significant skewing. Conclusion: The results do not confirm previous findings and suggest that the CTGF 2945 promoter polymorphism does not play a major role in SSc susceptibility or clinical phenotype. (Less)
Please use this url to cite or link to this publication:
author
; ; ; ; ; ; ; ; and , et al. (More)
; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; and (Less)
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Annals of the Rheumatic Diseases
volume
68
issue
10
pages
1618 - 1620
publisher
BMJ Publishing Group
external identifiers
  • wos:000269771800018
  • scopus:70349386180
  • pmid:19054816
ISSN
1468-2060
DOI
10.1136/ard.2008.100180
language
English
LU publication?
yes
id
79a0370e-ff66-4b44-8321-ee279e0a288d (old id 1492432)
date added to LUP
2016-04-01 13:50:48
date last changed
2022-04-06 07:22:58
@article{79a0370e-ff66-4b44-8321-ee279e0a288d,
  abstract     = {{Objective: To conduct a replication study to investigate whether the 2945 CTGF genetic variant is associated with systemic sclerosis (SSc) susceptibility or specific SSc phenotype. Methods: The study population comprised 1180 patients with SSc and 1784 healthy controls from seven independent case-control sets of European ancestry (Spanish, French, Dutch, German, British, Swedish and North American). The 2945 CTGF genetic variant was genotyped using a Taqman 59 allelic discrimination assay. Results: An independent association study showed in all the case-control cohorts no association of the CTGF 2945 polymorphism with SSc susceptibility. These findings were confirmed by a meta-analysis giving a pooled OR=1.12 (95% CI 0.99 to 1.25), p=0.06. Investigation of the possible contribution of the 2945 CTGF genetic variant to SSc phenotype showed that stratification according to SSc subtypes (limited or diffuse), selective autoantibodies (anti-topoisomerase I or anticentromere) or pulmonary involvement reached no statistically significant skewing. Conclusion: The results do not confirm previous findings and suggest that the CTGF 2945 promoter polymorphism does not play a major role in SSc susceptibility or clinical phenotype.}},
  author       = {{Rueda, B. and Simeon, C. and Hesselstrand, Roger and Herrick, A. and Worthington, J. and Ortego-Centeno, N. and Riemekasten, G. and Fonollosa, V. and Vonk, M. C. and van den Hoogen, F. H. J. and Sanchez-Roman, J. and Aguirre-Zamorano, M. A. and Garcia-Portales, R. and Pros, A. and Camps, M. T. and Gonzalez-Gay, M. A. and Gonzalez-Escribano, M. F. and Coenen, M. J. and Lambert, N. and Nelson, J. L. and Radstake, T. R. D. J. and Martin, J.}},
  issn         = {{1468-2060}},
  language     = {{eng}},
  number       = {{10}},
  pages        = {{1618--1620}},
  publisher    = {{BMJ Publishing Group}},
  series       = {{Annals of the Rheumatic Diseases}},
  title        = {{A large multicentre analysis of CTGF - 2945 promoter polymorphism does not confirm association with systemic sclerosis susceptibility or phenotype}},
  url          = {{http://dx.doi.org/10.1136/ard.2008.100180}},
  doi          = {{10.1136/ard.2008.100180}},
  volume       = {{68}},
  year         = {{2009}},
}