scispace - formally typeset
F

Fina A S Kurreeman

Researcher at Leiden University Medical Center

Publications -  59
Citations -  5949

Fina A S Kurreeman is an academic researcher from Leiden University Medical Center. The author has contributed to research in topics: Genome-wide association study & Single-nucleotide polymorphism. The author has an hindex of 32, co-authored 59 publications receiving 5515 citations. Previous affiliations of Fina A S Kurreeman include Leiden University & Harvard University.

Papers
More filters
Journal ArticleDOI

Genome-wide association study meta-analysis identifies seven new rheumatoid arthritis risk loci

Eli A. Stahl, +74 more
- 01 Jun 2010 - 
TL;DR: Seven new rheumatoid arthritis risk alleles were identified at genome-wide significance (P < 5 × 10−8) in an analysis of all 41,282 samples, and an additional 11 SNPs replicated at P < 0.05, suggesting that most represent genuine rhearatoid arthritisrisk alleles.
Journal ArticleDOI

Common variants at CD40 and other loci confer risk of rheumatoid arthritis

TL;DR: To identify rheumatoid arthritis risk loci in European populations, a meta-analysis of two published genome-wide association studies totaling 3,393 cases and 12,462 controls identified a common variant at the CD40 gene locus and identified evidence of association at four additional gene loci.
Journal ArticleDOI

Genetic variants at CD28, PRDM1, and CD2/CD58 are associated with rheumatoid arthritis risk

Soumya Raychaudhuri, +69 more
- 08 Nov 2009 - 
TL;DR: To discover new rheumatoid arthritis risk loci, GRAIL used Gene Relationships Across Implicated Loci (GRAIL), a computational method that applies statistical text mining to PubMed abstracts, to score these 179 loci for functional relationships to genes in 16 established RA disease loci.
Journal ArticleDOI

Meta-analysis of genome-wide association studies in celiac disease and rheumatoid arthritis identifies fourteen non-HLA shared loci

TL;DR: A meta-analysis of two published GWAS on celiac disease and rheumatoid arthritis confirmed that 4 gene loci previously established in either CD or RA are associated with the other autoimmune disease at combined P<5×10−8, and implicate antigen presentation and T-cell activation as a shared mechanism of disease pathogenesis.