FCGR3A-V158F polymorphism is a disease-specific pharmacogenetic marker for the treatment of psoriasis with Fc-containing TNF alpha inhibitors
PHARMACOGENOMICS JOURNAL
Authors: Mendrinoul, E.; Patsatsi, A.; Zafirious, E.; Papadopouloul, D.; Aggeloul, L.; Sarri, C.; Mannuris, Z.; Kyriakou, A.; Sotiriadis, D.; Roussaki-Schulze, A.; Sarafidou, T.; Vasilopoulos, Y.
Abstract
Psoriasis is a multifactorial skin disease affecting similar to 2% of world's population, causing a dramatic decrease in patients' quality of life and a significant increase in health-care expenses. Biological agents such as the anti-TNF alpha ones had an enormous impact in patients' therapy; however, a significant proportion of them do not respond well, an outcome attributed mainly to genetic factors. Recently, in a large European cohort of rheumatoid arthritis patients we have shown association with variation in the receptors that correspond to the Fc portion of the biological agents. As both diseases share common immunological fingerprints, we examined the hypothesis that they share common pharmacogenetic markers. Analysis of FCGR2A-H131R and FCGR3A-V158F polymorphisms in 100 psoriasis patients showed association only with respect to FCGR3A-V158F and response to etanercept (P=0.018). Interestingly, no association was found between FCGR2A-H131R and response to anti-TNFa therapy (P=0.882). This study suggests a role for FCGR3A-V158F polymorphism unique for psoriasis.
A pooled analysis of three studies evaluating genetic variation in innate immunity genes and non-Hodgkin lymphoma risk
BRITISH JOURNAL OF HAEMATOLOGY
Authors: Hosgood, H. Dean, III; Purdue, Mark P.; Wang, Sophia S.; Zheng, Tongzhang; Morton, Lindsay M.; Lan, Qing; Menashe, Idan; Zhang, Yawei; Cerhan, James R.; Grulich, Andrew; Cozen, Wendy; Yeager, Meredith; Holford, Theodore R.; Vajdic, Claire M.; Davis, Scott; Leaderer, Brian; Kricker, Anne; Schenk, Maryjean; Zahm, Shelia H.; Chatterjee, Nilanjan; Chanock, Stephen J.; Rothman, Nathaniel; Hartge, Patricia; Armstrong, Bruce
Abstract
P>Genetic variation in immune-related genes may play a role in the development of non-Hodgkin lymphoma (NHL). To test the hypothesis that innate immunity polymorphisms may be associated with NHL risk, we genotyped 144 tag single nucleotide polymorphisms (tagSNPs) capturing common genetic variation within 12 innate immunity gene regions in three independent population-based case-control studies (1946 cases and 1808 controls). Gene-based analyses found IL1RN to be associated with NHL risk (minP = 0 center dot 03); specifically, IL1RN rs2637988 was associated with an increased risk of NHL (per-allele odds ratio = 1 center dot 15, 95% confidence interval = 1 center dot 05-1 center dot 27; P(trend) = 0 center dot 003), which was consistent across study, subtype, and gender. FCGR2A was also associated with a decreased risk of the follicular lymphoma NHL subtype (minP = 0 center dot 03). Our findings suggest that genetic variation in IL1RN and FCGR2A may play a role in lymphomagenesis. Given that conflicting results have been reported regarding the association between IL1RN SNPs and NHL risk, a larger number of innate immunity genes with sufficient genomic coverage should be evaluated systematically across many studies.
COA
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