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2 articles matched your search query. Search Parameters:
Authors = Hakon Hakonarson

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HAKON (7) , HAKONARSON (2)

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Open AccessReview Association between Genetic Polymorphisms and Response to Anti-TNFs in Patients with Inflammatory Bowel Disease
Int. J. Mol. Sci. 2016, 17(2), 225; doi:10.3390/ijms17020225
Received: 11 January 2016 / Revised: 1 February 2016 / Accepted: 3 February 2016 / Published: 6 February 2016
Cited by 2 | Viewed by 1221 | PDF Full-text (438 KB) | HTML Full-text | XML Full-text
Abstract
Tumor necrosis factor (TNF) alpha is a major proinflammatory cytokine involved in the immune response in inflammatory bowel disease (IBD). Anti-TNF drugs such as infliximab and adalimumab are used to treat IBD; however, approximately 30% of patients do not respond to treatment. Individual
[...] Read more.
Tumor necrosis factor (TNF) alpha is a major proinflammatory cytokine involved in the immune response in inflammatory bowel disease (IBD). Anti-TNF drugs such as infliximab and adalimumab are used to treat IBD; however, approximately 30% of patients do not respond to treatment. Individual genetic differences could contribute to lack of efficacy. Genetic studies have tried to uncover the factors underlying differences in response, however, knowledge remains limited, and the results obtained should be validated, so that pharmacogenetic information can be applied in clinical practice. In this review, we gather current knowledge in the pharmacogenetics of anti-TNF drugs in patients with IBD. We observed a connection between the major genes described as possible predictors of response to anti-TNF drugs in IBD and the cytokines and molecules involved in the T helper (Th) 17 pathway. Full article
(This article belongs to the Special Issue Precision Medicine—From Bench to Bedside)
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Open AccessReview Genes Involved in Type 1 Diabetes: An Update
Genes 2013, 4(3), 499-521; doi:10.3390/genes4030499
Received: 31 July 2013 / Revised: 26 August 2013 / Accepted: 5 September 2013 / Published: 16 September 2013
Cited by 16 | Viewed by 2840 | PDF Full-text (1195 KB) | HTML Full-text | XML Full-text
Abstract
Type 1 Diabetes (T1D) is a chronic multifactorial disease with a strong genetic component, which, through interactions with specific environmental factors, triggers disease onset. T1D typically manifests in early to mid childhood through the autoimmune destruction of pancreatic β cells resulting in a
[...] Read more.
Type 1 Diabetes (T1D) is a chronic multifactorial disease with a strong genetic component, which, through interactions with specific environmental factors, triggers disease onset. T1D typically manifests in early to mid childhood through the autoimmune destruction of pancreatic β cells resulting in a lack of insulin production. Historically, prior to genome-wide association studies (GWAS), six loci in the genome were fully established to be associated with T1D. With the advent of high-throughput single nucleotide polymorphism (SNP) genotyping array technologies, enabling investigators to perform high-density GWAS, many additional T1D susceptibility genes have been discovered. Indeed, recent meta-analyses of multiple datasets from independent investigators have brought the tally of well-validated T1D disease genes to almost 60. In this mini-review, we address recent advances in the genetics of T1D and provide an update on the latest susceptibility loci added to the list of genes involved in the pathogenesis of T1D. Full article
(This article belongs to the Special Issue Genetics of Diabetes)

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