ABCC4 p.Thr587Gly
Predicted by SNAP2: | A: N (87%), C: N (93%), D: D (63%), E: N (57%), F: N (57%), G: N (72%), H: D (59%), I: N (87%), K: N (66%), L: N (72%), M: N (72%), N: N (82%), P: N (66%), Q: N (78%), R: N (72%), S: N (87%), V: N (97%), W: D (71%), Y: D (66%), |
Predicted by PROVEAN: | A: N, C: N, D: D, E: D, F: D, G: D, H: D, I: N, K: N, L: N, M: N, N: N, P: D, Q: N, R: N, S: N, V: N, W: D, Y: D, |
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[hide] Pharmacogenomics in the treatment of inflammatory ... Pharmacogenomics. 2010 Mar;11(3):421-37. Smith MA, Marinaki AM, Sanderson JD
Pharmacogenomics in the treatment of inflammatory bowel disease.
Pharmacogenomics. 2010 Mar;11(3):421-37., [PMID:20235796]
Abstract [show]
In recent years, the benefits of early aggressive treatment paradigms for inflammatory bowel disease have emerged. Symptomatic improvement is no longer considered adequate; instead, the aim of treatment has become mucosal healing and altered natural history. Nonetheless, we still fail to achieve these end points in a large number of our patients. There are many reasons why patients fail to respond or develop toxicity when exposed to drugs used for inflammatory bowel disease, but genetic variation is likely to account for a significant proportion of this. Some examples, notably thiopurine methyltransferase polymorphism in thiopurine treatment, are already established in clinical practice. We present a review of the expanding literature in this field, highlighting many interesting developments in pharmacogenomics applied to inflammatory bowel disease and, where possible, providing guidance on the translation of these developments into clinical practice.
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No. Sentence Comment
244 Mascheretti and colleagues tested an exploratory cohort of 90 patients for a total of 11 SNPs in TNF-a and its receptors and then sought confirmation of the two possible associations (SNP T587G Met196Arg in exon 6 of the TNF receptor II [TNFRII] gene and a linked silent SNP in exon 2) in a larger cohort of 444 patients.
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ABCC4 p.Thr587Gly 20235796:244:188
status: NEW