Title : Role of the UGT2B17 deletion in exemestane pharmacogenetics.

Pub. Date : 2018 Apr

PMID : 28534527






7 Functional Relationships(s)
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1 The aim of the present study was to determine the effects of UGT2B17 copy number variation on the levels of urinary and plasma 17beta-DHE-Gluc and 17beta-DHE in patients taking EXE. 17beta-dhe UDP glucuronosyltransferase family 2 member B17 Homo sapiens
2 The plasma levels of 17beta-DHE-Gluc was decreased 29-fold (P<0.0001) in subjects with the UGT2B17 (*2/*2) genotype vs subjects with UGT2B17 (*1/*1) genotype. 17beta-dhe UDP glucuronosyltransferase family 2 member B17 Homo sapiens
3 The plasma levels of 17beta-DHE-Gluc was decreased 29-fold (P<0.0001) in subjects with the UGT2B17 (*2/*2) genotype vs subjects with UGT2B17 (*1/*1) genotype. 17beta-dhe UDP glucuronosyltransferase family 2 member B17 Homo sapiens
4 The levels of plasma EXE-adjusted 17beta-DHE was 28% higher (P=0.04) in subjects with the UGT2B17 (*2/*2) genotype vs subjects with the UGT2B17 (*1/*1) genotype. 17beta-dhe UDP glucuronosyltransferase family 2 member B17 Homo sapiens
5 These data indicate that UGT2B17 is the major enzyme responsible for 17beta-DHE-Gluc formation in vivo and that the UGT2B17 copy number variant may play a role in inter-individual variability in 17beta-DHE levels in vivo. 17beta-dhe UDP glucuronosyltransferase family 2 member B17 Homo sapiens
6 These data indicate that UGT2B17 is the major enzyme responsible for 17beta-DHE-Gluc formation in vivo and that the UGT2B17 copy number variant may play a role in inter-individual variability in 17beta-DHE levels in vivo. 17beta-dhe UDP glucuronosyltransferase family 2 member B17 Homo sapiens
7 These data indicate that UGT2B17 is the major enzyme responsible for 17beta-DHE-Gluc formation in vivo and that the UGT2B17 copy number variant may play a role in inter-individual variability in 17beta-DHE levels in vivo. 17beta-dhe UDP glucuronosyltransferase family 2 member B17 Homo sapiens