標題: Cytochrome P450c17 alpha 5'-untranslated region T/C polymorphism in endometriosis
作者: Hsieh, YY
Chang, CC
Tsai, FJ
Lini, CC
Tsai, CH
生物科技學系
Department of Biological Science and Technology
關鍵字: cytochrome P450c17 CYP17;endometriosis;single nucleotide polymorphism
公開日期: 1-Aug-2004
摘要: Estrogen plays a role in the pathogenesis of endometriosis. The CYP17 gene codes for the cytochrome P450cl7alpha enzyme that is involved in the estrogen biosynthesis. We aimed to investigate if CYP 17 polymorphism could be used as marker to predict the susceptibility of endometriosis. Women were divided into two groups: (1) severe endometriosis (n= 119); (2) non-endometriosis groups (n=1 28). A 169-bp fragment encompassing the T/C polymorphic site in 5'-untranslated promoter region (5'-UTR) of the CYP17 was amplified by the polymerase chain reaction, treated with restriction enzyme MspA1I, and electrophoresis. The polymorphism was divided into restriction- enzyme indigestible (T homozygote), T/C heterozygote, and digestible (C homozygote). Genotypes and allelic frequencies for this polymorphism in both groups were compared. We observed a higher but non-significant percentage of T homozygote in the endometriosis women compared with the non-endometriosis women. Proportions of T homozygote/heterozygote/C homozygote for CYP17 in both groups were: (1) 26.1/46.2/27.7% and (2) 17.2/45.3/37.5% (p- value=0.13 1). T allele was related with higher susceptibility of endometriosis. T and C allele frequencies in both groups were: (1) 49.2/50.8%; (2) 39.8/60.2% (p- value=0.046). Despite the CYP17* T allele Appearing to be asscoiated with a trend of increased risk of endometriosis, CYP17 5'-UTR gene polymorphism might not be a useful marker for prediction of endometriosis susceptibility.
URI: http://hdl.handle.net/11536/26492
ISSN: 0022-1333
期刊: JOURNAL OF GENETICS
Volume: 83
Issue: 2
起始頁: 189
結束頁: 192
Appears in Collections:Articles


Files in This Item:

  1. 000224867100009.pdf

If it is a zip file, please download the file and unzip it, then open index.html in a browser to view the full text content.