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Now showing 1 - 7 of 7

Cytochrome P450c17 alpha 5'-untranslated region T/C polymorphism in endometriosis
(2004-08-01)
Hsieh, YY
;
Chang, CC
;
Tsai, FJ
;
Lini, CC
;
Tsai, CH
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.
Glutathione S-transferase M1*null genotype but not myeloperoxidase promoter G-463A polymorphism is associated with higher susceptibility to endometriosis
(2004-10-01)
Hsieh, YY
;
Chang, CC
;
Tsai, FJ
;
Lin, CC
;
Chen, JM
Glutathione S-transferase M1 (GSTM1), one member of the GST family, is responsible for metabolism of xenobiotics and carcinogens. Myeloperoxidase (MPO) plays an important role in the oxidation and activation of carcinogens and nitric oxide. Allelic variants of GSTM1 and MPO gene polymorphisms might impair detoxification function and increase the susceptibility to endometriosis. We aimed to investigate if these polymorphisms are useful markers for predicting endometriosis susceptibility. Women were divided into two groups: (i) endometriosis (n=150); (ii) non-endometriosis (n=159). Polymorphisms for GSTM1 and MPO were amplified by polymerase chain reaction and detected by electrophoresis after restriction digestion. The relative frequencies of the GSTM1*wild (+/+,+/0)/null (0/0) genotypes and MPO-463*G/A gene polymorphisms between both groups were compared. The distribution of GSTM1 polymorphisms was significantly different between the two groups. Proportions of GSTM1*wild/null alleles in both groups were: (i) 36.7/63.3%; (ii) 95/5% (P=0.001). In contrast, MPO-463 genotypes were not significantly different between the two groups. Proportions of MPO*A homozygote/heterozygote/G homozygote in both groups were: (i) 2.7/17.4/79.9% and (ii) 1.9/17/81.1% (P> 0.05). We conclude that the GSTM1*null genotype is associated with a higher risk of endometriosis development. MPO-463*G/A gene polymorphism is not related to the susceptibility of endometriosis.
Angiotensin I-converting enzyme ACE 2350*G and ACE-240*T-related genotypes and alleles are associated with higher susceptibility to endometriosis
(2005-01-01)
Hsieh, YY
;
Chang, CC
;
Tsai, FJ
;
Hsu, CM
;
Lin, CC
Endometriosis displays features similar to malignancy, ranging from neovascularization to local invasion and aggressive spread to distant organs. The altered vascular-related genes might be related to the development of endometriosis. This study investigates whether angiotensin I-converting enzyme (ACE) *A2350G and A-240T gene polymorphisms could be used as markers of susceptibility in endometriosis. Women were divided into two groups: (1) endometriosis group (n=150) and (2) non-endometriosis group (n=159). Genomic DNA was obtained from peripheral leukocytes. ACE A2350G and A-240T gene polymorphisms were amplified by PCR and detected after restriction enzyme digestion with BstUI and XbaI. Genotypes and allelic frequencies in both groups were compared. We observed that genotype distribution and allele frequency of ACE 2350 and ACE-240 gene polymorphisms in both groups were significantly different. Proportions of ACE 2350*A homozygote/heterozygote/G homozygote in both groups were: (1) 66.7/29.3/4% and (2) 96.2/3.1/0.7%. Proportions of ACE-240*A homozygote/heterozygote/T homozygote in both groups were: (1) 43.3/46/10.7% and (2) 62.9/35.8/1.3%. We concluded that ACE 2350*G and ACE-240*T-related genotypes and alleles are associated with higher susceptibility to endometriosis. ACE A2350G and A-240T gene polymorphisms might be associated with endometriosis development.
Polymorphism for transforming growth factor beta 1-509 (TGF-B1-509): Association with endometriosis
(2005-06-01)
Hsieh, YY
;
Chang, CC
;
Tsai, FJ
;
Peng, CT
;
Yeh, LS
Transforming growth factor beta (TGF-B) family members are multi-functional cytokines that play a key role in cellular growth, proliferation, and differentiation. The aim of the study was to investigate whether the TGF-B1-509 gene polymorphism could be used as a marker of susceptibility in endometriosis. Women were divided into two groups: endometriosis (n = 150) and non-endometriosis (n = 159). Polymorphisms for TGF-B1-509 genes were amplified by polymerase chain reaction and detected after restriction enzyme digestion. Genotypes and allelic frequencies in both groups were compared. Genotype proportions and allele frequencies of TGF-B1 gene polymorphisms differed significantly in both groups. Proportions of C homozygote, heterozygote, and T homozygote for TGF-B1 gene polymorphisms were 9.3/61.3/29.4% in the endometriosis group and 41.3/58.5/0% in the non-endometriosis group. Alleles C and T for TGF-B1 gene polymorphism were 40/60% (endometriosis) and 70.8/29.2% (non-endometriosis). Association of endometriosis with TGF-B1-509 gene polymorphism exists. T homozygote and T allele for TGF-B1 are associated with higher susceptibility to endometriosis.
Estrogen receptor alpha-351 XbaI*G and -397 PvuII*C-related genotypes and alleles are associated with higher susceptibilities of endometriosis and leiomyoma
(2007-02-01)
Hsieh, Y. -Y.
;
Wang, Y. -K.
;
Chang, C. -C.
;
Lin, C. -S.
;
生物科技學系
Endometriosis and leiomyoma are both common estrogen-related gynaecological diseases. We aimed to elucidate the association of estrogen receptor alpha (ER alpha)-351 A > G (XbaI) and -397 T > C (PvuII) gene polymorphisms with endometriosis and leiomyoma. Women were divided into three groups: (i) severe endometriosis (n = 112), (ii) leiomyoma (n = 106) and (iii) normal controls (n = 110). Genomic DNA was obtained from peripheral leukocytes. ER alpha-351 A/G XbaI and -397 T/C PvuII polymorphisms were assayed by the method of PCR and restriction fragment length polymorphism (RFLP). Genotypes and allelic frequencies in each group were compared. The genotype/allele frequencies of ER alpha-351 and -397 polymorphisms in endometriosis or leiomyoma groups were different from those of normal controls. ER alpha mutant-related genotypes/alleles (-351G and -397C) presented higher percentages in the endometriosis/leiomyoma population compared with normal controls. Proportions of ER alpha-351 AA/AG/GG genotypes and A/G alleles in each group were (i) 26.8/57.1/16.1 and 55.4/44.6%; (ii) 19.8/52.8/27.4 and 46.2/53.8% and (iii) 33.6/64.6/1.8 and 65.9/34.1%. Proportions of ER alpha-397 TT/TC/CC genotypes and T/C alleles in each group were (i) 24.1/60.7/15.2 and 54.5/45.5%; (ii) 23.6/70.8/5.6 and 59/41% and (iii) 54.5/40/5.5 and 74.5/25.5%. We concluded that ER alpha-351 XbaI*G- and -397 PvuII*C-related genotypes/alleles were correlated with higher susceptibilities of endometriosis or leiomyoma, which might be associated with related pathogeneses.
Angiotensin I-Converting enzyme insertion-related genotypes and allele are associated with higher susceptibility of endometriosis and leiomyoma
(2007-07-01)
Hsieh, Yao-Yuan
;
Lee, Cheng-Chun
;
Chang, Chi-Chen
;
Wang, Yu-Kuo
;
Yeh, Lian-Shun
Endometriosis and leiomyoma display features similar to malignancy, requiring neovascularization to proliferation and growth. Altered vascular-related genes might be related to the development of endometriosis and leiomyoma. Polymorphisms of the angiotensin-converting enzyme (ACE) insertion/deletion (I/D) genes have been linked with some vascular diseases. This study investigates whether ACE I/D gene polymorphisms could be used as markers of susceptibility in endometriosis and leiomyoma. Women were divided into three groups: (4) endometriosis (n = 125); (2) leiomyoma (n = 120); () normal controls (n = 128). Genomic DNA was obtained from peripheral leukocyte. ACE I/D gene polymorphisms in intron 16 were amplified by polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP) Genotypes and allelic frequencies in both groups were compared. We observed the genotype distribution and allele frequency of ACE I/ D gene polymorphisms in both groups were significantly different. Proportions of ACE(star)I homozygote/ heterozygote/D homozygote in both groups were: (1) 50.4/24/25.6%; (2) 25/23.33/51.67%; (3) 10.2/ 29.7/60.1%. Proportions of I/D alleles in each group Were: (1) 62.4/37.6%; (2) 36.7/63.3%; (3) 25/75%. We concluded that ACE(star)I/D gene polymorphisms are associated with endometriosis and leiomyoma suspeptibilities. ACE(star)I-related genotypes and allele are strongly related to the occurrence of endometriosis and moderately related to the occurrence of leiomyoma.
XRCC4 codon 247*A and XRCC4 promoter-1394*T related genotypes but not XRCC4 intron 3 gene polymorphism are associated with higher susceptibility for endometriosis
(2008-05-01)
Hsieh, Yao-Yuan
;
Bau, Da-Tian
;
Chang, Chi-Chen
;
Tsai, Chang-Hai
;
Chen, Chih-Ping
DNA repair systems act to maintain genome integrity in the face of replication errors, environmental insults, and the cumulative effects of age. Genetic variants in DNA repair genes such as X-ray repair cross-complementing group 4 (XRCC4) might influence the ability to repair damaged DNA. Herein we aimed to investigate whether some XRCC4-related polymorphisms were associated with endometriosis susceptibility. Women were divided: (1) severe endometriosis (rAFS stage IV, n = 136) and (2) nonendometriosis groups (n = 112). The polymorphisms of XRCC4 codon 247, XRCC4 promoter - 1394, and XRCC4 intron 3 insertion/deletion (I/D) polymorphism were amplified by PCR and detected by electrophoresis after restriction enzyme (BBS I, Hinc II) digestions. Genotypes and allelic frequencies in both groups were compared. We observed that XRCC4 codon 247*A and XRCC4 promoter - 1394*T related genotypes, but not XRCC4 intron 3 I/D polymorphism, are associated with higher susceptibility for endometriosis. Distributions of XRCC4 codon 247*C homozygote/heterozygote/A homozygote, and C/A allele in both groups were: (1) 89/9.5/1.5% and 93.7/6.3%; (2) 97.3/2.7/0%, and 98.7/1.3% (P < 0.05). Proportions of XRCC4 promoter -1394*T homozygote/heterozygote/G homozygote and T/Gallelein both groups were: (1) 94.1/5.2/0.7% and 96.7/3.3%, and (2) 79.4/17.9/2.7% and 88.4/11.6% (P < 0.005). Proportions of XRCC4*1 homozygote/heterozygote/D homozygote and A/C allele in both groups were: (1) 67.6/30.9/1.5% and 83.2/16.8%, and (2) 70.5/24.1/5.4% and 82.6/17.4% (nondifference). We conclude that XRCC4 codon 247*A and XRCC4 promoter -1394*T related genotypes and alleles, but not XRCC4 intron 3 I/D polymorphism, might be associated with endometriosis susceptibilities and pathogenesis.

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