Browsing by Author "Tsai, FJ"

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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.
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.
Estrogen receptor alpha dinucleotide repeat and cytochrorne P450c17 alpha gene polymorphisms are associated with susceptibility to endometriosis
(2005-03-01)
Hsieh, YY
;
Chang, CC
;
Tsai, FJ
;
Lin, CC
;
Tsai, CH
Objective: To investigate the association of endometriosis with estrogen receptor alpha (ER alpha) and cytochrome P450c17 alpha (CYP17) gene polymorphisms in light of the fact that estrogen plays a role in the pathogenesis of endometriosis and the CYP17 enzyme is involved with estrogen biosynthesis. Design: Prospective study. Setting: Genetics and gynecology units. Patient(s): All patients were divided into two groups: group 1, women with endometriosis (n = 119); group 2, normal controls (n = 108). Intervention(s): A dinucleotide (thymine-adenine [TA]) repeat polymorphism lying upstream of the ER alpha gene and A1/A2 polymorphism of the CYP17 gene were amplified by polymerase chain reaction, enzyme restriction, and electrophoresis. Main Outcome Measure(s): The ER Genotypes were classified into A through T (TA repeats, 10-29). The CYP17 genotypes included indigestible (A1 homozygote), heterozygote, and digestible (A2, homozygote). We compared these polymorphism distributions in both groups. Result(s): The percentage of genotypes D-G (TA, 13-16) in both groups were 110.5%, 29.4%, 13.0%, and 11.3% in group 1 and 7.9%, 16.7% 19.9%, and 17.6% in group 2. The genotype E (14 TA repeats) is associated with a higher risk of endometriosis. Proportions of Al homozygote/heterozygote/A2 homozygote for CYP17 were 26.1%/46.2%/27.7% for Group I and 14.8%/44.5%/40.7% for group 2, respectively. The Al homozygote and allele were associated with a higher susceptibility of endornetriosis. Conclusion(s): ER alpha* 14 TA repeats and the CYP17* Al allele are associated with an increased risk of endometriosis. Both polymorphisms are useful markers for predicting endometriosis susceptibility. (Fertil Steril (R) 2005:83:567-72. (c) 2005 by American Society for Reproductive Medicine.)
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.
Interleukin-2 receptor beta (IL-2R beta)-627*C homozygote but not IL-12R beta 1 codon 378 or IL-18 105 polymorphism is associated with higher susceptibility to endometriosis
(2005-08-01)
Hsieh, YY
;
Chang, CC
;
Tsai, FJ
;
Hsu, CM
;
Lin, CC
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.
T allele for VEGF gene-460 polymorphism at the 5 ''-untransiated region - Association with a higher susceptibility to endometriosis
(2004-06-01)
Hsieh, YY
;
Chang, CC
;
Tsai, FJ
;
Yeh, LS
;
Lin, CC
OBJECTIVE: To investigate whether vascular endothelial growth factor (VEGF) gene 5'-UTR-460 polymorphism could be used as a marker of susceptibility to endometriosis. STUDY DESIGN: Women were divided into 2 groups, endometriosis (n = 122) and nonendometriosis (n = 131). Polymorphisms for VEGF were detected by polymerase chain reaction and BstUI (New England Biolabs, Beverly, Massachusetts) restriction enzyme analysis. Genotypes and allelic frequencies between the groups were compared. RESULTS: Proportions of different VEGF polymorphisms in the groups were significantly different. Proportions of cuttable (C) homozygote/heterozygote/uncuttable (T) homozygote for VEGF in the groups were 0144.3155.7% and 0/63.4/36.6%, respectively. A higher percentage of T/T homozygote and T allele was present in the endometriosis population. The proportions of C/T alleles in the groups were 22.1/77.9% and 31.7/68.3%, respectively. CONCLUSION: T/T homozygotes and the T allele of the VEGF-460 gene are associated with a higher risk of endometriosis. Heterozygotes and C allele are related to the lower risk of endometriosis formation. VEGF polymorphism likely contributes to the pathogenesis of endometriosis and may become a useful marker for predicting endometriosis susceptibility.
T homozygote and allele of epidermal growth factor receptor 2073 gene polymorphism are associated with higher susceptibility to endometriosis and leiomyomas
(2005-03-01)
Hsieh, YY
;
Chang, CC
;
Tsai, FJ
;
Lin, CC
;
Tsai, CH
Epidermal growth factor receptor (EGER) is a regulator of angiogenesis and mediator of sex steroid-induced cell growth and differentiation. We observed that EGFR gene 2073*T-related genotypes and allele are associated with higher susceptibilities to endometriosis and leiomyoma. (c) 2005 by American Society for Reproductive Medicine.
Tumor necrosis factor-alpha-308 promoter and p53 codon 72 gene polymorphisms in women with leiomyomas
(2004-10-01)
Hsieh, YY
;
Chang, CC
;
Tsai, FJ
;
Lin, CC
;
Yeh, LS
Objective: Tumor necrosis factor-alpha (TNF-alpha), a proinflammatory cytokine, plays an important role in the process of autoimmune diseases. p53 is related to the regulation of cell growth and prevention of carcinogenesis. We propose to investigate whether gene polymorphisms for TNF-alpha-308 promoter and p53 could be used as markers of susceptibility in leiomyomas. Design: Prospective basic study. Setting: Departments of gynecology and genetics in a medical center. Patient(s): Group 1: leiomyoma (n = 159); group 2: non-leiomyoma (n = 13 1). Intervention(s): Genomic DNA was obtained from peripheral leukocyte. The TNF-alpha and p53 gene polymorphisms were amplified by polymerase chain reaction (PCR), enzyme restriction, and electrophoresis. Main Outcome Measure(s): Two gene polymorphisms were identified: [1] the A (cuttable)/G (uncuttable) polymorphisms of the TNF-alpha gene on chromosome 6p2l.3; [2] A (cuttable)/P (uncuttable) polymorphisms of the p53 gene on chromosome 17p. Genotype and allelic frequencies in both groups were compared. Result(s): Genotype distribution and allele frequency of TNF-a gene polymorphism in both groups were significantly different. Proportions of A homozygote/heterozygote/G homozygote for TNF-alpha in both groups were: (group 1) 61%/34.6%/4.4% and (group 2) 81.7%/14.5%/3.8%. Proportions of allele A/G for TNF-alpha in both groups were: (group 1) 78.3%/21.7% and (group 2) 88.9%/11.1%. Distributions of p53 polymorphisms in both groups were not different. The proportions of A homozygotes/heterozygotes/P homozygotes for p53 were (group 1) 32.7%/42.1%/25.2% and (group 2) 28.2%/48.9%/22.9%. Conclusion(s): G homozygote and G allele for TNF-alpha promoter are related to a higher risk of leiomyomas. The p53 codon 72 gene polymorphism is not associated with the susceptibility of leiomyomas. (C) 2004 by American Society for Reproductive Medicine.