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    P53 codon 11, 72, and 248 gene polymorphisms in endometriosis
    (2006-01-01)
    Hsieh, Yao-Yuan
    ;
    Lin, Chich-Sheng
    ;
    生物科技學系
    ;
    Department of Biological Science and Technology
    Objective: Mutated p53 gene is related to the instability of cell growth and cell cycle progression. We aimed to evaluate the association between endometriosis and p53 codon 11, 72 and 248 gene polymorphisms. Patients and methods: Women were divided into two groups: (1) moderate/severe endometriosis (n=148), and (2) non-endometriosis groups (n=150). P53 gene polymorphisms include codon11 Glu/Gln or Lys (GAG->CAG or AAG), codon 72 Arg/Pro (CGC->CCC), and codon 248 Arg/Thr (CGG->TCG). These gene polymorphisms were amplified by polymerase chain reaction and detected by electrophoresis after restriction enzyme (Taq I, BstU I, Hap II) digestions. Associations between the endometriosis and p53 polymorphisms were evaluated. Results: The distributions of p53 codon 72 polymorphisms in both groups were significantly different. The proportions of Arg homozygotes/heterozygotes/Pro homozygotes in both groups were 9.5/66.2/24.3% and 30.7/50/19.3%. The proportions of Arg/Pro alleles were 42.6/57.4% and 56/44%. The distributions of p53 codon 11 and 248 polymorphisms in both groups were non-significantly different. All individuals appeared the wild genotypes (Glu11 and Arg248 homozygotes). Conclusion: Association between endometriosis and p53 codon 72 polymorphism exists. P53 codon 72*Pro-related genotype and allele are related with higher susceptibility of endometriosis. P53 codon 11 and 248 polymorphisms are not related with endometriosis susceptibility.
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    The cuttable C-related genotype and allele for the E-cadherin 3 '-UTR Pml I polymorphism are associated with higher susceptibility to endometriosis
    (2005-12-01)
    Hsieh, Yao-Yuan
    ;
    Chang, Chi-Chen
    ;
    Tsai, Fuu-Jen
    ;
    Hsu, Chin-Moo
    ;
    Lin, Cheng-Chieh
    Epithelial cadherin (E-cadherin; CDH1) may influence pericellular proteolysis and intracellular signal transduction, which plays an essential part of tumor invasion. In our study we investigated the correlation between CDH1 gene polymorphism and endometriosis in two groups of pre-menopausal Taiwanese women, group 1 (n = 150) consisting of women with severe stage IV enclometriosis and group 2 (n = 159) of women with no enclometriosis. The polymerase chain reaction (PCR) was used to identify the cuttable (C) and uncuttable (T) polymorphism of the CDH1-Pm/ l gene (rs1801026) located on the T-untranslated region (3'-UTR) of chromosome 16 and compare the genotypes and allelic frequencies of this gene in both groups. We found that the genotype and allele distributions of the CDH1-Pml/ l C/T polymorphism were significantly different in both groups. In group 1 the CDH1*C frequency was 47.7% and the T frequency 52.3%, while the CC homozygote frequency was 6.7%, the TT homozygote 11.3% and the CT heterozygote 82%. In group 2 the CDH1*C frequency was 17% and the T frequency 83%, while the CC frequency was 0.6%, the TT 66.1% and the CT 33.3%. These data indicate that the CDH1 gene polymorphism may be associated with the development of severe endometriosis and that the CDH1 gene C allele is related to higher susceptibility to enclometriosis.
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    Interleukin (IL)-12 receptor beta 1 codon 378 G homozygote and allele, but not IL-1 (beta-511 promoter, 3953 exon 5, receptor antagonist), IL-2 114, IL-4-590 intron 3, IL-8 3 '-UTR 2767, and IL-18 105, are associated with higher susceptibility to leiomyoma
    (2007-04-01)
    Hsieh, Yao-Yuan
    ;
    Chang, Chi-Chen
    ;
    Tsai, Chang-Hai
    ;
    Lin, Cheng-Chieh
    ;
    Tsai, Fuu-Jen
    Objective: To investigate whether certain polymorphisms are correlated with leiomyoma susceptibility, i.e., interleukin (IL)-1, IL-2, IL-4, IL-8, IL-12, and IL-18, which are all immunomodulatory cytokines that play important roles in host immune responses against cancers. Setting: Departments of gynecology and genetics in a medical center. Patient(s): Women were divided into: [1] a leiomyoma group (n = 162) and [2] a nonleiomyoma group (n = 156). Intervention(s): Genotyping for the IL-1 beta-511 promoter, IL-1 beta exon 5, IL-1Ra, IL-2 114, IL-4 -590 intron 3, IL-8 3'-UTR 2767, IL-12R beta 1 codon 378, and IL-18 105 were evaluated by polymerase chain reaction-restriction fragment length polymorphism. Main Outcome Measurement(s): Genotypes and allelic frequencies in both groups were compared. Result(s): Proportions of IL-12R beta 1 codon 378 *CC/CG/GG in the leiomyoma and nonleiomyoma groups were: [1] 7.4%/43.8%/48.8% and [2] 11.5%/54.5%/34%, respectively. Distributions of other polymorphisms in both groups were not significantly different. Proportions of IL-1 beta-511 promoter *CC/CT/TT were: [1] 22.8%/50%/ 27.2% and [2] 21.8%/57.1%/21.1% in the leiomyoma and nonleiomyoma groups, respectively. The IL-1 beta exon 5 *E1 homozygote/heterozygote/E2 homozygote were: [1] 96.3%/3.7%/0% and [2] 96.9%/3.1%/0% in the leiomyoma and nonleiomyoma groups, respectively. Alleles I/II/III/IV/V for IL-1Ra were: [1] 92.6%/7.1%/0.3%/ 0/0% and [2] 93.9%/5.7%/0%/0.4/0% in the leiomyoma and nonleiomyoma groups, respectively. The IL-2 114 G homozygote/heterozygote/T homozygote were: [1] 27.8%/49.4%/22.8% and [2] 20.5%/53.2%/26.3% in the leiomyoma and nonleiomyoma groups, respectively. The IL-4 -590 intron 3 *RP1 homozygote/heterozygote/ RP2 homozygote were: [1] 64.8%/32.7%/2.5% and [2] 69.2%/26.9%/3.9% in the leiomyoma and nonleiomyoma groups, respectively. The IL-8 3'-UTR 2767 A homozygote/heterozygote/G homozygote were: [1] 14.2%/ 43.8%/42% and [2] 20.5%/41.7%/37.8% in the leiomyoma and nonleiomyoma groups, respectively. The IL-18 *AA/AC/CC were: [1] 56.8%/40.7%/2.5% and [2] 59%/39.7%/1.3% in the leiomyoma and nonleiomyoma groups, respectively. Conclusion(s): The IL-12R beta 1 codon 378 *G homozygote and G allele are related to a higher susceptibility to leiomyoma. The IL-1 beta-511 promoter, IL-1 beta exon 5, and IL-1Ra, IL-2 114, IL-4 -590 intron 3, IL-8 3'-UTR 2767, and IL-18 105 gene polymorphisms are not correlated with the development of leiomyoma.