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  • 1
    Electronic Resource
    Electronic Resource
    Lack of association between pro-inflammatory cytokine (IL-6, IL-8 and TNF-α) gene polymorphisms and Graves’ disease (2005)
    Oxford, UK : Blackwell Science Ltd
    International journal of immunogenetics 32 (2005), S. 0 
    Details
    ISSN: 1744-313X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Graves’ disease (GD) is a common, autoimmune disease involving the thyroid gland, and it has been previously suggested that pro-inflammatory cytokines are involved in the disease's pathogenesis. The aim of this study was to test whether the interleukin (IL)-6 gene promoter region, or tumour necrosis factor (TNF)-α or IL-8 gene 3′-untranslated region (3′-UTR) polymorphisms could provide useful genetic markers for an individual's susceptibility to GD. A normal control group of 60 healthy people and 95 patients featuring GD were examined. Polymerase chain reaction (PCR)-based restriction analysis was performed for the three gene polymorphisms using endonucleases BsrBI, NcoI and ApaLI, respectively. We found no significant difference between the frequencies of genotype and allelic variants for the IL-6 gene promoter (−572 G/C), the TNF-α gene promoter (−308 A/G) and the IL-8 gene 3′-UTR (2767 A/G) for GD patients and for normal controls. Cytokines are a large group of proteins that may elicit multiple effects upon immunological reactions. It still appears to be very worthwhile to continue to aggressively search for cytokine gene polymorphisms in order to predict the development of such disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1744-313X.2005.00536.x
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  • 2
    Electronic Resource
    Electronic Resource
    Distributions of p53 codon 72 polymorphism in bladder cancer – proline form is prominent in invasive tumor (2000)
    Springer
    Urological research 28 (2000), S. 293-296 
    Details
    ISSN: 1434-0879
    Keywords: Key words p53 codon 72 polymorphism ; Bladder cancer ; Proline form ; Arginine form
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Abnormal function of p53 is commonly associated with various cancer formations. High-grade and late-stage bladder cancers have been reported to have mutated or become inactive p53 when using immunohistochemical stains. Recently, p53 codon 72 polymorphism was extensively studied to determine the risk factors responsible for cancer formation. There was a general population of codon 72 sequence polymorphism of the wild type p53. A single base change from G to C caused the alteration of amino acid residue 72 from arginine to proline. The arginine form is considered to be a significant risk factor in the development of cancer. However, various reports had indicated discrepancies with regard to this polymorphism; some showed no significant difference between the control and cancer groups, while other series were associated with high risks in the proline form homozygotes. To resolve the undefined distribution of this polymorphism in bladder cancers, 58 patients with bladder cancer were enrolled onto this study. When checked using the Chi-squared test (P=0.952) there were no differences between the control subjects and bladder cancer patients in the distribution of polymorphism. However, proline form homozygotes were more frequently found in the invasive group than the non-invasive group by Fisher's exact test (25% and 2.9%, respectively, P 〈 0.001). More than 70% of the non-invasive bladder cancers were the arginine form homozygotes. This result is consistent with those reported for hepatocellular carcinoma that showed a history of chronic liver disease and proline form homozygotes in a report by Yu et al. Our data suggest that proline form homozygotes are associated with invasive bladder cancer.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002400000117
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  • 3
    Electronic Resource
    Electronic Resource
    Molecular analysis of Wilson disease in Taiwan: identification of one novel mutation and evidence of haplotype-mutation association (2000)
    Springer
    Journal of human genetics 45 (2000), S. 275-279 
    Details
    ISSN: 1435-232X
    Keywords: Key words Wilson disease (WND) ; ATP7B ; Mutation analysis ; Haplotype analysis ; Short tandem repeat (STR) markers ; Taiwanese
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Wilson disease (WND) is caused by a deficiency of the copper-transporting enzyme, P-type ATPase (ATP7B). Twelve different mutations have previously been identified in Taiwan Chinese with Wilson disease. We, herein, report another 4 missense mutations, 1 of which is novel. We did haplotype analysis of Taiwanese WND chromosomes, using three well characterized short tandem repeat markers (haplotype was assigned in the order of D13S314-D13S301-D13S316). Association correlation was found between the mutations and their respective haplotypes. Haplotype-deduced pedigree analysis was shown to be helpful in the mutation analysis of WND chromosomes and in the molecular assessment of both pre-symptomatic WND patients and carriers. Given the complexity and heterogeneity of the mutation spectrum of ATP7B, we suggest that haplotype analysis should be performed before full-scale mutation analysis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s100380070015
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