No association of two Fas gene polymorphisms with Hashimoto's thyroiditis and Graves' disease

Stuck, Bettina J.; Pani, Michael A.; Besrour, Foued; Segni, Maria; Krause, Maren; Usadel, K. H.; Badenhoop, Klaus

doi:10.1530/eje.0.1490393

Cited by 7 publications

(6 citation statements)

References 22 publications

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“…No such association has also been revealed in other diseases like Hashimoto's thyroiditis [45], Grave's disease, and inflammatory bowel disease [46]. As far as our study is concerned, although the Fas G allele frequency and genotypes were not significantly different between the KBD patients and the controls, we were unable to confirm no association of Fas A670G with the disease, and we also need to conduct in-depth research for the gene.…”

Section: Discussioncontrasting

confidence: 57%

Association of TNF-α and Fas gene promoter polymorphism with the risk of Kashin–Beck disease in Northwest Chinese population

et al. 2012

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The objective of this study is to investigate the relationship between single-nucleotide polymorphisms (SNPs) of the tumor necrosis factor-α (TNF-α) and Fas genes and Kashin-Beck disease (KBD) in Shaanxi province, Northwest in China. Blood samples of 388 residents were collected from 14 KBD villages in Linyou and Yongshou counties, Shaanxi, Northern of China. One hundred eighty-six cases with KBD and 202 cases of health in KBD areas were diagnosed by "Diagnosis Criterion of Kashin-Beck disease in China (WS/T207- 2010)". The TNF-α -308G/A, TNF-α -238G/A, and Fas -670A/G SNPs were determined by polymerase chain reaction-restriction fragment length polymorphism in combination with sequence analysis in KBD and healthy control groups. The genotypes and allele frequencies distribution of these SNPs were then analyzed. TNF-α -308A allele frequency in KBD patients were significantly higher than that in healthy controls. Although TNF-α -238 genotypes and allele frequencies were not significantly different between KBD patients and the healthy controls, GA genotype and A allele frequency in KBD patients were higher than those in healthy controls. The TNF-α -308G/A SNPs were associated with the susceptibility of KBD.

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Section: Discussioncontrasting

confidence: 57%

Association of TNF-α and Fas gene promoter polymorphism with the risk of Kashin–Beck disease in Northwest Chinese population

et al. 2012

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“…Two common Fas gene polymorphisms (670 G<A in the promoter region and 154C<T in exon 7) have shown no significant association with Graves' disease and Hashimoto thyroiditis (Stuck et al 2003). The silent exon 7 polymorphism that has been detected in this study (988C<T) has also been reported in patients with marginal zone B cell lymphoma (Bertoni et al 2000) and in LES patients (SNP: ss4479789).…”

Section: Discussioncontrasting

confidence: 54%

Thyroid papillary carcinoma: preliminary evidence for a germ-line single nucleotide polymorphism in the Fas gene

Basolo

Giannini²,

Faviana³

et al. 2004

Journal of Endocrinology

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The expression of Fas in thyroid tumours and Graves' disease was analysed by mRNA transcript expression. As compared with unaffected thyroid tissue, Fas expression was enhanced in Graves' disease, adenomas, and papillary and follicular carcinomas. This pattern was also reflected in immunohistochemical studies. The PCR single-strand conformational polymorphism (SSCP) method and DNA sequencing were used to analyse Fas exons 1-9. The study was carried out on five different histotypes of thyroid tumours (n=93) and tissue from Graves' disease patients. As compared with a group of healthy blood donors (n=64), a significant association (P=0.006) emerged between papillary thyroid carcinoma and a silent single nucleotide polymorphism (SNP, 988C-->T) in exon 7 of the Fas gene. Other forms of thyroid pathology were not associated with the above polymorphism. Patients with neoplasia showed the same SNP in tumour tissue, in the unaffected contralateral thyroid lobe, and in peripheral blood cells. Thus, the 988C-->T polymorphism appeared to be of germ-line origin.

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“…In contrast, À844C/C genotype did not increase disease susceptibility risk in Caucasians in previous studies of autoimmune-related diseases, including SLE, type I insulin-independent diabetes mellitus, and autoimmune thyroid diseases. 31,[36][37][38] Moreover, the frequency of -844C/T polymorphism was not significantly different in patients with positive vs negative clinical manifestations and autoantibodies. These findings indicate that lupus pathogenesis is complex and multiple genetic defects might be required for development of the full-blown disease.…”

Section: Discussionmentioning

confidence: 83%

The −844C/T polymorphism in the Fas ligand promoter associates with Taiwanese SLE

Chen¹,

Wang²,

Chi³

et al. 2005

Genes Immun

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FasL expression is critical in T-cell activation-induced apoptosis, which is involved in lupus pathogenesis. This study identified two SNPs in the FasL promoter regions from -1145 to -45 by genomic DNA sequencing. The -844C/T polymorphism was previously described by its location in and affect on the CCAAT/enhancer-binding protein b (C/EBPB b)-binding site and the other (-1094A/C, a novel polymorphism) was located at the NF-kB transcription-binding site. FasL gene promoter polymorphisms were genotyped in 260 systemic lupus erythematosus (SLE) patients and 280 healthy controls using MassArray matrix-assisted laser desorption ionization-time-of-flight (MALDI-TOF) mass spectrometry. The distribution of FasL promoter -844C/C genotype, predominant in Taiwanese, was skewed in Taiwanese SLE patients (odds ratio: 1.53; P-value ¼ 0.014). FasL promoter À844C/T polymorphism genotype distributions of Taiwanese, African Americans, and Caucasians differed. Moreover, no particular clinical association of À844C/T and À1094A/C polymorphisms with SLE was found in patients in Taiwan. This study confirmed that À844C/C genotype is associated with lupus susceptibility. The -1094A/C polymorphism is not significantly associated with lupus disease susceptibility, albeit the role of NF-kB pathway in FasL promoter activation remains unclear. Fas/FasL pathway may contribute to SLE polygenic disease entity.

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No association of two Fas gene polymorphisms with Hashimoto's thyroiditis and Graves' disease

Cited by 7 publications

References 22 publications

Association of TNF-α and Fas gene promoter polymorphism with the risk of Kashin–Beck disease in Northwest Chinese population

Association of TNF-α and Fas gene promoter polymorphism with the risk of Kashin–Beck disease in Northwest Chinese population

Thyroid papillary carcinoma: preliminary evidence for a germ-line single nucleotide polymorphism in the Fas gene

The −844C/T polymorphism in the Fas ligand promoter associates with Taiwanese SLE

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