Single nucleotide polymorphism at Fas promoter is associated with cervical carcinogenesis

Lai, Hung Cheng; Sytwu, Huey Kang; Sun, Chien An; Mu, Yu; Yu, Cheng; Liu, Hang Seng; Chang, Cheng‐Chang; Chu, Tang-Yuan

doi:10.1002/ijc.10800

Cited by 101 publications

(77 citation statements)

References 45 publications

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“…7,8 In addition, polymorphisms in the FAS gene and perhaps also in the FASL gene that impair apoptotic signal transduction are associated with a high risk of cancer in various models. [9][10][11][12][13][14][15][16][17][18][19][20][21][22] Thus, the FAS/FASL system appears to have a role in the development and progression of cancer.…”

Section: Introductionmentioning

confidence: 99%

Association between FAS polymorphism and prostate cancer development

Lima

Morais

Lobo

et al. 2007

Prostate Cancer Prostatic Dis

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The role of FAS polymorphisms in prostate cancer has not been studied. Using the PCR-based restriction fragment-length polymorphism methodology, we evaluated FAS gene locus À670 genotypes in DNA from 904 men: 657 prostate cancer patients and 247 healthy controls. We found that carriers of AG or GG genotypes have a statistically significant protection (odds ratio (OR) ¼ 0.30; confidence interval (CI): 0.20-0.44 and OR ¼ 0.22; CI: 0.12-0.74, respectively) for disease with extra-capsular invasion. Taken together, a 72% protection was found for G allele carriers (OR ¼ 0.28; CI: 0.19-0.41). Fas exist as membrane-bound and soluble forms and with opposite roles. They derive from the same gene by alternative splicing. Membrane Fas receptors trigger apoptosis whereas, on the other hand, soluble Fas (sFas) bind to Fas ligand antagonizing Fas-Fas ligand apoptotic pathway. Our results suggest that G allele may reduce sFas levels preventing the apoptotic inhibition caused by the soluble form.

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Section: Introductionmentioning

confidence: 99%

Association between FAS polymorphism and prostate cancer development

Lima

Morais

Lobo

et al. 2007

Prostate Cancer Prostatic Dis

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“…28 -30 Our previous study showed that a single nucleotide polymorphism (SNP) creating an IFN-␥ response element in the Fas(CD95) promoter was associated with increased risk of cervical cancer, indicating differential activation-induced cell death (AICD) of lymphocytes as a susceptibility factor to cervical carcinogenesis. 26 Whether the higher-expression allele of IFN-␥ gene induces higher or earlier AICD of lymphocytes resulting in increased risk of cervical cancer requires further investigation.…”

Section: Discussionmentioning

confidence: 99%

“…HPV genotypes were grouped into group 16, group 18 and group 58 according to the phylogenetic similarity described previously. 26 …”

Section: Hpv Detection and Genotypingmentioning

confidence: 99%

Genetic polymorphism of the interferon‐γ gene in cervical carcinogenesis

Lai

Chang

Lin

et al. 2004

Intl Journal of Cancer

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Beyond human papillomavirus (HPV) infection, host genetic factors may contribute to cervical carcinogenesis. This study aims to test the hypothesis that CA-dinucleotide repeat polymorphism in the first intron of the interferon-gamma (IFN-␥) gene is associated with HPV-initiated cervical carcinogenesis. A hospital-based casecontrol study including patients with low-grade squamous intraepithelial lesions (LSILs; n ‫؍‬ 93), high-grade squamous intraepithelial lesions (HSILs; n ‫؍‬ 123) and invasive carcinomas (n ‫؍‬ 153) of the uterine cervix, as well as 1:1 age-matched controls, was conducted. The IFN-␥ genotype was determined by PCR and capillary electrophoresis with internal standards. HPV genotype was determined by consensus PCR and reverse line blot hybridization. Genotypes containing the 12 or 14 allele (12 or 14 CA repeats) were significantly more common in patients with HSILs than in controls (46% vs. 22%; OR ‫؍‬ 3.0; 95% CI ‫؍‬ 1.7-5.2; p < 0.0001). In contrast, genotypes containing 13 and 18 were significantly more common in controls than in patients with HSILs (76% vs. 53%; OR ‫؍‬ 0.3; 95% CI ‫؍‬ 0.2-0.6; p ‫؍‬ 0.0001) or squamous cell carcinomas (74% vs. 63%; OR ‫؍‬ 0.6; 95% CI ‫؍‬ 0.4 -1.0; p ‫؍‬ 0.037). The frequency of the 12 and 14 genotypes increased significantly in accordance with the severity of cervical carcinogenesis (p test for trend ‫؍‬ 0.0002), whereas the 13 and 18 genotypes showed the opposite trend (p test for trend ‫؍‬ 0.007). Comparing IFN-␥ genotype and HPV status, 18-containing genotypes were more frequently found in HPV ؉ LSILs, and 12-containing genotypes were less frequently found in HPV ؉ HSILs. Compared with non-13 genotypes, 13 genotype HSILs were more frequently infected with HPV58 (70% vs. 45%) and less frequently infected with HPV18 (0% vs. 16%; p‫؍‬ 0.007). Genetic polymorphism of the IFN-␥ gene is associated with individual susceptibility to cervical carcinogenesis. This polymorphism correlates with HPV infection in a disease-and type-specific manner.

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“…26 An involvement in cancer susceptibility has been also suggested for the SNPs located in the FAS promoter region. 12,27,28 There is a series of publications assessing a tumor-associated role of the noncoding G4C14-to-A4T14 allelism. 29 Protective effects have been observed for the DR4 polymorphism and bladder cancer risk, and for the CASP8 variant and breast cancer proneness.…”

Section: Polymorphic Variations In Apoptotic Genes In Cancer Patientsmentioning

confidence: 99%