Fas gene promoter -670 polymorphism in gynecological cancer

Ueda, Masatsugu; Kanda, Koji; Kanemura, Masanori; Takehara, Mikio; Yamaguchi, Hiroyuki; Nishiyama, K.; Yasuda, Masayuki; Ueki, Minoru

doi:10.1111/j.1525-1438.2006.00505.x

Cited by 30 publications

(31 citation statements)

References 14 publications

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“…It has been suggested that the reduction of Fas membrane receptor would reduce apoptosis and be associated with a malignant potential. 9,16,17 However, our results may be in accordance with the recently published studies suggesting the opposite hypothesis. [41][42][43][44] Fas exists as membrane-bound and soluble forms with opposite roles on triggering apoptosis.…”

Section: Discussioncontrasting

confidence: 47%

“…A significantly associated risk was found for FAS À670 A/G polymorphism in bladder, 13 cervical cancer, 11,16,22 cutaneous malignant melanoma, 12 esophageal and head and neck squamous cell carcinoma, 15,21 lung and nasopharyngeal cancer. 9,17,20 We analyzed the frequency of FAS genotypes in the normal control population.…”

Section: Discussionmentioning

confidence: 98%

“…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%

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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: Discussioncontrasting

confidence: 47%

Section: Discussionmentioning

confidence: 98%

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Association between FAS polymorphism and prostate cancer development

Lima

Morais

Lobo

et al. 2007

Prostate Cancer Prostatic Dis

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“…Although evidence of an association between FAS/FASL polymorphisms and cervical cancer risk has been reported, the findings remain controversial (11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22). Therefore, we performed a meta-analysis of all published studies on the association between the FAS/FASL polymorphisms and cervical cancer.…”

Section: Introductionmentioning

confidence: 99%

Lack of association between the FAS/FASL polymorphisms and cervical cancer risk: A meta-analysis

Pan

2013

Biomedical Reports

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Abstract. FAS/FASL gene promoter polymorphisms are associated with cervical cancer risk, however, results from previous studies have been conflicting. To obtain a more precise estimation of the association between these polymorphisms and cancer risk, a meta-analysis was performed. All eligible studies up to November 1st, 2012, concerning FAS-670 A/G, FAS-1377 G/A and FASL-844 T/C polymorphisms and cervical cancer risk, were collected from the following electronic databases: PubMed, Excerpta Medica Database and Chinese Biomedical Literature Database. The odds ratio (OR) and 95% confidence interval (95% CI) were used to assess the strength of the association via the additive, codominant, dominant and recessive models. In total, 10 publications with 11 case-control studies (10 on FAS-670 A/G, 5 on FAS-1377 G/A and 6 on FASL-844 T/C polymorphisms) were included in this meta-analysis. No association between FAS-670 A/G, FAS-1377 G/A and FASL-844 T/C polymorphisms and cervical cancer susceptibility for all the genetic models was identified. Following stratification of the studies by ethnicity or source of controls, similar results were obtained. In conclusion, our findings showed that the FAS-670 A/G, FAS-1377 G/A and FASL-844 T/C polymorphisms are not associated with cervical cancer risk. Future studies with larger sample sizes are required to further evaluate these associations.

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“…Fas gene mutations and single-nucleotide polymorphisms (SNP) in the promoter region have also been described for endometrial cancers (Ueda et al 2006). However, the impact of these mutations on response to therapy and prognosis is not well defined and is yet to be understood in endometrial cancer.…”

Section: The Extrinsic Death Receptor Pathwaymentioning

confidence: 99%

Resistance to chemotherapy and hormone therapy in endometrial cancer

Chaudhry¹,

Asselin²

2009

Endocrine-Related Cancer

111

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Endometrial cancer is the most common gynecological malignancy in developed countries and represents the eighth leading cause of cancer related death in women. The growing incidence of endometrial cancer leads scientists and oncologists to identify effective preventive measures and also molecular markers for diagnosis and prognosis. Chemotherapy and hormone therapy is the mainstay treatment option for advanced and recurrent endometrial cancer and response to therapy is one of the most important factor which favors prognosis and overall survival. In recent years, there have been major advances in the treatment of patients with endometrial cancer. Despite advances made in the treatment of this cancer, the overall survival of patients has not significantly improved because considerable number of patients harbor tumor refractory to these therapies and the majority of the initially responsive tumors become refractory to treatments. Therefore, determination of sensitivity/resistance is becoming increasingly important for individualization of endometrial cancer therapy. The aim of this review is to present the existing knowledge about the molecular markers that could play a crucial role in determining resistance to chemo-and hormone therapy. Extensive literature search for the cell signaling pathways and factors responsible for chemoresistance have been performed and reviewed. Several recent studies suggest that deregulations in the apoptotic pathways (such as p53, Fas/FasL, Bcl-2 family proteins, inhibitor of apoptosis proteins), survival pathways (PI3K/AKT, MAPK), hormone receptor signaling pathways (progesterone receptor), Cyclooxygenase-2 and Her-2 are considered as key factors involved in the onset and maintenance of therapeutic resistance, suggesting that resistance is a multi-factorial phenomenon.

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Fas gene promoter -670 polymorphism in gynecological cancer

Cited by 30 publications

References 14 publications

Association between FAS polymorphism and prostate cancer development

Association between FAS polymorphism and prostate cancer development

Lack of association between the FAS/FASL polymorphisms and cervical cancer risk: A meta-analysis

Resistance to chemotherapy and hormone therapy in endometrial cancer

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