Polymorphisms of death pathway genes FAS and FASL and risk of premalignant gastric lesions

Ping I. Hsu, Pei-Jung Lu, E. Ming Wang, Luo Ping Ger, Gin Ho Lo, Feng Woei Tsay, Tai An Chen, Hsiao Bai Yang, Hui Chun Chen, Weir Sen Lin, Kwok Hung Lai

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Abstract

Background: Tumorigenesis is a multistep process that begins with the abrogation of normal controls of apoptosis and cell proliferation, and the FAS receptor-ligand system is a key regulator of apoptosis. The aim of this study was to investigate whether functional polymorphisms of death pathway genes (FAS and FASL) are associated with the development of gastric atrophy and intestinal metaplasia. Patients and Methods: Genotypes in the promoter regions of the FAS (-1377G/A and -670A/G) and FASL (-844T/C) genes of 101 healthy individuals and 86 gastric cancer patients were determined by PCR-RFLP. Additionally, gastric histological changes were examined according to the updated Sydney System. Results: The carriage of FASL -844C allele significantly increased the risk of atrophy in the gastric corpus, with an adjusted odds ratio (OR) of 5.0 [95% confidence interval (CI), 1.5-6.8]. There were no gene-gene interactions among FASL -844T/C, FAS -1377G/A and FAS -670A/G polymorphisms in developing premalignant gastric lesions. In the 109 individuals with Helicobacter pylori infection, carrying the FAS -1377A allele was a protective factor for developing intestinal metaplasia in the antrum (OR, 0.3; 95% CI, 0.1-0.9), while carrying the FASL -844C allele was a risk factor for developing gastric atrophy in the corpus (OR 9.4; 95% CI, 1.7-53.4). Conclusion: FAS and FASL genotypes of the hosts are important determinants in the pathogenesis of gastric atrophy and intestinal metaplasia in H. pylori-infected individuals.

Original languageEnglish
Pages (from-to)97-104
Number of pages8
JournalAnticancer research
Volume28
Issue number1 A
Publication statusPublished - 2008 Jan 1

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Stomach
Atrophy
Metaplasia
Genes
Alleles
Odds Ratio
Confidence Intervals
Helicobacter pylori
Genotype
Apoptosis
Helicobacter Infections
Genetic Promoter Regions
Restriction Fragment Length Polymorphisms
Stomach Neoplasms
Carcinogenesis
Cell Proliferation
Ligands
Polymerase Chain Reaction

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

Cite this

Hsu, P. I., Lu, P-J., Wang, E. M., Ger, L. P., Lo, G. H., Tsay, F. W., ... Lai, K. H. (2008). Polymorphisms of death pathway genes FAS and FASL and risk of premalignant gastric lesions. Anticancer research, 28(1 A), 97-104.
Hsu, Ping I. ; Lu, Pei-Jung ; Wang, E. Ming ; Ger, Luo Ping ; Lo, Gin Ho ; Tsay, Feng Woei ; Chen, Tai An ; Yang, Hsiao Bai ; Chen, Hui Chun ; Lin, Weir Sen ; Lai, Kwok Hung. / Polymorphisms of death pathway genes FAS and FASL and risk of premalignant gastric lesions. In: Anticancer research. 2008 ; Vol. 28, No. 1 A. pp. 97-104.
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title = "Polymorphisms of death pathway genes FAS and FASL and risk of premalignant gastric lesions",
abstract = "Background: Tumorigenesis is a multistep process that begins with the abrogation of normal controls of apoptosis and cell proliferation, and the FAS receptor-ligand system is a key regulator of apoptosis. The aim of this study was to investigate whether functional polymorphisms of death pathway genes (FAS and FASL) are associated with the development of gastric atrophy and intestinal metaplasia. Patients and Methods: Genotypes in the promoter regions of the FAS (-1377G/A and -670A/G) and FASL (-844T/C) genes of 101 healthy individuals and 86 gastric cancer patients were determined by PCR-RFLP. Additionally, gastric histological changes were examined according to the updated Sydney System. Results: The carriage of FASL -844C allele significantly increased the risk of atrophy in the gastric corpus, with an adjusted odds ratio (OR) of 5.0 [95{\%} confidence interval (CI), 1.5-6.8]. There were no gene-gene interactions among FASL -844T/C, FAS -1377G/A and FAS -670A/G polymorphisms in developing premalignant gastric lesions. In the 109 individuals with Helicobacter pylori infection, carrying the FAS -1377A allele was a protective factor for developing intestinal metaplasia in the antrum (OR, 0.3; 95{\%} CI, 0.1-0.9), while carrying the FASL -844C allele was a risk factor for developing gastric atrophy in the corpus (OR 9.4; 95{\%} CI, 1.7-53.4). Conclusion: FAS and FASL genotypes of the hosts are important determinants in the pathogenesis of gastric atrophy and intestinal metaplasia in H. pylori-infected individuals.",
author = "Hsu, {Ping I.} and Pei-Jung Lu and Wang, {E. Ming} and Ger, {Luo Ping} and Lo, {Gin Ho} and Tsay, {Feng Woei} and Chen, {Tai An} and Yang, {Hsiao Bai} and Chen, {Hui Chun} and Lin, {Weir Sen} and Lai, {Kwok Hung}",
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Hsu, PI, Lu, P-J, Wang, EM, Ger, LP, Lo, GH, Tsay, FW, Chen, TA, Yang, HB, Chen, HC, Lin, WS & Lai, KH 2008, 'Polymorphisms of death pathway genes FAS and FASL and risk of premalignant gastric lesions', Anticancer research, vol. 28, no. 1 A, pp. 97-104.

Polymorphisms of death pathway genes FAS and FASL and risk of premalignant gastric lesions. / Hsu, Ping I.; Lu, Pei-Jung; Wang, E. Ming; Ger, Luo Ping; Lo, Gin Ho; Tsay, Feng Woei; Chen, Tai An; Yang, Hsiao Bai; Chen, Hui Chun; Lin, Weir Sen; Lai, Kwok Hung.

In: Anticancer research, Vol. 28, No. 1 A, 01.01.2008, p. 97-104.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Polymorphisms of death pathway genes FAS and FASL and risk of premalignant gastric lesions

AU - Hsu, Ping I.

AU - Lu, Pei-Jung

AU - Wang, E. Ming

AU - Ger, Luo Ping

AU - Lo, Gin Ho

AU - Tsay, Feng Woei

AU - Chen, Tai An

AU - Yang, Hsiao Bai

AU - Chen, Hui Chun

AU - Lin, Weir Sen

AU - Lai, Kwok Hung

PY - 2008/1/1

Y1 - 2008/1/1

N2 - Background: Tumorigenesis is a multistep process that begins with the abrogation of normal controls of apoptosis and cell proliferation, and the FAS receptor-ligand system is a key regulator of apoptosis. The aim of this study was to investigate whether functional polymorphisms of death pathway genes (FAS and FASL) are associated with the development of gastric atrophy and intestinal metaplasia. Patients and Methods: Genotypes in the promoter regions of the FAS (-1377G/A and -670A/G) and FASL (-844T/C) genes of 101 healthy individuals and 86 gastric cancer patients were determined by PCR-RFLP. Additionally, gastric histological changes were examined according to the updated Sydney System. Results: The carriage of FASL -844C allele significantly increased the risk of atrophy in the gastric corpus, with an adjusted odds ratio (OR) of 5.0 [95% confidence interval (CI), 1.5-6.8]. There were no gene-gene interactions among FASL -844T/C, FAS -1377G/A and FAS -670A/G polymorphisms in developing premalignant gastric lesions. In the 109 individuals with Helicobacter pylori infection, carrying the FAS -1377A allele was a protective factor for developing intestinal metaplasia in the antrum (OR, 0.3; 95% CI, 0.1-0.9), while carrying the FASL -844C allele was a risk factor for developing gastric atrophy in the corpus (OR 9.4; 95% CI, 1.7-53.4). Conclusion: FAS and FASL genotypes of the hosts are important determinants in the pathogenesis of gastric atrophy and intestinal metaplasia in H. pylori-infected individuals.

AB - Background: Tumorigenesis is a multistep process that begins with the abrogation of normal controls of apoptosis and cell proliferation, and the FAS receptor-ligand system is a key regulator of apoptosis. The aim of this study was to investigate whether functional polymorphisms of death pathway genes (FAS and FASL) are associated with the development of gastric atrophy and intestinal metaplasia. Patients and Methods: Genotypes in the promoter regions of the FAS (-1377G/A and -670A/G) and FASL (-844T/C) genes of 101 healthy individuals and 86 gastric cancer patients were determined by PCR-RFLP. Additionally, gastric histological changes were examined according to the updated Sydney System. Results: The carriage of FASL -844C allele significantly increased the risk of atrophy in the gastric corpus, with an adjusted odds ratio (OR) of 5.0 [95% confidence interval (CI), 1.5-6.8]. There were no gene-gene interactions among FASL -844T/C, FAS -1377G/A and FAS -670A/G polymorphisms in developing premalignant gastric lesions. In the 109 individuals with Helicobacter pylori infection, carrying the FAS -1377A allele was a protective factor for developing intestinal metaplasia in the antrum (OR, 0.3; 95% CI, 0.1-0.9), while carrying the FASL -844C allele was a risk factor for developing gastric atrophy in the corpus (OR 9.4; 95% CI, 1.7-53.4). Conclusion: FAS and FASL genotypes of the hosts are important determinants in the pathogenesis of gastric atrophy and intestinal metaplasia in H. pylori-infected individuals.

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M3 - Article

VL - 28

SP - 97

EP - 104

JO - Anticancer Research

JF - Anticancer Research

SN - 0250-7005

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