Interactions between pork consumption, CagA status and IL-1B-31 genotypes in gastric cancer

Xiao Qin Wang, Paul Terry, Li Cheng, Hong Yan, Jian Sheng Wang, Wen An Wu, Sen Ke Hu

Research output: Contribution to journalArticle

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Abstract

Aim: To explore potential interactions among Helicobacter pylori (H. pylori), CagA status, interleukin (IL)- 1B-31 genotypes, and non-cardiac gastric cancer (GC) risk. Methods: A case-control study of non-cardia GC was performed at 3 hospitals located in Xi'an, China, between September 2008 and July 2010. We included 171 patients with histologically diagnosed primary noncardia GC and 367 population based controls (matched by sex, age and city of residence). A standardized questionnaire was used to obtain information regarding potential risk factors, including pork consumption. H. pylori CagA status was assessed by enzyme-linked immunosorbent assay, and IL-1B-31 genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism. Multivariate unconditional logistic regression was used to explore potential interactions among the factors. Results: The CagA appeared to confer an increased risk of GC (OR = 1.81, 95%CI: 1.25-2.61). The main associations with IL-1B-31C allele here were 0.98 (95%CI: 0.59-1.63) for CC vs TT and 0.99 (95%CI: 0.64-1.51) for C Carriers vs TT. However, no associations were observed for CagA or IL-1B-31 genotype status among subjects who reported low pork consumption (P for interaction = 0.11). In contrast, high pork consumption and IL-1B-31C genotypes appeared to synergistically increase GC risk (P for interaction = 0.048) after adjusting for confounding factors, particularly among subjects with CagA (OR = 3.07, 95%CI: 1.17-10.79). We did not observe effect modification of pork consumption by H. pylori CagA status, or between H. pylori CagA status and IL-1B-31 genotypes after adjustment for pork consumption and other factors. Conclusion: These interaction relationships among CagA, IL-1B-31 and pork consumption may have implications for development of the preventive strategies for the early detection of non-cardiac GC.

Original languageEnglish (US)
Pages (from-to)8151-8157
Number of pages7
JournalWorld Journal of Gastroenterology
Volume20
Issue number25
DOIs
StatePublished - Jan 1 2014
Externally publishedYes

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Interleukins
Stomach Neoplasms
Genotype
Helicobacter pylori
Population Control
Red Meat
Restriction Fragment Length Polymorphisms
Case-Control Studies
China
Logistic Models
Enzyme-Linked Immunosorbent Assay
Alleles
Polymerase Chain Reaction

All Science Journal Classification (ASJC) codes

  • Gastroenterology

Cite this

Interactions between pork consumption, CagA status and IL-1B-31 genotypes in gastric cancer. / Wang, Xiao Qin; Terry, Paul; Cheng, Li; Yan, Hong; Wang, Jian Sheng; Wu, Wen An; Hu, Sen Ke.

In: World Journal of Gastroenterology, Vol. 20, No. 25, 01.01.2014, p. 8151-8157.

Research output: Contribution to journalArticle

Wang, Xiao Qin ; Terry, Paul ; Cheng, Li ; Yan, Hong ; Wang, Jian Sheng ; Wu, Wen An ; Hu, Sen Ke. / Interactions between pork consumption, CagA status and IL-1B-31 genotypes in gastric cancer. In: World Journal of Gastroenterology. 2014 ; Vol. 20, No. 25. pp. 8151-8157.
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abstract = "Aim: To explore potential interactions among Helicobacter pylori (H. pylori), CagA status, interleukin (IL)- 1B-31 genotypes, and non-cardiac gastric cancer (GC) risk. Methods: A case-control study of non-cardia GC was performed at 3 hospitals located in Xi'an, China, between September 2008 and July 2010. We included 171 patients with histologically diagnosed primary noncardia GC and 367 population based controls (matched by sex, age and city of residence). A standardized questionnaire was used to obtain information regarding potential risk factors, including pork consumption. H. pylori CagA status was assessed by enzyme-linked immunosorbent assay, and IL-1B-31 genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism. Multivariate unconditional logistic regression was used to explore potential interactions among the factors. Results: The CagA appeared to confer an increased risk of GC (OR = 1.81, 95{\%}CI: 1.25-2.61). The main associations with IL-1B-31C allele here were 0.98 (95{\%}CI: 0.59-1.63) for CC vs TT and 0.99 (95{\%}CI: 0.64-1.51) for C Carriers vs TT. However, no associations were observed for CagA or IL-1B-31 genotype status among subjects who reported low pork consumption (P for interaction = 0.11). In contrast, high pork consumption and IL-1B-31C genotypes appeared to synergistically increase GC risk (P for interaction = 0.048) after adjusting for confounding factors, particularly among subjects with CagA (OR = 3.07, 95{\%}CI: 1.17-10.79). We did not observe effect modification of pork consumption by H. pylori CagA status, or between H. pylori CagA status and IL-1B-31 genotypes after adjustment for pork consumption and other factors. Conclusion: These interaction relationships among CagA, IL-1B-31 and pork consumption may have implications for development of the preventive strategies for the early detection of non-cardiac GC.",
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T1 - Interactions between pork consumption, CagA status and IL-1B-31 genotypes in gastric cancer

AU - Wang, Xiao Qin

AU - Terry, Paul

AU - Cheng, Li

AU - Yan, Hong

AU - Wang, Jian Sheng

AU - Wu, Wen An

AU - Hu, Sen Ke

PY - 2014/1/1

Y1 - 2014/1/1

N2 - Aim: To explore potential interactions among Helicobacter pylori (H. pylori), CagA status, interleukin (IL)- 1B-31 genotypes, and non-cardiac gastric cancer (GC) risk. Methods: A case-control study of non-cardia GC was performed at 3 hospitals located in Xi'an, China, between September 2008 and July 2010. We included 171 patients with histologically diagnosed primary noncardia GC and 367 population based controls (matched by sex, age and city of residence). A standardized questionnaire was used to obtain information regarding potential risk factors, including pork consumption. H. pylori CagA status was assessed by enzyme-linked immunosorbent assay, and IL-1B-31 genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism. Multivariate unconditional logistic regression was used to explore potential interactions among the factors. Results: The CagA appeared to confer an increased risk of GC (OR = 1.81, 95%CI: 1.25-2.61). The main associations with IL-1B-31C allele here were 0.98 (95%CI: 0.59-1.63) for CC vs TT and 0.99 (95%CI: 0.64-1.51) for C Carriers vs TT. However, no associations were observed for CagA or IL-1B-31 genotype status among subjects who reported low pork consumption (P for interaction = 0.11). In contrast, high pork consumption and IL-1B-31C genotypes appeared to synergistically increase GC risk (P for interaction = 0.048) after adjusting for confounding factors, particularly among subjects with CagA (OR = 3.07, 95%CI: 1.17-10.79). We did not observe effect modification of pork consumption by H. pylori CagA status, or between H. pylori CagA status and IL-1B-31 genotypes after adjustment for pork consumption and other factors. Conclusion: These interaction relationships among CagA, IL-1B-31 and pork consumption may have implications for development of the preventive strategies for the early detection of non-cardiac GC.

AB - Aim: To explore potential interactions among Helicobacter pylori (H. pylori), CagA status, interleukin (IL)- 1B-31 genotypes, and non-cardiac gastric cancer (GC) risk. Methods: A case-control study of non-cardia GC was performed at 3 hospitals located in Xi'an, China, between September 2008 and July 2010. We included 171 patients with histologically diagnosed primary noncardia GC and 367 population based controls (matched by sex, age and city of residence). A standardized questionnaire was used to obtain information regarding potential risk factors, including pork consumption. H. pylori CagA status was assessed by enzyme-linked immunosorbent assay, and IL-1B-31 genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism. Multivariate unconditional logistic regression was used to explore potential interactions among the factors. Results: The CagA appeared to confer an increased risk of GC (OR = 1.81, 95%CI: 1.25-2.61). The main associations with IL-1B-31C allele here were 0.98 (95%CI: 0.59-1.63) for CC vs TT and 0.99 (95%CI: 0.64-1.51) for C Carriers vs TT. However, no associations were observed for CagA or IL-1B-31 genotype status among subjects who reported low pork consumption (P for interaction = 0.11). In contrast, high pork consumption and IL-1B-31C genotypes appeared to synergistically increase GC risk (P for interaction = 0.048) after adjusting for confounding factors, particularly among subjects with CagA (OR = 3.07, 95%CI: 1.17-10.79). We did not observe effect modification of pork consumption by H. pylori CagA status, or between H. pylori CagA status and IL-1B-31 genotypes after adjustment for pork consumption and other factors. Conclusion: These interaction relationships among CagA, IL-1B-31 and pork consumption may have implications for development of the preventive strategies for the early detection of non-cardiac GC.

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