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Different etiological role of Helicobacter pylori (Hp) infection in carcinogenesis between differentiated and undifferentiated gastric cancers: a nested case-control study using IgG titer against Hp surface antigen.
Acta Oncol 2008; 47(3):360-5AO

Abstract

BACKGROUND

The present study epidemiologically clarified the different roles of Helicobacter pylori (Hp) infection in carcinogenesis between two major histological types of noncardia gastric cancer (ncGC), intestinal (=differentiated) and diffuse (=undifferentiated), by analyzing IgG antibody titer against Hp surface antigen on the data set of a nested case-control study in a large cohort study conducted in Japan.

METHODS

A total of 36,745 subjects aged 40 to 69 years in the Japan Health Center-based prospective study who responded to the baseline questionnaire and provided blood were followed over 15 years; 350 ncGC cases (differentiated=242, undifferentiated=108) matched to controls were used. Using baseline blood samples, plasma IgG titer was measured using ELISA. The level of IgG titer >10 U (cut-off value) was classified into three grades in groups of equal number: low, middle, and high.

RESULTS

IgG titer of Hp was significantly (p<0.01) higher in undifferentiated cases than in differentiated ones. Among the three grades of Hp IgG titer, the high titer was more closely associated with risk of undifferentiated ncGC (odds ratio (OR) for high=7.8, 95% confidence interval (CI)=2.4-24.9 vs. OR for low=6.4, 95% CI=2.1-19.6), while the low titer was a better predictor of differentiated ncGC (OR for high=3.2, 95% CI=1.6-6.4 vs. OR for low=5.9, 95% CI=3.0-11.6, trend p < 0.05). The high titer group had the lowest risk to develop differentiated ncGC with <7 years (OR=3.2, 95% CI=1.3-7.7), whereas the high titer group demonstrated the highest risk for undifferentiated ncGC developing (OR=11.6 95% CI=2.3-59.1).

CONCLUSION

Our study epidemiologically confirmed that atrophic changes caused by Hp infection determine the development of differentiated-type ncGC, and the inflammation itself induced by Hp infection promotes the development of undifferentiated-type ncGC.

Authors+Show Affiliations

Epidemiology and Prevention Division, Research Center for Cancer Prevention and Screening, National Cancer Center, Chuo-ku, Tokyo, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article

Language

eng

PubMed ID

18347999

Citation

Tatemichi, Masayuki, et al. "Different Etiological Role of Helicobacter Pylori (Hp) Infection in Carcinogenesis Between Differentiated and Undifferentiated Gastric Cancers: a Nested Case-control Study Using IgG Titer Against Hp Surface Antigen." Acta Oncologica (Stockholm, Sweden), vol. 47, no. 3, 2008, pp. 360-5.
Tatemichi M, Sasazuki S, Inoue M, et al. Different etiological role of Helicobacter pylori (Hp) infection in carcinogenesis between differentiated and undifferentiated gastric cancers: a nested case-control study using IgG titer against Hp surface antigen. Acta Oncol. 2008;47(3):360-5.
Tatemichi, M., Sasazuki, S., Inoue, M., & Tsugane, S. (2008). Different etiological role of Helicobacter pylori (Hp) infection in carcinogenesis between differentiated and undifferentiated gastric cancers: a nested case-control study using IgG titer against Hp surface antigen. Acta Oncologica (Stockholm, Sweden), 47(3), pp. 360-5. doi:10.1080/02841860701843035.
Tatemichi M, et al. Different Etiological Role of Helicobacter Pylori (Hp) Infection in Carcinogenesis Between Differentiated and Undifferentiated Gastric Cancers: a Nested Case-control Study Using IgG Titer Against Hp Surface Antigen. Acta Oncol. 2008;47(3):360-5. PubMed PMID: 18347999.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Different etiological role of Helicobacter pylori (Hp) infection in carcinogenesis between differentiated and undifferentiated gastric cancers: a nested case-control study using IgG titer against Hp surface antigen. AU - Tatemichi,Masayuki, AU - Sasazuki,Shizuka, AU - Inoue,Manami, AU - Tsugane,Shoichiro, AU - ,, PY - 2008/3/19/pubmed PY - 2008/10/10/medline PY - 2008/3/19/entrez SP - 360 EP - 5 JF - Acta oncologica (Stockholm, Sweden) JO - Acta Oncol VL - 47 IS - 3 N2 - BACKGROUND: The present study epidemiologically clarified the different roles of Helicobacter pylori (Hp) infection in carcinogenesis between two major histological types of noncardia gastric cancer (ncGC), intestinal (=differentiated) and diffuse (=undifferentiated), by analyzing IgG antibody titer against Hp surface antigen on the data set of a nested case-control study in a large cohort study conducted in Japan. METHODS: A total of 36,745 subjects aged 40 to 69 years in the Japan Health Center-based prospective study who responded to the baseline questionnaire and provided blood were followed over 15 years; 350 ncGC cases (differentiated=242, undifferentiated=108) matched to controls were used. Using baseline blood samples, plasma IgG titer was measured using ELISA. The level of IgG titer >10 U (cut-off value) was classified into three grades in groups of equal number: low, middle, and high. RESULTS: IgG titer of Hp was significantly (p<0.01) higher in undifferentiated cases than in differentiated ones. Among the three grades of Hp IgG titer, the high titer was more closely associated with risk of undifferentiated ncGC (odds ratio (OR) for high=7.8, 95% confidence interval (CI)=2.4-24.9 vs. OR for low=6.4, 95% CI=2.1-19.6), while the low titer was a better predictor of differentiated ncGC (OR for high=3.2, 95% CI=1.6-6.4 vs. OR for low=5.9, 95% CI=3.0-11.6, trend p < 0.05). The high titer group had the lowest risk to develop differentiated ncGC with <7 years (OR=3.2, 95% CI=1.3-7.7), whereas the high titer group demonstrated the highest risk for undifferentiated ncGC developing (OR=11.6 95% CI=2.3-59.1). CONCLUSION: Our study epidemiologically confirmed that atrophic changes caused by Hp infection determine the development of differentiated-type ncGC, and the inflammation itself induced by Hp infection promotes the development of undifferentiated-type ncGC. SN - 1651-226X UR - https://www.unboundmedicine.com/medline/citation/18347999/Different_etiological_role_of_Helicobacter_pylori__Hp__infection_in_carcinogenesis_between_differentiated_and_undifferentiated_gastric_cancers:_a_nested_case_control_study_using_IgG_titer_against_Hp_surface_antigen_ L2 - http://www.tandfonline.com/doi/full/10.1080/02841860701843035 DB - PRIME DP - Unbound Medicine ER -