Zhonghua zhong liu za zhi [Chinese journal of oncology] · 2008
[Interaction between an insertion/deletion polymorphism in pepsinogen C and Helicobacter pylori infection in the development of gastric cancer].
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Sun Li-Ping, Zhang Ye, Liu Yun-En, Chen Wei, Yuan Yuan
Аннотация
OBJECTIVE: This study was designed to investigate the interaction between pepsinogen C(PGC) insertion/deletion polymorphism and Helicobacter pylori(Hp) infection, together with its different subtype strains, in the development of gastric cancer (GC).
METHODS: PGC Genotypes were determined by polymerase chain reaction (PCR) assay in 564 subjects with superficial gastritis (NOR), gastric ulcer (GU), atrophic gastritis (AG) and GC, who were frequency-matched as 1:1. Serum Hp-IgG antibodies were determined by an enzyme linked immunoadsorbent assay (ELISA). Hp genetic subtypes in 171 patients with Hp infection were determined by PCR methods.
RESULTS: In GU, AG and GC, the OR of interaction was 8.69 (P = 0.049), 11.16 (P = 0.02), and 10.61 (P = 0.03), respectively; the interaction index of PGC homozygous allele 1 genotype and Hp infection was 5.40, 6.48 or 4.34, respectively; the attributable proportions were 0.721, 0.770 and 0.697, respectively. In AG and GC, no significant interactions were observed between PGC polymorphism and Hp genetic subtypes.
CONCLUSION: The findings of this study suggest that PGC insertion/deletion polymorphism and Hp infection seem to present a positive interaction in the development of gastric cancer. While no interactions may be present between PGC polymorphism and Hp genetic subtypes.
METHODS: PGC Genotypes were determined by polymerase chain reaction (PCR) assay in 564 subjects with superficial gastritis (NOR), gastric ulcer (GU), atrophic gastritis (AG) and GC, who were frequency-matched as 1:1. Serum Hp-IgG antibodies were determined by an enzyme linked immunoadsorbent assay (ELISA). Hp genetic subtypes in 171 patients with Hp infection were determined by PCR methods.
RESULTS: In GU, AG and GC, the OR of interaction was 8.69 (P = 0.049), 11.16 (P = 0.02), and 10.61 (P = 0.03), respectively; the interaction index of PGC homozygous allele 1 genotype and Hp infection was 5.40, 6.48 or 4.34, respectively; the attributable proportions were 0.721, 0.770 and 0.697, respectively. In AG and GC, no significant interactions were observed between PGC polymorphism and Hp genetic subtypes.
CONCLUSION: The findings of this study suggest that PGC insertion/deletion polymorphism and Hp infection seem to present a positive interaction in the development of gastric cancer. While no interactions may be present between PGC polymorphism and Hp genetic subtypes.