Human gastric cancer risk screening: From rat pepsinogen studies to the ABC method

We examined the development of gastric cancer risk screening, from rat pepsinogen studies in an experimental rat gastric carcinogenesis model induced with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and human pepsinogen studies in the 1970s and 1980s to the recent ABC method for human gastric cancer risk screening. First, decreased expression or absence of a major pepsinogen isozyme, PG1, was observed in the rat gastric mucosa from the early stages of gastric carcinogenesis to adenocarcinomas following treatment with MNNG. In the 1980s, decreases in PGI in the human gastric mucosa and serum were identified as markers of atrophic gastritis. In the 1990s, other researchers revealed that chronic infection with Helicobacter pylori (Hp) causes atrophic gastritis and later gastric cancer. In the 2000s, a gastric cancer risk screening method combining assays to detect serum anti-Hp IgG antibody and serum PGI and PGII levels, the ABC method, was established. Eradication of Hp and endoscopic follow-up examination after the ABC method are recommended to prevent gastric cancer.

Automated summary

The development of gastric cancer risk screening involves studies from rat pepsinogen research to human pepsinogen studies, identifying key markers such as decreased PG1 in early stages of gastric carcinogenesis, decreased PGI in atrophic gastritis, and the link between Hp infection and gastric cancer. The ABC method, combining serum anti-Hp IgG antibody and serum PGI and PGII levels, has been established for gastric cancer risk screening, with Hp eradication and follow-up examination recommended for prevention.