Modulation of gastric carcinogenesis: updated model based on intragastric nitrosation.

The etiological model of gastric carcinogenesis is discussed. Its complexity and flexibility may be more applicable to human situations than experimental models utilizing high doses of carcinogens in homogeneous animal populations. The limitations of the epidemiological method and the use of a collaborative approach by epidemiologists and experimentalists are described. The need for markers of exposure to N-nitroso compounds is stressed.