Gastric cancer etiology: a biochemical hypothesis.
We have proposed a two-stage biochemical model for the etiology of "intestinal" gastric cancer. The model postulates that the gastric mucosal barrier is biochemically pierced as a result of chemical interactions between the mucoproteins and mucopolysaccharides of the barrier and ingested polysaccharrides (starches). This would allow the growth of gastric flora which could produce carcinogenic nitrosamines and/or nitrosamides. Observational and experimental evidence in favor of the model is provided. The model suggests various research initiatives, the results of which might provide the basis for biochemical and physiological methods for the prevention and/or treatment of gastric cancer. Various ways in which the model may be tested are also noted.
D000328:Adult; D001789:Blood Group Antigens; D004032:Diet / Q000009:adverse effects; D005260:Female; D005770:Gastrointestinal Neoplasms / Q000097:blood / Q000209:etiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D008954:Models, Biological; D009088:Mucoproteins / Q000378:metabolism*; D011134:Polysaccharides / Q000378:metabolism*; D011230:Precancerous Conditions; D013213:Starch / Q000009:adverse effects*; D013270:Stomach / Q000503:physiopathology
D001789:Blood Group Antigens; D009088:Mucoproteins; D011134:Polysaccharides; D013213:Starch