Abstract
The adenomatous stomach lesion which occurs spontaneously in strain I mice did not occur in mice of other strains when they were kept in pens with strain I mice or when they were fed the lesion. Feeding tissues of the lesion to young strain I mice did not hasten its appearance or increase its degree of development in the young animals. The stomach lesion was not communicable and was not, apparently, caused by an infectious agent. The lesion did not regress in older strain I mice fed a vit. A rich diet and occurred in young strain I mice fed a diet rich in vit. A. The lesion was evidently not the result of vit. A deficiency. The lesion was more pronounced in young strain I mice kept on a dog chow diet which contained roughage than in those fed diets rich or deficient in vit. A but which contained very little roughage. This suggested that the physical state of the diet exerted some influence upon the development of the lesion. The vit. A deficient diet caused hypertrophy and hyperkeratosis of the lining in the forestomachs of mice from 3 inbred strains but the strains varied in their responses to the deficient diet. The implication of this variation in response was discussed and it was suggested that inbred strains of mice might be of some use in the study of vits.

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