This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Silverstone, H. Articles by Tannenbaum, A. Search for Related Content PubMed PubMed Citation Articles by Silverstone, H. Articles by Tannenbaum, A.

Proportion of Dietary Protein and the Formation of Spontaneous Hepatomas in the Mouse^{* ,}

( Department of Cancer Research, Medical Research Institute, Michael Reese Hospital, Chicago 16, Ill.)

C3H male mice ingesting a diet containing 9 per cent casein as the principal source of protein developed a significantly lower incidence of hepatomas than mice on a diet containing 18 per cent casein. This occurred whether the daily rations were isocaloric or were adjusted to maintain equivalent body weights. Changing the proportion of dietary casein from 18 to 45 per cent had no noteworthy effect on the incidence of hepatomas.

The amount of dietary protein per se was not the factor responsible for the striking difference in the rate of formation of hepatomas between mice on 9 per cent and those on 18 per cent casein diets. Adding 9 per cent gelatin to the 9 per cent casein ration had little effect. On the other hand, supplementing the 9 per cent casein ration with methionine and cystine increased the incidence of hepatomas to that of mice on an 18 per cent casein diet. Thus, the reduced incidence of hepatomas in the mice on the 9 per cent casein rations was a consequence of inadequate amounts of dietary sulfurcontaining amino acids. The supplements of these amino acids may have acted directly in the carcinogenic process or, more likely, produced their effect by augmenting the nutritional adequacy of the dietary protein.

^* Presented, in part, at the Fifth International Cancer Congress, Paris, July 19, 1950.

This work was supported by a Grant-in-Aid from the American Cancer Society upon recommendation of the Committee on Growth of the National Research Council.

Supported, in part, by the Michael Reese Research Foundation and the Foundation for Cancer Research, Chicago.

Received 1/25/51.