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Department of Internal Medicine, The University of Texas Southwestern Medical School, Dallas, Texas, and Laboratory of Biochemistry, National Cancer Institute, NIH, Bethesda, Maryland
The studies reported here were carried out in an effort to extend our previous observation that the cholesterol negative feedback system is deleted in 3 varieties of hepatoma. In the present study the status of this feedback system has been examined in 10 additional transplantable hepatomas and in 1 human hepatoma. Although active cholesterol synthesis could be demonstrated in each of these tumors, in every case the cholesterol feedback system was found to be absent. Furthermore, the deletion of this feedback system from the highly differentiated Morris hepatoma 7787 suggests that this derangement of cholesterol feedback control may be a property of malignancy per se rather than a nonspecific effect of dedifferentiation. In conclusion, the deletion of the cholesterol feedback system in a total of 14 hepatomas so far examined, together with the demonstration of this lesion in a very highly differentiated liver tumor, suggests that the loss of this feedback system may be characteristic of malignancy in the liver.
1 This study was supported by grants from the Damon Runyon Memorial Fund and the USPHS (CA-05090).
2 Recipient, Research Career Award, National Heart Institute.
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