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Role of Injury and Hyperplasia in the Induction of Hepatocellular Carcinoma

Stanley Goldfarb, M.D.; Frederick G. Zak, M.D.

JAMA. 1961;178(7):729-731. doi:10.1001/jama.1961.73040460007007b.

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THE INDUCTION of hepatocellular carcinoma is not dependent on continuous feeding of carcinogen. Short periods of exposure to carcinogen may result in tumors many weeks or months after drug withdrawal.¹ Nevertheless, hepatocellular injury and hyperplasia apparently precede the development of hepatomas. The persistence, regression, or alteration of early hepatocellular injury and hyperplasia were studied in rats after withdrawal of 3'-methyl-4-dimethylamino azobenzene (methyl butter yellow, MeBY), a potent carcinogen. Since 26 days of drug feeding causes a low incidence of hepatocellular carcinoma and 40 days a high incidence of hepatomas,² 2 groups of rats fed the drug for these intervals were compared. Morphologic changes that were more prominent in the second group might be associated with hepatoma induction. The formation and persistence of nodules of hydropic, weakly basophilic cells, deficient in glucose-6-phosphatase (G-6-P' ase) that are closely associated with hepatocellular carcinoma will be described.

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Goldfarb S, Zak FG. Role of Injury and Hyperplasia in the Induction of Hepatocellular Carcinoma. JAMA. 1961;178(7):729-731. doi:10.1001/jama.1961.73040460007007b.

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