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[Cancer Research 23, 987-994, August 1, 1963]
© 1963 American Association for Cancer Research

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Comparative Biochemistry of Hepatomas

III. Carbohydrate Enzymes in Liver Tumors of Different Growth Rates*

George Weber and Harold P. Morris

( Department of Pharmacology, Indiana University School of Medicine, Indianapolis, Ind.; and Laboratory of Biochemistry, National Cancer Institute, N.I.H., P.H.S., Bethesda, Md.)

The behavior of carbohydrate enzymes was examined in a spectrum of hepatomas of different growth rates, and results were evaluated in the light of data obtained in Hepatoma 5123-D and the Novikoff tumor. The studied biochemical parameters can be classified according to their relation to hepatoma growth rate. There are factors which correlate, others which do not correlate, and, finally, parameters which are decreased or increased in all or most of the tumors.

Marked differences in cellularity, nitrogen content, and enzyme activities were found between normal livers and host livers. Therefore, the values of hepatomas were compared with those of normal livers.

Certain metabolic features were correlated with the growth rate of liver tumors. Nitrogen content showed a trend to decrease with increasing growth rate, with lowest values found in the rapidly growing tumors. Glucose-6-phosphatase and fructose-1,6-diphosphatase activities in slowly growing tumors were one-half to one-third of normal liver values, and they further decreased in more rapidly growing tumors with no activities in the fastest growing hepatomas. No correlation with growth rate was noted for cellularity or for the enzymes, phosphohexose isomerase, lactic dehydrogenase, and 6-phosphogluconate dehydrogenase.

Phosphoglucomutase was significantly decreased in all examined tumors. In contrast, glucose-6-phosphate dehydrogenase was increased in all hepatomas with the exception of 5123-D.

The presented results were evaluated in terms of the molecular basis and possible biochemical grading of hepatomas exhibiting different biological behavior.

* This work was supported in part by grants from the Damon Runyon Memorial Fund for Cancer Research, Inc. (DRG-542); American Cancer Society (No. E-254); and National Cancer Institute, National Institutes of Health, U.S. Public Health Service (CY-5034).

Received 2/13/63.


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[Abstract] [Full Text] [PDF]




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Copyright © 1963 by the American Association for Cancer Research.