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The Comparative Enzymology and Cell Origin of Rat Hepatomas

IV. Pyrimidine Metabolism in Minimal-Deviation Tumors^*

Tetsuo Ono, D. G. R. Blair, Van R. Potter and H. P. Morris

( McArdle Memorial Laboratories, The Medical School, University of Wisconsin, Madison, Wisconsin and National Cancer Institute, National Institutes of Health, Bethesda, Maryland)

A series including both "new" and "old" transplantable rat hepatomas were compared with the Morris 5123 Hepatoma with respect to enzymes of pyrimidine metabolism, particularly those that are considered to be "markers" for liver. The latter included carbamyl phosphate synthetase, ornithine transcarbamylase, uracil reductase, and thymine reductase.

The new hepatomas included the Morris 7316, Morris 7800, and Reuber H-35, all of which were categorized with the Morris 5123 as "minimal-deviation" hepatomas because they all possessed significant though reduced levels of the liver "marker" enzymes, in contrast to the Novikoff hepatoma, which possessed little if any of the "marker" enzymes.

Other pyrimidine enzymes studied included aspartic transcarbamylase, orotic decarboxylase, and enzymes converting orotic acid via orotidylic acid to the uridine nucleotides. These anabolic enzymes are known to be widely distributed and were found in near normal amounts in the hepatomas which were studied.

It was concluded that the Morris 5123 Hepatoma is not the only example of a minimal-deviation hepatoma and that additional examples are available in transplant form and can be obtained as primary tumors if desired.

Assays for ornithine transcarbamylase, uracil reductase, and thymine reductase in minimal-deviation hepatomas showed that deletion or diminution of these catabolic enzymes could not be considered essential to the malignant process in hepatoma cells. Moreover, the absence of these enzymes in the fast-growing Novikoff hepatoma could not be considered as proof that growth rate was stimulated by decreased activity of these catabolic enzymes, although this remains a possibility.

^* This work was supported in part by a grant (No. C-646) from the National Cancer Institute, National Institutes of Health, U.S. Public Health Service.

On leave from the Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.

Present address: Dept. of Cancer Research, University of Saskatchewan, Saskatoon, Canada.

Received 8/16/62.