Infection of the chorioallantoic membrane (CAM)2 of the chick embryo with Rous sarcoma virus (RSV) results in a 10-fold increase in uridine kinase activity of cell-free extracts prepared from the resulting tumor tissue. This enhancement of enzymatic activity is 1st evident 4 days after infection, when pocks are 1st noticed on the CAM. Maximal enzymatic activity is reached 6 or 7 days after infection, when there is a confluent tumor on the CAM. Uridine kinase activity is increased by infection with either the Bryan or the Schmidt-Ruppin strain of RSV.

RSV-induced tumors fail to exhibit a general increase in nucleoside kinase activities. Besides uridine, only cytidine and the analog 6-azauridine of several ribonucleosides and deoxyribonucleosides tested are phosphorylated to a much greater degree in infected CAM than in uninfected CAM.

The increase in phosphorylation of uridine in RSV-induced tumors is not a result of differential rates of catabolism of the substrate, uridine, or the product of the uridine kinase reaction, uridine-5′-phosphate (UMP), since activities of uridine phosphorylase and uracil ribonucleotide phosphatase are similar in control and infected CAM.

1

Aided by grants from the National Cancer Institute, C-3811, and the Atomic Energy Commission, AT (30-1)-910.

2

The abbreviations used are: CAM, chorioallantoic membrane; RSV, Rous sarcoma virus; UMP, uridine-5′-phosphate; ATP, adenosine triphosphate; Tris, tris(hydroxymethyl)aminomethane; and EDTA, ethylenediaminetetraacetic acid.

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©1966 American Association for Cancer Research.
1966
Cancer Research, Inc.