Cancer Research Infection and Cancer: Biology, Therapeutics, and Prevention  Susan G. Komen for the Cure-AACR Outstanding Investigator Award for Breast Cancer Research
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Cell Growth & Differentiation

[Cancer Research 26, 748-751, April 1, 1966]
© 1966 American Association for Cancer Research

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Gelbard, A. S.
Right arrow Articles by Eidinoff, M. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gelbard, A. S.
Right arrow Articles by Eidinoff, M. L.

Nucleoside Kinase Activities in Tissues Infected with Rous Sarcoma Virus1

A. S. Gelbard, S. H. Kim and M. L. Eidinoff

Biophysics Division, Sloan-Kettering Institute for Cancer Research, New York, New York

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.

Received 7/ 8/65. Revised 10/22/65.





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Cell Growth & Differentiation
Copyright © 1966 by the American Association for Cancer Research.