
[Cancer Research 12, 399-406, June 1, 1952]
© 1952 American Association for Cancer Research
Tissue Culture Screening of Purines and Purine Nucleosides for Selective Damage to Mouse Sarcoma Cells*
John J. Biesele,
Ruth E. Berger and
Marilyn Clarke
( Cell Growth Section of the Division of Experimental Chemotherapy, Sloan-Kettering Institute for Cancer Research, New York 21, N.Y.)
- 1. Comparative toxic effects of 96 purines and 28 purine nucleosides on embryonic mouse skin cells and Crocker mouse Sarcoma 180 cells in tissue culture are reported.
- 2. Compounds causing the greatest differential damage to Sarcoma 180 cells were most prominent among the adenines and the 2,6-diaminopurines. The 2-aminopurines, guanines, hypoxanthines, and xanthines were less effective.
- 3. The most effective compounds were certain 2-substituted adenines, particularly 2-chloroadenine, 2,6-diaminopurine, 2-methyladenine, 2-iodoadenine, and certain 2,6-diamino-8-arylpurines.
- 4. Additional substituents at other positions reduced the effectiveness of 2-substituted adenines.
- 5. The five nucleosides that caused more than slight damage in 1 day of exposure were ribofuranosyladenines or xylofuranosyladenines substituted, if at all, only in position 2 of adenine. The most toxic was 2-chloroadenosine.
- 6. Purine nucleosides, with the major exception of 2-hydroxyadenosine, tended to be less toxic to Sarcoma 180 cells than the corresponding free purines. For example, 2-aminoadenosine was about 1/40th as toxic to Sarcoma 180 cells as was 2,6-diaminopurine. Some nucleosides were more toxic to embryonic cells than were the free purines.
- 7. Consequently, embryonic and sarcomatous mouse cells were damaged to about the same extent by purine nucleosides.
* This work was supported in part by grants from the American Cancer Society; the National Cancer Institute, of the National Institutes of Health, Public Health Service; and the Damon Runyon Memorial Fund for Cancer Research.
Received 9/12/51.
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Rational Cancer Chemotherapy
Science,
January 15, 1954;
119(3081):
77 - 80.
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Copyright © 1952 by the American Association for Cancer Research.