Cancer Research Infection and Cancer: Biology, Therapeutics, and Prevention
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[Cancer Research 47, 3988-3994, August 1, 1987]
© 1987 American Association for Cancer Research

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DNA Cross-Linking Responses of Human Malignant Glioma Cell Strains to Chloroethylnitrosoureas, Cisplatin, and Diaziquone

Eric Sariban1, Kurt W. Kohn2, Chana Zlotogorski3, Guy Laurent4, Mauricio D'Incalci5, Rufus Day, III6, Barry H. Smith, Paul L. Kornblith7 and Leonard C. Erickson8

Laboratory of Molecular Pharmacology [E. S., K. W. K., C. Z., G. L., M. D'I., L. C. E.] and Laboratory of Molecular Carcinogenesis [R. D.], National Cancer Institute, and Surgical Neurology Branch, National Institute of Neurological Communicative Disease and Stroke [B. H. S., P. L. K.], Bethesda, Maryland 20892

Cell strains derived by culture of malignant glioma (astrocytoma grade III–IV) surgical specimens were tested for the production of DNA interstrand cross-links (ISC) and DNA-protein cross-links following treatment in vitro with 1-(2-chloroethyl)-1-nitrosourea, 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU, carmustine), 1-(2-chloroethyl)-3-(2,6-dioxo-1-piperidyl)-1-nitrosourea (PCNU), cis-dichlorodiammineplatinum(II) (cisplatin), and 3,6-diaziridinyl-2,5-bis(carboethoxyamino)-1,4-benzoquinone (diaziquone). ISC and DNA-protein crosslinks were measured by means of the DNA alkaline elution technique. Large differences among the cell strains were observed in DNA cross-linking responses to individual agents. The DNA responses to the chloroethylnitrosoureas, cisplatin, and diaziquone were largely independent of each other, except for a weak correlation between ISC responses to chloroethylnitrosoureas and cisplatin. ISC responses among the cell strains to chloroethylnitrosoureas were distributed bimodally, in accord with a phenotypic distinction between Mer+ and Mer- cells. ISC responses to cisplatin and diaziquone showed significant variation among cell strains, but the distributions were not bimodal. The results demonstrate the existence of diverse DNA cross-linking response patterns among cell strains from different tumors of a given histological type.

1 Present address: Dana Farber Cancer Institute, Boston, MA 02115.

2 To whom requests for reprints should be addressed, at Building 37, Room 5A19, NIH, Bethesda, MD 20892.

3 Present address: Mevasserot, Zion, Israel.

4 Present address: Laboratoire de Chimie Physiologique, UCL 75.39, Avenue Hippocrate 75, B-1200 Bruxelles, Belgium.

5 Present address: Mario Negri Institute, VIA Eritrea 62, 20157, Milan, Italy.

6 Present address: Department of Medicine, Cross Cancer Institute, 11560 University Avenue, Edmonton, Alberta T6G-1Z2, Canada.

7 Present address: Department of Neurosurgery, Albert Einstein College of Medicine, Montefiore Medical Center, Bronx, NY 10461.

8 Present address: Oncology Section, Building 54, Room 050, Loyola University Medical Center, 2160 South First Avenue, Maywood, IL 60153.

Received 8/13/86. Revised 2/26/87. Accepted 5/ 7/87.




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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 Meeting Abstracts Online
Copyright © 1987 by the American Association for Cancer Research.