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Differential Repair of 1-(2-Chloroethyl)-3-(4-methylcyclohexyl)-1-nitrosourea-induced DNA Damage in Two Human Colon Tumor Cell Lines

Laboratories of Molecular Pharmacology [L. C. E., K. W. K.] and Chemical Pharmacology [R. O.], Developmental Therapeutics Program, Division of Cancer Treatment, National Cancer Institute, NIH, Bethesda, Maryland 20014

Two human colon tumor cell lines were examined for their responses to 1-(2-chloroethyl)-3-(4-methylcyclohexyl)-1-nitrosourea treatment when maintained as cultured cell lines and xenograft tumors in nude mice. One tumor line, HT, was resistant to 1-(2-chloroethyl)-3-(4-methylcyclohexyl)-1-nitrosourea treatment both in tissue culture and in vivo. The other tumor line, BE, was sensitive to 1-(2-chloroethyl)-3-(4-methylcyclohexyl)-1-nitrosourea treatment in vitro and in vivo. The DNA of tissue-cultured cells treated with 1-(2-Chloroethyl)-3-(4-methylcyclohexyl)-1-nitrosourea was examined by alkaline elution for DNA damage. 1-(2-Chloroethyl)-3-(4-methylcyclohexyl)-1-nitrosourea was found to produce DNA strand breaks and DNA cross-links in both cell types. The DNA cross-links appear to be completely repaired in the resistant HT line over the 48-hr period following drug removal, but in the sensitive BE line little or no cross-link repair was observed during this interval.

¹ To whom requests for reprints should be addressed.

² Present address: Innere Klinik (Tumorforschung), Hufelandstr. 55, D-43 Essen 1, Federal Republic of Germany.

Received 6/20/77. Accepted 12/ 8/77.