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Circumvention of Deficient Activation in Mitomycin C-resistant Human Colonic Carcinoma Cells by the Mitomycin C Analogue BMY25282

Circumvention of Deficient Activation in Mitomycin C-resistant Human Colonic Carcinoma Cells by... BMY25282, a newly designed analogue of mitomycin C (MMC) with the substitution of an amidine group at position 7 of MMC, can circumvent MMC resistance in a series of human colonic carcinoma cells that were selected for resistance to MMC (J. K. V. Willson et al. , Cancer Res., 45: 5281–5286, 1985). In this study MMC resistance was found to be associated with an inability of the resistant cells to activate MMC. However, both the MMC-sensitive and -resistant cells were observed to metabolize BMY25282 extensively in vitro to a reactive species capable of alkylating 4-( p -nitrobenzyl)pyridine (a trapping agent for activated drug). The results of these studies suggested that the deficient cellular reductive activating mechanism was associated with MMC resistance and that analogue BMY25282 was able to overcome this deficiency in MMC-resistant cells by virtue of its enhanced activation. 1 Supported in part by NIH Grant CA40449. 2 To whom requests for reprints should be addressed. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Cancer Research American Association of Cancer Research

Circumvention of Deficient Activation in Mitomycin C-resistant Human Colonic Carcinoma Cells by the Mitomycin C Analogue BMY25282

Circumvention of Deficient Activation in Mitomycin C-resistant Human Colonic Carcinoma Cells by the Mitomycin C Analogue BMY25282

Cancer Research , Volume 46 (7): 3456 – Jul 1, 1986

Abstract

BMY25282, a newly designed analogue of mitomycin C (MMC) with the substitution of an amidine group at position 7 of MMC, can circumvent MMC resistance in a series of human colonic carcinoma cells that were selected for resistance to MMC (J. K. V. Willson et al. , Cancer Res., 45: 5281–5286, 1985). In this study MMC resistance was found to be associated with an inability of the resistant cells to activate MMC. However, both the MMC-sensitive and -resistant cells were observed to metabolize BMY25282 extensively in vitro to a reactive species capable of alkylating 4-( p -nitrobenzyl)pyridine (a trapping agent for activated drug). The results of these studies suggested that the deficient cellular reductive activating mechanism was associated with MMC resistance and that analogue BMY25282 was able to overcome this deficiency in MMC-resistant cells by virtue of its enhanced activation. 1 Supported in part by NIH Grant CA40449. 2 To whom requests for reprints should be addressed.

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Publisher
American Association of Cancer Research
Copyright
Copyright © 1986 by the American Association for Cancer Research.
ISSN
0008-5472
Publisher site

Abstract

BMY25282, a newly designed analogue of mitomycin C (MMC) with the substitution of an amidine group at position 7 of MMC, can circumvent MMC resistance in a series of human colonic carcinoma cells that were selected for resistance to MMC (J. K. V. Willson et al. , Cancer Res., 45: 5281–5286, 1985). In this study MMC resistance was found to be associated with an inability of the resistant cells to activate MMC. However, both the MMC-sensitive and -resistant cells were observed to metabolize BMY25282 extensively in vitro to a reactive species capable of alkylating 4-( p -nitrobenzyl)pyridine (a trapping agent for activated drug). The results of these studies suggested that the deficient cellular reductive activating mechanism was associated with MMC resistance and that analogue BMY25282 was able to overcome this deficiency in MMC-resistant cells by virtue of its enhanced activation. 1 Supported in part by NIH Grant CA40449. 2 To whom requests for reprints should be addressed.

Journal

Cancer ResearchAmerican Association of Cancer Research

Published: Jul 1, 1986

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