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- W2033351384 abstract "Nitrogen mustard resistance in B-cell chronic lymphocytic leukemia (B-CLL) has been associated with enhanced DNA repair and increased expression of DNA repair enzymes. Lymphocytes from patients with nitrogen mustard resistant B-CLL displayed a fivefold increase in resistance to melphalan in vitro as compared to those from untreated patients concordant with our definition of clinical resistance. We have performed Northern analysis using a cohort consisting of 11 untreated and 12 treated-resistant patients. Increased expression of ERCC-1 was not found to be associated with nitrogen mustard resistance, nor did we find altered expression of the DNA repair enzymes: ERCC-2, DNA polymerase β, or topoisomerase I. There was also no difference in the levels of ERCC-1 protein between melphalan sensitive and resistant B-CLL lymphocytes. Analysis of genes involved in nitrogen mustard detoxification revealed that metallothionein was weakly expressed, while transcripts encoding glutathione-S-transferase α were undetectable. Thus, it is unlikely either of these proteins plays a role in the resistance. The results of the cytotoxicity assay validate the use of B-CLL as a model to study nitrogen mustard resistance. This model allows us to perform in vitro studies using a tumor which develops resistance in vivo. The results of this study suggest that nucleotide excision repair, as represented by ERCC-1 and ERCC-2, is not the limiting step in B-CLL nitrogen mustard resistance." @default.
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- W2033351384 date "1968-08-01" @default.
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- W2033351384 title "Permeability difference as a source of resistance to alkylating agents in Ehrlich tumor cells" @default.
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- W2033351384 doi "https://doi.org/10.1016/0006-291x(68)90288-x" @default.
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