Drug resistance and DNA repair in XXXX .

@entity1 @entity5 @entity1072 @entity57964 @entity1778 @entity375
Most cytotoxic agents exert their action via damage of DNA. Therefore, the repair of such lesions is of major importance for the sensitivity of malignant cells to chemotherapeutic agents. The underlying mechanisms of various DNA repair pathways have extensively been studied in @entity375 , bacteria and @entity1 cells. Sensitive and @entity5 cell lines have provided models for analysis of the contribution of DNA repair to chemosensitivity. However, the validity of results obtained by laboratory experiments with regard to the clinical situation is limited. In both @entity1778 , the emergence of drug resistant cells is a major cause for treatment failure. Recently, assays have become available to measure cellular DNA repair capacity in clinical specimens at the single-cell level. Application of these assays to isolated lymphocytes from @entity1 with @entity1072 ( @entity1072 ) revealed large interindividual differences in DNA repair rates. Accelerated @entity57964 elimination from DNA and faster processing of repair-induced single-strand breaks were found in @entity1072 lymphocytes from @entity1 nonresponsive to chemotherapy with alkylating agents compared to untreated or treated sensitive @entity1 . Moreover, modulators of DNA repair with different target mechanisms were identified which also influence the sensitivity of @entity5 cells to alkylating agents. In this article, we review the current knowledge about the contribution of DNA repair to drug resistance in @entity1 @entity1778 .
