作者: Mark R. Müller , Jürgen Thomale , Manfred F. Rajewsky , Siegfried Seeber
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摘要: Most cytotoxic agents exert their action via damage of DNA. Therefore, the repair such lesions is major importance for sensitivity malignant cells to chemotherapeutic agents. The underlying mechanisms various DNA pathways have extensively been studied in yeast, bacteria and mammalian cells. Sensitive drug resistant cancer cell lines provided models analysis contribution chemosensitivity. However, validity results obtained by laboratory experiments with regard clinical situation limited. In both acute chronic leukaemias, emergence a cause treatment failure. Recently, assays become available measure cellular capacity specimens at single-cell level. Application these isolated lymphocytes from patients lymphatic leukaemia (CLL) revealed large interindividual differences rates. Accelerated O6-ethylguanine elimination faster processing repair-induced single-strand breaks were found CLL nonresponsive chemotherapy alkylating compared untreated or treated sensitive patients. Moreover, modulators different target identified which also influence this article, we review current knowledge about resistance human leukaemia.