trp mutation, which is found in the backbone of the DHFR molecule rather than in the active site, is currently under study. It is now important to carefully examine human neoplams to determine if alterations in DHFR lead to intrinsic or acquired drug resistance. The possibility that inherent or natural resistance of ANLL to MTX is due to the presence of an altered form of DHFR in blasts of untreated patients has been suggested by the observations of Dedhar et al.

McGrath T, Center MS (1988) Mechanisms of multidrug resistance in HL60 cells: evidence that a surface membrane protein distinct from P-glycoprotein contributes to reduced cellular accumulation of drug. Cancer Res 48: 3959-3963 9. Beck WT (1990) Mechanisms of multidrug resistance in human tumor cells. The roles of P-glycoprotein, DNA topoisomerase II, and other factors. Cancer Treat Rev 17 (Suppl A): 11-20 10. Danks MK, Yalowich JC, Beck WT (1987) Atypical multiple drug resistance in a human leukemic cell line selected for resistance to teniposide (VM-26).

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