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Titlebook: Cytotoxic Drug Resistance Mechanisms; Robert Brown,Uta B?ger-Brown Book 1999 Humana Press 1999

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樓主: Negate
21#
發(fā)表于 2025-3-25 07:16:06 | 只看該作者
22#
發(fā)表于 2025-3-25 09:32:10 | 只看該作者
23#
發(fā)表于 2025-3-25 13:33:02 | 只看該作者
https://doi.org/10.1007/978-1-4842-2424-3ance. Reversal studies are best performed in diseases in which this mechanism represents the major component of drug resistance. The clearest approach to identifying these is to measure .-1 mRNA or P-glycoprotein in tumors at diagnosis, at the time of disease recurrence, and before and after treatment with P-glycoprotein reversal agents.
24#
發(fā)表于 2025-3-25 16:27:36 | 只看該作者
Scripting Languages & Server Side Includes, This is important, because despite considerable progress in the understanding of the mechanistic basis of apoptosis, morphological analysis remains unquestionably the “gold standard” for its assessment and quantitation.
25#
發(fā)表于 2025-3-25 23:42:16 | 只看該作者
https://doi.org/10.1007/978-1-4842-2424-3odimer and forms a covalent bond with the 5′-terminus of the DNA double-strand break with a four base-pairs overhang (.) (.–.). No energy cofactor is required for top1 activity, whereas top2 hydrolyzes adenosine triphosphate (ATP) during its catalytic cycle.
26#
發(fā)表于 2025-3-26 03:28:34 | 只看該作者
27#
發(fā)表于 2025-3-26 05:54:46 | 只看該作者
28#
發(fā)表于 2025-3-26 10:42:56 | 只看該作者
Topoisomerase I and II Activity Assays,odimer and forms a covalent bond with the 5′-terminus of the DNA double-strand break with a four base-pairs overhang (.) (.–.). No energy cofactor is required for top1 activity, whereas top2 hydrolyzes adenosine triphosphate (ATP) during its catalytic cycle.
29#
發(fā)表于 2025-3-26 12:43:35 | 只看該作者
Measuring Drug-DNA Adducts in Individual Cells, methods, to determine the extent of drug-DNA interaction in cells. These techniques however, rely on the measurement of adducts on DNA isolated from millions of cells (described by Tilby in . and .. and .).
30#
發(fā)表于 2025-3-26 20:11:48 | 只看該作者
Drug Resistance,d in the discovery of numerous mechanisms present within tumor cells that act to reduce their cytotoxic effects. However, the failure to translate this basic laboratory research into improved clinical outcome for patients remains one of the most pressing problems in contemporary cancer research.
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