By Val R. Adams
A severe evaluation our present figuring out of camptothecins, their shortcomings, and of the chances for bettering their scientific functionality. The authors talk about new camptothecin analog improvement, drug supply matters for optimizing their anticancer job, and their strength use in a number of assorted cancers. extra chapters describe what's recognized in regards to the biochemistry, the pharmacology, and the chemistry of the camptothecins, together with the mechanism of topoisomerase and the way camptothecins poison this enzyme, using animal versions in defining the anticancer power of camptothecins, and the query of camptothecin resistance.
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Additional info for Camptothecins in Cancer Therapy (Cancer Drug Discovery and Development)
A) Models of illegitimate recombination using nicked and gapped DNA oligonucleotide substrates. (B) TOP-I–mediated ligation of a nicked substrate. (Tables 1 and 3). However, ligation of inhibition of the gapped DNA substituted was effected only by CPT itself and by 20-deoxy CPT (21), the latter of which failed to inhibit any of the other ligation reactions. Thus it seems clear that differential inhibition of individual TOP-I-mediated transformations should be possible. 54 Hecht Table 3 Inhibition of the TOP-I-Mediated Ligation of Nicked and Gapped DNA Oligonucleotides by CPTs Extent of inhibition ligation (%) CPT analoga Nicked substrateb 1 21 22 23 24 62 5 21 37 32 a50 Gapped substrate 47 13 0 0 0 μM concentration.
Ann N Y Acad Sci 803:74–92. 139. Liu LF, Desai SD, Li TK, Mao Y, Sun M, Sim SP. 2000 Mechanism of action of camptothecin. Ann N Y Acad Sci 922:1–10. 140. Desai SD, Mao Y, Sun M, Li TK, Wu J, Liu LF. 2000 Ubiquitin, SUMO-1 and UCRP in camptothecin sensitivity and resistance. Ann N Y Acad Sci 922:306–308. 141. Desai SD, Li TK, Rodriguez-Bauman A, Rubin E, Liu LF. 2001 Ubiquitin/26S proteasome-mediated degradation of topoisomerase I as a resistance mechanism to camptothecin in tumor cells. Cancer Res 61:5926–5932.
Each of these structures contained unresolvable portions of the protein in the connector region (Pro635–Phe640). Moreover, the reconstituted enzyme has altered kinetics and is not sensitive to camptothecin in a plasmid relaxation assay (35). Hence, the structures reported here are the first structures of a fully active human TOP-I in covalent complex with DNA in the absence and presence of bound drug. (C) Comparison of the 22mer duplex oligonucleotides of the drug-bound (blue) and nondrug-bound (yellow).