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Titlebook: Concepts, Mechanisms, and New Targets for Chemotherapy; F. M. Muggia Book 1995 Springer Science+Business Media New York 1995 DNA.breast ca

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書(shū)目名稱Concepts, Mechanisms, and New Targets for Chemotherapy
編輯F. M. Muggia
視頻videohttp://file.papertrans.cn/235/234960/234960.mp4
叢書(shū)名稱Cancer Treatment and Research
圖書(shū)封面Titlebook: Concepts, Mechanisms, and New Targets for Chemotherapy; F. M. Muggia Book 1995 Springer Science+Business Media New York 1995 DNA.breast ca
描述.Concepts, Mechanisms, and New Targets for Chemotherapy.describes new interconnections between rationally designed andempirically discovered compounds. One route that has not beentravelled previously is that of protein kinase C inhibition. Thispathway may be exploited to give potent inhibitors, such as thebryostatins, now in clinical trial. A summary is given of the currentstatus of topoisomerase, focusing on recent clinical advances withcamptothecin analogs based on connecting empiricism with concepts ofdrug selectivity. .Modification of existing therapies based on the pursuit of leadsarising from mechanistic studies is also being applied clinically on awide scale. Greater understanding should follow from the studies ofreversal of the multidrug resistant phenotype, on the use ofhydroxyurea to reverse resistance mediated by extrachromosomal DNA,and on various aspects of the fluoropyrimidine pathways. .Successful applications of chemotherapy to the treatment of specificdiseases include the growing applications of systemic therapy usingvarious skin malignancies. In prostate cancer, estramustine phosphatewill likely play an expanding role. Taxanes are restructuringtreatment regimens i
出版日期Book 1995
關(guān)鍵詞DNA; breast cancer; cancer; carcinoma; chemotherapy; clinical trial; diseases; neoplasm; prostate cancer; sys
版次1
doihttps://doi.org/10.1007/978-1-4615-2007-8
isbn_softcover978-1-4613-5829-9
isbn_ebook978-1-4615-2007-8Series ISSN 0927-3042 Series E-ISSN 2509-8497
issn_series 0927-3042
copyrightSpringer Science+Business Media New York 1995
The information of publication is updating

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Recent clinical advances with camptothecin analoguesn, demonstrated encouraging activity in early clinical testing but was abandoned due to unpredictable toxicity. In 1985, Hsaing and Liu observed that the cytotoxic effect of camptothecin requires the nuclear enzyme topoisomerase I [2]. This finding coincided with the development of the semisynthetic
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The reversal of multidrug resistanceaboratory, tumor cells can be selected for resistance to a particular cytotoxin by repeated exposure to that drug. The selected cells often display crossresistance to a number of functionally and structurally distinct drugs. This drug-resistant phenotype is referred to as . (MDR). Currently, the bes
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Fluoropyrimidine catabolismtes for important enzymatic reactions required in vital cell biologic processes, e.g., synthesis of DNA and RNA. Several reviews on the metabolism of antimetabolite drugs have recently been published, providing a general background on these drugs [1–5]. The pyrimidine antimetabolite drugs consist of
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Aspects of one-carbon folate cycling related to fluoropyrimidine and antifolate therapyxyuridylate (FdUMP) inhibition of thymidylate synthase (TS) occurs by the ordered, sequential binding of TS, FdUMP, and then 5-10-methylenetetrahydrofolate (CH.FH.) [.–.]. In cell-free kinetic systems, CH.FH. must be in excess for maximal TS-FdUMP-CH.FH. ternary complex formation and complete inhibi
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High-dose chemotherapy with peripheral blood progenitor autograftinglinic, this strategy also results in increased toxicity to normal tissues. For those cytotoxics that are primarily dose-limited by myelosuppression (e.g., alkylating agents, carboplain, and etoposide), the use of autologous bone marrow transplantation (ABMT) has facilitated substantial dose escalati
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