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Titlebook: Drug Resistance; William N. Hait Book 1996 Kluwer Academic Publishers 1996 DNA.Drogen.apoptosis.breast cancer.cancer.chemotherapy.drug.dru

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書目名稱Drug Resistance
編輯William N. Hait
視頻videohttp://file.papertrans.cn/284/283116/283116.mp4
叢書名稱Cancer Treatment and Research
圖書封面Titlebook: Drug Resistance;  William N. Hait Book 1996 Kluwer Academic Publishers 1996 DNA.Drogen.apoptosis.breast cancer.cancer.chemotherapy.drug.dru
描述Resistance to treatment represents the final common outcome forfar too many patients with cancer. Even our most promising new drugsfall victim to drug resistance. Hormones and newer biologicaltherapies, though safe and active, also lose their activity over time..In this volume of .Drug Resistance., leading investigators in thefield have reviewed the most basic mechanisms of drug resistance, andhave proposed ways to modulate resistance. This comprehensive volumeshould be of value for basic and clinical scientists who wish to delvemore deeply into this intriguing problem in the laboratory anddevastating problem in the clinic.
出版日期Book 1996
關(guān)鍵詞DNA; Drogen; apoptosis; breast cancer; cancer; chemotherapy; drug; drug resistance; hormones; immunodeficienc
版次1
doihttps://doi.org/10.1007/978-1-4613-1267-3
isbn_softcover978-1-4612-8540-3
isbn_ebook978-1-4613-1267-3Series ISSN 0927-3042 Series E-ISSN 2509-8497
issn_series 0927-3042
copyrightKluwer Academic Publishers 1996
The information of publication is updating

書目名稱Drug Resistance影響因子(影響力)




書目名稱Drug Resistance影響因子(影響力)學(xué)科排名




書目名稱Drug Resistance網(wǎng)絡(luò)公開度




書目名稱Drug Resistance網(wǎng)絡(luò)公開度學(xué)科排名




書目名稱Drug Resistance被引頻次




書目名稱Drug Resistance被引頻次學(xué)科排名




書目名稱Drug Resistance年度引用




書目名稱Drug Resistance年度引用學(xué)科排名




書目名稱Drug Resistance讀者反饋




書目名稱Drug Resistance讀者反饋學(xué)科排名




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Multidrug Resistance Associated with Overexpression of MRP of tumors, such as non-small cell lung carcinomas, this resistance is inherent, while in others (e.g., acute myelogenous leukemia) it is acquired during treatment. The problem of drug resistance has been studied in the laboratory primarily by using drug-selected, cultured tumor cell lines as model
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Mechanisms of Resistance to Alkylating Agentse result of the induction of a variety of protective mechanisms or the result of the selection of resistant clones. In some cases, neoplastic cells may also have a high intrinsic level of resistance [2]. Alkylating agents, particularly agents that alkylate preferentially at the O6 position of guanin
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Glutathione S-Transferaseschemoprotectant. In the human, levels of GSH range from 30μM in plasma to 3mM in kidney proximal tubules; tumors of various organs can contain up to 10mM GSH [1]. GSH is synthesized via the γ-glutamyl cycle (Figure 4–1). The rate-limiting step is catalyzed by γ-glutamylcysteine synthetase (γ-GCS) to
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Role of DNA Repair in Resistance to Drugs that Alkylate O6 of Guaninents includes the methylating agents, temozolomide, procarbazine, dacarbazine (DTIC), and steptozotocin, and the chloroethylating agents, carmustine (1,3 bis-chloroethyl 2-nitrosourea, BCNU), lomustine (3-cyclohexyl-1-chloroethyl-nitrosourea, CCNU), (2-chloroethyl)-3-sarcosinamide-1-nitrosourea (SarC
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Cellular Resistance to Topoisomerase Poisonstous in nature and are required for the regulation of DNA structure (topology) in the cell. Specifically, DNA topoisomerases regulate the coiling of the DNA double helix, a parameter critical for processes such as replication and transcription. Topoisomerases alter DNA coiling by transiently cleavin
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