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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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书目名称Drug Resistance
编辑William N. Hait
视频video
丛书名称Cancer Treatment and Research
图书封面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
关键词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

书目名称Drug Resistance影响因子(影响力)




书目名称Drug Resistance影响因子(影响力)学科排名




书目名称Drug Resistance网络公开度




书目名称Drug Resistance网络公开度学科排名




书目名称Drug Resistance被引频次




书目名称Drug Resistance被引频次学科排名




书目名称Drug Resistance年度引用




书目名称Drug Resistance年度引用学科排名




书目名称Drug Resistance读者反馈




书目名称Drug Resistance读者反馈学科排名




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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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