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Titlebook: Organ Directed Toxicities of Anticancer Drugs; Proceedings of the F Miles P. Hacker,John S. Lazo,Thomas R. Tritton Conference proceedings 1

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發(fā)表于 2025-3-21 16:10:40 | 只看該作者 |倒序瀏覽 |閱讀模式
書目名稱Organ Directed Toxicities of Anticancer Drugs
副標(biāo)題Proceedings of the F
編輯Miles P. Hacker,John S. Lazo,Thomas R. Tritton
視頻videohttp://file.papertrans.cn/704/703740/703740.mp4
叢書名稱Developments in Oncology
圖書封面Titlebook: Organ Directed Toxicities of Anticancer Drugs; Proceedings of the F Miles P. Hacker,John S. Lazo,Thomas R. Tritton Conference proceedings 1
描述The addition of chemotherapy as an effective means to treat cancer has had a major impact on selected human malignancies. Due to a general inability to dif- ferentiate between normal and neoplastic cells, little selectivity exists in currently used oncolytic drugs. Consequently, significant toxicity to the patient is expected when systemic cancer chemotherapy is chosen as an appropriate therapeutic in- tervention. Much of this toxicity, such as damage to the bone marrow, gastroin- testinal tract, or hair follicles, is predictable based upon the fact that anticancer drugs kill actively dividing cells. These types of toxicities, while serious, are usually manageable and reversible and are, therefore, not often considered to be dose limiting. Unfortunately, several of the most important anticancer drugs also damage tissues in which the growth fraction is relatively small. Such toxicities can not be predicted based on the chemical structure of the drugs, are often not detected in preclinical studies, and are encountered frequently for the first time in clinical studies. Further, unlike most of the proliferative-dependent toxicities, the unpre- dicted toxicities are usually irreversible
出版日期Conference proceedings 1988
關(guān)鍵詞cancer; cell; chemotherapy; clinical trial; drug; kidney; research; toxicity
版次1
doihttps://doi.org/10.1007/978-1-4613-2023-4
isbn_softcover978-1-4612-9205-0
isbn_ebook978-1-4613-2023-4
copyrightMartinus Nijhoff Publishing, Boston 1988
The information of publication is updating

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Role of Iron in Anthracycline Actiononly relatively recently that attention has focused on the role of iron chemistry in this process. Interest in this problem is bound to increase as a result of recent clinical and preclinical studies which demonstrate that ICRF-187, an EDTA derivative, effectively prevents doxorubicin-induced cardia
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Role of Reactive Oxygen Production in Doxorubicin Cardiac Toxicity lymphomas, and carcinomas of the breast, lung, and thyroid (1). The clinical usefulness of these drugs may, however, be compromised by the development of a dose related, congestive cardiomyopathy that is sometimes fatal (2). Over the past decade, a substantial body of experimental data has been pub
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Adriamycin Cardiac Toxicity — An Assessment of Approaches to Cardiac Monitoring and Cardioprotectionrolonged use could lead to progressive, refractory, irreversible and almost uniformly fatal congestive heart failure has been a major impediment to its more widespread use in the curative treatment of early cancer and to prolonging its use in responding patients with advanced disease.
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A Trial of ICRF-187 to Selectively Protect Against Chronic Adriamycin Cardiac Toxicity: Rationale ane drugs, particularly doxorubicin (Adriamycin.), constitute some of the most active compounds available to the clinical oncologist. They have activity in both hematologic malignancies and solid tumors. Numerous efforts to improve upon their activity through analogue development or a better dose sche
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Bleomycin Induced Lung Injuryoxicity varies widely, from 2 to 40% (1). Risk factors in developing toxicity include age, cumulative dose, use with other cytotoxic drugs, radiation therapy and oxygen (1). The most frequent manifestation of bleomycin induced pulmonary injury is the development of a diffuse alveolar damage frequent
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