Organ Directed Toxicities of Anticancer Drugs

1. Front Matter

   Pages i-xii

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2. Keynote Address

   1. Front Matter

      Pages 1-1

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   2. The Irrelevant Toxicities of Anticancer Drugs

      • I. H. Krakoff

      Pages 3-10

3. Anthracycline Induced Cardiotoxicity

   1. Front Matter

      Pages 11-11

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   2. Overview

      • T. R. Tritton

      Pages 13-16

   3. Role of Iron in Anthracycline Action

      • C. E. Myers

      Pages 17-30

   4. Role of Reactive Oxygen Production in Doxorubicin Cardiac Toxicity

      • J. H. Doroshow

      Pages 31-40

   5. Adriamycin Cardiac Toxicity — An Assessment of Approaches to Cardiac Monitoring and Cardioprotection

      • R. S. Benjamin, S. P. Chawla, M. S. Ewer, G. N. Hortobagyi, B. Mackay, S. S. Legha et al.

      Pages 41-55

   6. Pretreatment with ICRF-187 Protects Against the Chronic Cardiac Toxicity Produced by Very Large Cumulative Doses of Doxorubicin in Beagle Dogs

      • V. J. Ferrans, E. H. Herman, R. L. Hamlin

      Pages 56-63

   7. A Trial of ICRF-187 to Selectively Protect Against Chronic Adriamycin Cardiac Toxicity: Rationale and Preliminary Results of a Clinical Trial

      • J. L. Speyer, M. D. Green, C. Ward, J. Sanger, E. Kramer, M. Rey et al.

      Pages 64-73

4. Bleomycin Induced Pulmonary Toxicity

   1. Front Matter

      Pages 75-75

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   2. Overview

      • J. S. Lazo

      Pages 77-78

   3. Base Propenals and the Toxicity of Bleomycin

      • A. P. Grollman

      Pages 79-90

   4. Bleomycin Induced Lung Injury

      • A. F. Tryka

      Pages 91-106

   5. Immunoregulation of Growth Factor Release in Bleomycin Induced Lung Disease

      • J. Kelley, M. Absher, E. J. Kovacs

      Pages 107-117

   6. Pulmonary Toxicity of Anticancer Drugs: Alterations in Endothelial Cell Function

      • J. D. Catravas

      Pages 118-127

   7. Pulmonary Metabolic Inactivation of Bleomycin and Protection from Drug-Induced Lung Injury

      • J. S. Lazo, J. E. Mignano, S. M. Sebti

      Pages 128-139

   8. Biochemical and Molecular Bases of Bleomycin-Induced Pulmonary Fibrosis: Glucocorticoid Intervention

      • K. R. Cutroneo, D. Cockayne, K. M. Sterling Jr.

      Pages 140-151

5. Platinum Induced Nephrotoxicity

   1. Front Matter

      Pages 153-153

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   2. Overview

      • M. P. Hacker

      Pages 155-158

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 or only partially reversible upon cessation of drug administration. Because of this, the unpredicted toxicities are referred to as dose limiting. They represent a significant barrier to the ultimate efficacy of several of our most important anticancer drugs.

• cancer
• cell
• chemotherapy
• clinical trial
• drug
• kidney
• research
• toxicity

• Vermont Regional Cancer Center, Burlington, USA

  Miles P. Hacker, Thomas R. Tritton

• Yale University School of Medicine, New Haven, USA

  John S. Lazo

Policies and ethics