Strategies to mitigate the toxicity of cancer therapeutics /

Detalles Bibliográficos
Clasificación:Libro Electrónico
Otros Autores: Gewirtz, David A., Fisher, Paul B.
Formato: eBook
Idioma:Inglés
Publicado: Cambridge, MA : Academic Press, 2022.
Colección:Advances in cancer research ; v. 155.
Temas:
Cancer > Treatment > Complications.
Iatrogenic diseases > Prevention.
Drug-Related Side Effects and Adverse Reactions > therapy
Antineoplastic Agents > adverse effects
Radiotherapy > adverse effects
Neoplasms > therapy
Cancer > Traitement > Complications et s�equelles.
Radioth�erapie > Complications et s�equelles.
Cancer > Treatment > Complications
Acceso en línea:Texto completo
Tabla de Contenidos:
  • Intro
  • Strategies to Mitigate the Toxicity of Cancer Therapeutics
  • Copyright
  • Contents
  • Contributors
  • Preface
  • Chapter One: An overview of chemotoxicity and radiation toxicity in cancer therapy
  • 1. Introduction
  • 2. Cardiotoxicity
  • 3. Pulmonary toxicity
  • 4. Renal toxicity
  • 5. Gastrointestinal toxicity
  • 5.1. Chemotherapy-induced nausea and vomiting (CINV)
  • 5.2. Severe delayed onset diarrhea
  • 5.3. Mucositis
  • 6. Neuromuscular toxicity
  • 6.1. Chemotherapy-induced peripheral neuropathy (CIPN)
  • 7. Cognitive dysfunction associated with chemotherapy: ``Chemobrain or chemo fog��
  • 8. Myalgias and arthralgias
  • 9. Cutaneous toxicity
  • 10. Secondary malignancies
  • 11. Side effects of immune checkpoint inhibitors
  • 12. Radiation therapy
  • 12.1. CNS
  • 12.2. Head and neck
  • 12.3. Breast
  • 12.4. Lung
  • 12.5. Upper abdomen
  • 12.6. Lower abdomen and pelvis
  • 13. Mitigating/circumventing chemotoxicity
  • 14. Conclusion
  • References
  • Chapter Two: Chemobrain: A review on mechanistic insight, targets and treatments
  • 1. Introduction
  • 2. Impact of chemobrain in patients
  • 3. Symptoms and epidemiology
  • 4. Mechanisms contributing to chemobrain
  • 4.1. Oxidative stress
  • 4.1.1. Occurrence of ROS and its activity
  • 4.1.2. Antioxidants and their protective role
  • 4.2. Absence of spinal and dendritic arborization
  • 4.3. Inflammatory cytokines
  • 4.4. Neurotransmitters
  • 4.5. Apoptosis and autophagy
  • 4.6. MAPK signalling pathway
  • 4.7. Genetic factors and epigenetic modulations
  • 5. Targets and treatment options
  • 5.1. Targeting oxidative stress
  • 5.2. Targeting neurogenesis
  • 5.3. Targeting neuroinflammation
  • 5.4. Targeting arborization
  • 5.5. Targeting genetic factors
  • 6. Current status and personalized therapy
  • 7. Future perspectives
  • 8. Conclusion
  • Reference
  • Further reading.
  • Chapter Three: Nephrotoxicity in cancer treatment: An update
  • 1. Introduction
  • 2. Risk factors for renal toxicities in cancer therapy
  • 2.1. General risk factors for nephrotoxicity of anticancer drugs and treatment
  • 2.2. Patient-specific factors
  • 2.3. Kidney-specific factors
  • 2.3.1. Genetic polymorphisms, sex and other kidney-related factors in renal enzymes
  • 2.4. Drug-specific factors
  • 3. Nephrotoxicity of chemotherapeutic agents and management
  • 3.1. Platinum agents
  • 3.1.1. Prospective use of diabetes drugs
  • 3.1.2. Prospective use of antihypertensive agents
  • 3.1.3. Prospective use of other clinically available drugs
  • 3.1.4. Prospective targets and other compounds
  • 3.2. Alkylating agents
  • 3.3. Antitumor antibiotics
  • 3.4. Antimetabolites cancer drugs
  • 3.5. Epidermal growth factor receptor pathway inhibitors (EGFR inhibitors)
  • 3.6. Vascular endothelial growth factor pathway inhibitors (VEGF inhibitors)
  • 3.7. Immune checkpoint inhibitors
  • 3.8. Proteasome inhibitors
  • 3.9. mTOR protein kinase inhibitors
  • 3.10. Biologic agents
  • 3.11. BRAF inhibitors
  • 3.12. Anaplastic lymphoma kinase inhibitor
  • 4. Renoprotective effects of some novel anticancer therapeutics
  • 4.1. The immune system
  • 4.2. Sphingolipid signaling
  • 4.3. DNA repair pathway
  • 4.3.1. Poly(ADP-ribose) polymerase (PARP), PARP-1
  • 4.4. Histone modifications
  • 4.4.1. Histone acetyltransferases (HATs)
  • 4.4.2. Histone deacetylases (HDACs)
  • 4.4.3. Sirtuins (SIRT)
  • 4.5. Non-coding RNAs
  • 5. Conclusions
  • References
  • Chapter Four: Chemotherapy induced gastrointestinal toxicities
  • 1. Introduction
  • 2. Chemotherapy-induced diarrhea
  • 3. Chemotherapy-induced mucositis (CIM)
  • 3.1. Intestinal epithelium
  • 3.2. Pathobiological mechanisms of CIM
  • 3.3. Chemotherapeutics implicated in CIM and CID
  • 3.4. CIM and the microbiome.
  • 4. Emerging mechanisms underlying chemotherapy-induced gastrointestinal toxicity
  • 5. Treatment of CID
  • 5.1. Current and emerging pre-clinical strategies for treating CIM
  • 6. The gut and chemotherapy-induced peripheral neuropathy
  • 7. Conclusion
  • References
  • Chapter Five: Cardiac complications of cancer therapies
  • 1. Introduction
  • 2. Cancer therapeutic agents
  • 2.1. Anthracyclines
  • 2.1.1. Mechanisms of anthracycline cardiotoxicity
  • 2.1.1.1. ROS and oxidative damage
  • 2.1.1.2. Topoisomerase II
  • 2.1.1.3. Apoptosis
  • 2.1.1.4. Ferroptosis
  • 2.1.1.5. Pyroptosis
  • 2.2. Tyrosine kinase inhibitors
  • 2.2.1. Mechanisms of tyrosine kinase inhibitor cardiotoxicity
  • 2.2.1.1. QT prolongation
  • 2.2.1.2. Left ventricular dysfunction
  • 2.2.1.3. Hypertension
  • 2.3. Fluorouracil and other anti-metabolites
  • 2.3.1. Fluorouracil and anti-metabolites induced cardiac toxicity
  • 2.4. Immune therapies
  • 2.4.1. IC-associated cardiotoxicities
  • 2.5. Radiation therapy
  • 2.5.1. Cardiotoxicity due to radiation therapy
  • 2.6. Alkylating agents
  • 2.6.1. Cardiotoxicity of alkylating agents
  • 2.7. Platinum-based agents
  • 2.7.1. Cardiotoxicity of platinum-based agents
  • 2.8. Proteasome inhibitors
  • 2.8.1. Cardiotoxicity from proteasome inhibitors
  • 3. Current and promising therapies to prevent chemotherapy-induced cardiotoxicity
  • 3.1. Dexrazoxane
  • 3.2. Neurohormonal blockade
  • 3.3. Statins
  • 3.4. Exercise therapy
  • 3.5. Remote ischemic preconditioning intervention
  • 4. Conclusions
  • Acknowledgments
  • References
  • Chapter Six: Strategies to mitigate the toxicity of cancer therapeutics
  • 1. Overview of organ specific toxicities
  • 2. Cancer related cognitive impairment
  • 3. Ocular toxicities
  • 4. Ototoxicity
  • 5. Oral mucosal toxicities
  • 6. Gastrointestinal toxicities
  • 7. Renal toxicity.
  • 8. Aromatase inhibitor-associated musculoskeletal syndrome
  • 9. Chemotherapy induced peripheral neuropathy (CIPN)
  • 10. Immunotherapy-induced autoimmunity
  • 11. Putting it all together. What is the future of symptom science?
  • References.

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