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Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists01:28

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Neurokinin 1 (NK1) receptors are distributed across the GI tract, vagal afferents, and key CNS regions including the central vomiting center and chemoreceptor trigger zone (CTZ) Chemotherapy agents stimulate enterochromaffin cells in the gastrointestinal (GI) tract to release large amounts of substance P (SP). SP is a neuropeptide released by specific sensory nerves in response to many different stressors, including those in the GI mucosa affected by chemotherapy.  SP binds and activates...
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Dopamine receptor antagonists, also known as antipsychotic agents, are critical in managing chemotherapy-induced vomiting. These antiemetic agents block dopamine receptors in the chemoreceptor trigger zone (CTZ), inhibiting signal transmission to the vomiting center. Antipsychotic agents encompass phenothiazines (PTZ), butyrophenones, benzamides, and thienobenzodiazepines (Zyprexa), which are utilized for their antiemetic and sedative properties.
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5-HT3 receptor antagonists, such as dolasetron, granisetron (Kytril), ondansetron (Zofran), and palonosetron (Axoli), are crucial in managing chemotherapy-induced nausea and vomiting (CINV) and postoperative nausea. These drugs selectively block 5-HT3 receptors in the visceral vagal and spinal afferent nerves, chemoreceptor trigger zone, and the vomiting center. They have a rapid onset of action and can be given as a single dose before chemotherapy. Ondansetron and granisetron, in particular,...
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Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
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Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity
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Chemotherapy-induced peripheral neuropathy.

Jill C Fehrenbacher1

  • 1Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, Indiana, USA; Stark Neuroscience Research Institute, Indiana University School of Medicine, Indianapolis, Indiana, USA; Department of Anesthesiology, Indiana University School of Medicine, Indianapolis, Indiana, USA.

Progress in Molecular Biology and Translational Science
|March 7, 2015
PubMed
Summary
This summary is machine-generated.

Chemotherapy-induced peripheral neuropathy (CIPN) affects cancer survivors, causing sensory issues. Understanding the varied mechanisms of chemotherapy drugs is crucial for developing effective treatments for this common side effect.

Keywords:
BortezomibChemotherapyCisplatinMechanismsNeuropathyOxaliplatinPaclitaxelPainPeripheral sensory neuronVinca alkaloids

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Area of Science:

  • Neuroscience
  • Oncology
  • Pharmacology

Background:

  • Chemotherapy-induced peripheral neuropathy (CIPN) is a frequent and debilitating side effect of cancer treatment.
  • CIPN significantly impacts patient survivability and long-term quality of life.
  • Current therapeutic options for CIPN are limited due to an incomplete understanding of its underlying mechanisms.

Purpose of the Study:

  • To highlight the need for further research into the specific mechanisms driving CIPN.
  • To underscore the importance of understanding how different chemotherapy classes induce neuropathy.
  • To address the paucity of effective pharmacological agents for preventing or treating CIPN.

Main Methods:

  • Review of existing literature on CIPN mechanisms.
  • Analysis of clinical presentations of CIPN across different chemotherapy classes.
  • Evaluation of preclinical findings and their translation to clinical efficacy.

Main Results:

  • CIPN presents with abnormal sensory discrimination (touch, vibration, thermal, pain).
  • Despite similar clinical symptoms, different chemotherapeutic agents may induce neuropathy via distinct mechanisms.
  • Many agents developed from preclinical studies have failed to show efficacy in clinical trials for CIPN.

Conclusions:

  • A deeper understanding of chemotherapy-specific neuropathy mechanisms is essential.
  • Targeted therapeutic strategies require elucidation of how each chemotherapy class affects sensory neurons.
  • Further research is critical to identify and validate novel targets for CIPN prevention and treatment.