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

Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists

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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.
Phenothiazines, such as prochlorperazine...
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Chemotherapy-Induced Nausea and Vomiting: 5-HT3 Receptor Antagonists01:27

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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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Tetrahydrocannabinol (THC) is a phytocannabinoid that primarily interacts with the CB1 receptor, a type of G protein-coupled receptor (GPCR) predominantly in and around the chemoreceptor trigger zone (CTZ) and emetic center. THC also blocks the serotonin receptor activity in the dorsal vagal complex (DVC) by inhibiting serotonin release. THC exerts its anti-emetic effects through these interactions, which are beneficial for patients undergoing chemotherapy.
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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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Cancer therapies are various modes of treatment, such as surgery, radiation therapy, and chemotherapy that are administered to cancer patients.
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Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity
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Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity

Published on: April 26, 2012

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Chemotherapy-induced peripheral neurotoxicity.

Guido Cavaletti1, Paola Marmiroli

  • 1Experimental Neurology Unit, Department of Surgery and Translational Medicine, University of Milano-Bicocca, Monza, Italy.

Current Opinion in Neurology
|July 22, 2015
PubMed
Summary

Chemotherapy-induced peripheral neurotoxicity (CIPN) is a common side effect impacting cancer survivors. Understanding and standardizing assessment of CIPN is crucial for better management and developing new treatments.

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Area of Science:

  • Oncology
  • Neuroscience
  • Pharmacology

Background:

  • Chemotherapy-induced peripheral neurotoxicity (CIPN) is a frequent and dose-limiting side effect of cancer treatment.
  • CIPN significantly impacts cancer survivors' quality of life, with no effective treatments currently available.
  • Understanding CIPN mechanisms is essential for improving patient outcomes and treatment strategies.

Purpose of the Study:

  • To review the clinical relevance and management challenges of chemotherapy-induced peripheral neurotoxicity.
  • To highlight the need for standardized assessment tools and further research into CIPN.
  • To emphasize the importance of monitoring neurotoxicity from both conventional and newer targeted therapies.

Main Methods:

  • Review of current literature on chemotherapy-induced peripheral neurotoxicity.
  • Analysis of clinical features and impact of CIPN on cancer patients.
  • Discussion of assessment methodologies and research priorities.

Main Results:

  • Conventional chemotherapy agents commonly cause sensory neurotoxicity.
  • Newer chemotherapeutic compounds and targeted drugs can also induce peripheral neurotoxicity, including motor impairment.
  • CIPN presents challenges due to varying patient and provider perceptions of severity.

Conclusions:

  • Standardizing CIPN assessment using validated measures is a key research objective.
  • Continued vigilance regarding the neurotoxicity of recently introduced drugs is necessary.
  • Preclinical studies are vital for identifying therapeutic targets to prevent or mitigate CIPN.