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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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Chemotherapy-Induced Nausea and Vomiting: Dopamine Receptor Antagonists01:29

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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

Chemotherapy-Induced Nausea and Vomiting: 5-HT3 Receptor Antagonists

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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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Chemotherapy-Induced Nausea and Vomiting: Cannabinoids01:21

Chemotherapy-Induced Nausea and Vomiting: Cannabinoids

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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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Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

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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 Therapies02:49

Cancer Therapies

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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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Updated: Apr 4, 2026

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity
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Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity

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[Chemotherapy-induced Peripheral Neuropathy].

I Bobylev1, T Elter2, C Schneider1

  • 1Klinik und Poliklinik für Neurologie, Universitätsklinikum Köln.

Fortschritte Der Neurologie-Psychiatrie
|September 2, 2015
PubMed
Summary
This summary is machine-generated.

Chemotherapy-induced peripheral neuropathy (CIPN) is a common side effect of cancer drugs. Research is uncovering its causes, like mitochondrial issues and immune responses, and exploring ways to prevent it.

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Chemotherapy-induced Vascular Toxicity - Real-time In vivo Imaging of Vessel Impairment
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Area of Science:

  • Neuroscience
  • Oncology
  • Pharmacology

Context:

  • Chemotherapy-induced peripheral neuropathy (CIPN) is a significant adverse effect of numerous antineoplastic agents.
  • CIPN impacts patient quality of life and can necessitate dose reductions or treatment cessation.
  • Understanding CIPN's mechanisms is crucial for developing supportive care strategies.

Purpose:

  • To review the current understanding of the pathogenetic mechanisms underlying CIPN.
  • To discuss experimental strategies for preventing or mitigating the neurotoxic effects of chemotherapy.
  • To provide an overview of recent advancements in CIPN research.

Summary:

  • CIPN results from complex interactions including mitochondrial toxicity, impaired axonal transport, Schwann cell damage, and immune system activation.
  • In vivo and in vitro models have been instrumental in elucidating these pathogenic pathways.
  • Current research focuses on identifying therapeutic targets to manage chemotherapy-related nerve damage.

Impact:

  • This review synthesizes current knowledge on CIPN pathogenesis, aiding researchers and clinicians.
  • It highlights potential avenues for developing novel neuroprotective therapies against chemotherapy side effects.
  • Improved understanding may lead to better patient management and treatment adherence in oncology.