Mechanism of taxane neurotoxicity

  title={Mechanism of taxane neurotoxicity},
  author={Hiroki Hagiwara and Yoshihide Sunada},
  journal={Breast Cancer},
The two taxanes (paclitaxel and docetaxel) are widely employed in standard antineoplastic practice. Although these agents are now well established, some toxic side effects have been reported. Toxicity of these agents includes bone marrow suppression (principally neutropenia), hypersensitivity reactions, cutaneus reactions, edema and neurotoxicity. The most prominent neurotoxicity is a sensory neuropathy. Controlling neuropathy is crucial for maintaining the quality of life of patients because… 
Comparison of neuropathy-inducing effects of eribulin mesylate, paclitaxel, and ixabepilone in mice.
Overall, the findings indicate that eribulin mesylate induces less neuropathy in mice than paclitaxel or ixabepilone at equivalent MTD-based doses.
Mechanisms of Chemotherapy-Induced Neurotoxicity
The main effects of chemotherapy on the peripheral and central nervous systems, including neuropathic pain, chemobrain, enteric neuropathy, as well as nausea and emesis are discussed.
Proposed medications for taxane-induced myalgia and arthralgia (Review).
The aim of this review was to examine the topical choices available for the protective management of taxane-induced neurotoxicity monitored in preliminary case studies and clinical trials.
Melatonin, a Promising Role in Taxane-Related Neuropathy
Patients receiving melatonin during taxane chemotherapy had a reduced incidence of neuropathy, andMelatonin may be useful in the prevention or reduction of taxane-induced neuropathy and in maintaining quality of life.
Overview of neuropathy associated with taxanes for the treatment of metastatic breast cancer
The toxicity profile (i.e., neuropathy) of each of the taxanes used in the treatment of MBC will be focused on, updates on tools used for the assessment of neuropathy will be provided, and newly discovered predictors of taxane-related neuropathy are highlighted.
Lithium attenuates peripheral neuropathy induced by paclitaxel in rats.
Lithium at these doses, as an inexpensive and relatively safe salt, may be useful clinically in preventing the neuropathy induced by paclitaxel treatment, and suggests that lithium, at subtherapeutic doses, can prevent both motor and sensory components of pac litaxel neuropathy in rats.
Docetaxel‐induced peripheral neuropathy: protective effects of dihydroprogesterone and progesterone in an experimental model
It is demonstrated that treatment with dihydroprogesterone (DHP) or progesterone (P) counteracts docetaxel‐induced neuropathy, preventing nerve conduction and thermal threshold changes, and degeneration of skin nerves in the foodpad.
Neuropathy-Inducing Effects of Eribulin Mesylate Versus Paclitaxel in Mice with Preexisting Neuropathy
Preclinical data suggest that eribulin mesylate may have reduced tendency to exacerbate preexisting paclitaxel-induced PN in clinical settings.
2 Predictors of Chemotherapy-Induced Peripheral Neuropathy
The predictors for CIPN are discussed, including bortezomib, taxanes, oxaliplatin or vincristine, and other studies are reviewed.


Managing taxane toxicities
If patients are monitored closely (e.g., for hypersensitivity reactions, bone marrow suppression) the taxanes have a favorable side effect profile, and it is currently uncommon for treatment to be discontinued because of the development of excessive toxicity.
Chemotherapy-induced peripheral neuropathy.
This review describes the pathogenesis, clinical presentation, neurophysiologic findings, nerve biopsies and the relation between cumulative dosage/dosage per cycle and neuropathy for the cytostatic drugs for which neurotoxicity is an important side-effect: cisplatin, vincristine, paclitaxel, docetaxel and suramin.
Paclitaxel-induced neuropathy.
Using 3-weekly 3-hour infusions of paclitaxel, dose-limiting neurotoxicity can be expected in patients treated with 250 mg/m2 or more each cycle, and follow-up data of 12 patients after discontinuation of pac litaxel therapy showed that pac Litaxel-induced neuropathy is at least partially reversible.
Peripheral neurotoxicity induced by docetaxel
It is concluded that docetaxel produces a mild and predominantly sensory neuropathy in a high proportion of treated patients and this neurotoxicity appeared to be dose dependent and may be severe and disabling at higher dose levels.
Chemotherapy-induced peripheral neuropathy
A general predisposition for developing a chemotherapy-induced neuropathy has been observed in nerves previously damaged by diabetes mellitus, alcohol or inherited neuropathy and no drug is available to reliably prevent or cure chemotherapy- induced neuropathy.
Peripheral neuropathy secondary to docetaxel (Taxotere)
Docetaxel produced a sensorimotor peripheral neuropathy in 11% of the patient population, delineating clinically and electrophysiologically the characteristics of a peripheral Neuropathy due to docetaxe.
Neurotoxicity of Taxol.
The neuromuscular effects of Taxol, including symptoms, physical and electrophysiological manifestations, and predisposing factors, as well as agents that may be used for neuroprotection, are discussed in this report.
Patients treated with antitumor drugs displaying neurological deficits are characterized by a low circulating level of nerve growth factor.
  • S. De Santis, A. Pace, L. Aloe
  • Medicine, Biology
    Clinical cancer research : an official journal of the American Association for Cancer Research
  • 2000
The results clearly suggest that NGF might become a useful agent to prevent neuropathies induced by antineoplastic drugs and restore peripheral nerve dysfunction induced by these pharmacological compounds.
Reduction of paclitaxel-induced peripheral neuropathy with glutamine.
Glutamine may reduce the severity of peripheral neuropathy associated with high-dose paclitaxel; however, results from randomized, placebo-controlled clinical trials will be needed to fully assess its impact, if any.
Nerve growth factor prevents toxic neuropathy in mice
Administration of nerve growth factor to mice resulted in a profound sensory neuropathy characterized by decreases in dorsal root ganglion content of the peptide neurotransmitter, substance P, elevated threshold to thermally induced pain, and diminished amplitude of the compound action potential in the caudal nerve.