12 research outputs found
Diffuse tensor imaging of lower extremities: a novel MR imaging technique for chemotherapy-induced peripheral neuropathy
Uniformity under in vitro conditions: Changes in the phenotype of cancer cell lines derived from different medulloblastoma subgroups
An asymptomatic mutation complicating severe chemotherapy-induced peripheral neuropathy (CIPN): a case for personalised medicine and a zebrafish model of CIPN
Low Levels of NDRG1 in Nerve Tissue Are Predictive of Severe Paclitaxel-Induced Neuropathy
Chemotherapy-induced peripheral neuropathy: evidence from genome-wide association studies and replication within multiple myeloma patients
Epigenetic pathway inhibitors represent potential drugs for treating pancreatic and bronchial neuroendocrine tumors
National Cancer Institute-supported chemotherapy-induced peripheral neuropathy trials: outcomes and lessons
Taxane and epothilone-induced peripheral neurotoxicity: From pathogenesis to treatment
Taxane-induced peripheral neurotoxicity (TIPN) is the most common nonhematological side effect of taxane-based chemotherapy, and may result in dose
reductions and discontinuations, having as such a detrimental effect on patients'
overall survival. Epothilones share similar mechanism of action with taxanes. The typical TIPN clinical presentation is mainly comprised of numbness and paresthesia, in a
stocking-and-glove distribution and may progress more proximally over time, with
paclitaxel being more neurotoxic than docetaxel. Motor and autonomic involvement
is less common, whereas an acute taxane-induced acute pain syndrome is frequent.
Patient reported outcomes questionnaires, clinical evaluation, and instrumental tools
offer complementary information in TIPN. Its electrodiagnostic features include reduced/abolished sensory action potentials, and less prominent motor involvement, in
keeping with a length-dependent, axonal dying back predominately sensory neuropathy. TIPN is dose-dependent and may be reversible within months after the end of
chemotherapy. The single and cumulative delivered dose of taxanes is considered the
main risk factor of TIPN development. Apart from the cumulative dose, other risk factors for TIPN include demographic, clinical, and pharmacogenetic features with several single-nucleotide polymorphisms potentially linked with increased susceptibility
of TIPN. There are currently no neuroprotective strategies to reduce the risk of TIPN,
and symptomatic treatments are very limited. This review critically examines the
pathogenesis, incidence, risk factors (both clinical and pharmacogenetic), clinical phenotype and management of TIP