Chemotherapy-induced peripheral neurotoxicity (CIPN): An update

Argyriou, Andreas A.; Bruna, Jordi; Marmiroli, P; Cavaletti, Guido

doi:10.1016/j.critrevonc.2011.04.012

Cited by 460 publications

(437 citation statements)

References 234 publications

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“…Oxaliplatin possesses a relative low hematological and gastrointestinal toxicity, but CIN can limit its clinical use [33,34]. Therefore, many efforts have been addressed to find adjuvant strategies to reduce CIN.…”

Section: Discussionmentioning

confidence: 99%

Effect of the SOD mimetic MnL4 on in vitro and in vivo oxaliplatin toxicity: Possible aid in chemotherapy induced neuropathy

Mannelli

Zanardelli

Landini³

et al. 2016

Free Radical Biology and Medicine

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Section: Discussionmentioning

confidence: 99%

Effect of the SOD mimetic MnL4 on in vitro and in vivo oxaliplatin toxicity: Possible aid in chemotherapy induced neuropathy

Mannelli

Zanardelli

Landini³

et al. 2016

Free Radical Biology and Medicine

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“…However, up to half of the patients with CIPN experience long-term neuropathic symptoms, including neuropathic pain, ataxia, and distal weakness. There are excellent reviews on CIPN and details of clinical presentations and potential mechanisms of actions of various chemotherapeutic drugs, but they will not be discussed here [76,77]. Instead, the focus in this article is on the animal models and the outcome measures used to evaluate them, and how faithfully these models mimic the human disease.…”

Section: Chemotherapy-induced Peripheral Neuropathymentioning

confidence: 99%

Animal Models of Peripheral Neuropathies

Höke

2012

Neurotherapeutics

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Peripheral neuropathies are common neurological diseases, and various animal models have been developed to study disease pathogenesis and test potential therapeutic drugs. Three commonly studied disease models with huge public health impact are diabetic peripheral neuropathy, chemotherapy-induced peripheral neuropathy, and human immunodeficiency virus-associated sensory neuropathies. A common theme in these animal models is the comprehensive use of pathological, electrophysiological, and behavioral outcome measures that mimic the human disease.

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“…OXA appears for the most part to impair the calciumdependent lymph node axonal SCNAs rather than potassium channels, thereby resulting in hyperexcited motor sensory nerves and muscles because of the reduction in the overall sodium current. 6,20 To our knowledge to date, there is no evidence that the other cytotoxic drugs contained in the FOLFOX or XELOX regimens (5-fluorouracil or capecitabine) may affect the ion channels. The pathogenic hallmark of cumulative OXAIPN is the decreased cellular metabolism and axoplasmic transport resulting from the accumulation of OXA in dorsal root ganglia (DRG) cells, together with mitochondrial dysfunction and oxidative stress, thus producing DRG neuron apoptosis.…”

Section: Discussionmentioning

confidence: 99%

“…4 Although clinical predictors for both acute and chronic OXAIPN have been suggested, to the best of our knowledge no reliable genetic or molecular biomarkers have been identified to date with which to detect those patients at high risk of developing OXAIPN. [5][6][7] The voltage-gated sodium channels (SCNAs) are fundamental to facilitate the initiation and propagation of action potentials in neurons and other electrically excitable cells. These membrane proteins are encoded by > 10 genes in mammals, whereas mutations in SCNAs are associated with diseases of both the central and peripheral nervous system (PNS).…”

Section: Introductionmentioning

confidence: 99%

Voltage‐gated sodium channel polymorphisms play a pivotal role in the development of oxaliplatin‐induced peripheral neurotoxicity: Results from a prospective multicenter study

Cavaletti

Antonacopoulou

Genazzani³

et al. 2013

Cancer

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BACKGROUND:The current prospective, multicenter study sought to identify single nucleotide polymorphisms of voltage-gated sodium channels (SCNAs) genes that might confer susceptibility to an increased incidence and severity of oxaliplatin-induced peripheral neuropathy (OXAIPN) in patients treated with either leucovorin, 5-fluorouracil, and oxaliplatin (FOLFOX) or oxaliplatin plus capecitabine (XELOX) for colorectal cancer (CRC). METHODS: A total of 200 patients with CRC were genotyped with real-time polymerase chain reaction using locked nucleic acid hydrolysis probes or allele-specific primers. All patients had received oxaliplatin-based chemotherapy, either in the adjuvant or metastatic setting. The incidence and severity of cumulative OXAIPN was graded using the clinical version of the Total Neuropathy Score and the neurosensory National Cancer Institute Common Toxicity Criteria (version 3.0). The incidence of acute OXAIPN was assessed using a descriptive questionnaire (yes=no response format) at each clinical evaluation. Acute OXAIPN was present in 169 of 200 patients (84.5%), whereas after treatment discontinuation, the cumulative=chronic form of neurotoxicity occurred in 145 of 200 patients (72.5%). RESULTS: In the logistic regression analysis adjusted for confounding factors, the overdominant model (CT vs CC 1 TT) of 2 single nucleotide polymorphisms (ie, SCN4A-rs2302237 and SCN10A-rs1263292) emerged as being significantly associated with an increased incidence of acute OXAIPN (rs2302237: odds ratio of 2.62 [95% confidence interval (95% CI), 1.15-6.00]; P 5.019; and rs12632942: OR of 0.39 [95% CI, 0.17-0.88]; P 5.023). However, only SCN4A-rs2302237 emerged as also being predictive of the clinical severity of acute OXAIPN (OR, 2.50 [95% CI, 1.35-4.63]; P 5.0029) and the occurrence of cumulative=chronic OXAIPN (OR, 2.47 [95% CI, 1.04-5.85]; P 5.037). CONCLUSIONS: The results of the current study provide evidence to support a causal relationship between SCNA polymorphisms and OXAIPN. However, further studies from independent groups are warranted to confirm these results. Cancer 2013;119:3570-7.

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Chemotherapy-induced peripheral neurotoxicity (CIPN): An update

Cited by 460 publications

References 234 publications

Effect of the SOD mimetic MnL4 on in vitro and in vivo oxaliplatin toxicity: Possible aid in chemotherapy induced neuropathy

Effect of the SOD mimetic MnL4 on in vitro and in vivo oxaliplatin toxicity: Possible aid in chemotherapy induced neuropathy

Animal Models of Peripheral Neuropathies

Voltage‐gated sodium channel polymorphisms play a pivotal role in the development of oxaliplatin‐induced peripheral neurotoxicity: Results from a prospective multicenter study

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