Cancer-treatment-induced neurotoxicity—focus on newer treatments

Stone, Jacqueline B.; DeAngelis, Lisa M.

doi:10.1038/nrclinonc.2015.152

Cited by 209 publications

(183 citation statements)

References 139 publications

(62 reference statements)

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“…Vincristine‐induced cranial neuropathies have also been reported. The neuropathy is usually severe but reversible within months after therapy discontinuation, even if it can present or worsen after therapy withdrawal (coasting effect) . A progressive increase in the risk of developing vincristine peripheral neuropathy seems to be associated with older age and higher cumulative dose .…”

Section: Chemotherapy‐induced Neurotoxicitymentioning

confidence: 99%

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Peripheral nervous system involvement in lymphomas

Briani

Visentin

Campagnolo

et al. 2019

J Peripheral Nervous Sys

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The peripheral nervous system may be involved at any stage in the course of lymphoproliferative diseases. The different underlying mechanisms include neurotoxicity secondary to chemotherapy, direct nerve infiltration (neurolymphomatosis), infections, immune‐mediated, paraneoplastic or metabolic processes and nutritional deficiencies. Accordingly, the clinical features are heterogeneous and depend on the localization of the damage (ganglia, roots, plexi, and peripheral nerves) and on the involved structures (myelin, axon, and cell body). Some clinical findings, such a focal or diffuse involvement, symmetric or asymmetric pattern, presence of pain may point to the correct diagnosis. Besides a thorough medical history and neurological examination, neurophysiological studies, cerebrospinal fluid analysis, nerve biopsy (in selected patients with suspected lymphomatous infiltration) and neuroimaging techniques (magnetic resonance neurography and nerve ultrasound) may be crucial for a proper diagnostic workup.

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Section: Chemotherapy‐induced Neurotoxicitymentioning

confidence: 99%

“…Methotrexate can be part of the treatment regimen of high‐grade lymphomas and has been rarely associated with peripheral neuropathy. However, sporadic cases of lumbosacral plexopathy have been reported …”

Section: Chemotherapy‐induced Neurotoxicitymentioning

confidence: 99%

Peripheral nervous system involvement in lymphomas

Briani

Visentin

Campagnolo

et al. 2019

J Peripheral Nervous Sys

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“…Symptoms can include allodynia, pain, increased sensitivity to cold, loss of proprioception, loss of touch, and reduced tendon reflexes. Unlike for other major side effects of chemotherapy (e.g., nausea, hair loss, or bone marrow failure) (Zafar et al, 2010), there are currently no U.S. Food and Drug Administration-approved interventions or prevention strategies for CIPN (Hershman et al, 2014;Stone and DeAngelis, 2016). s This article has supplemental material available at jpet.aspetjournals.org.…”

Section: Introductionmentioning

confidence: 99%

Identification and Characterization of New Chemical Entities Targeting Apurinic/Apyrimidinic Endonuclease 1 for the Prevention of Chemotherapy-Induced Peripheral Neuropathy

Kelley

Wikel

Guo

et al. 2016

J Pharmacol Exp Ther

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Chemotherapy-induced peripheral neuropathy (CIPN) is a potentially debilitating side effect of a number of chemotherapeutic agents. There are currently no U.S. Food and Drug Administration-approved interventions or prevention strategies for CIPN. Although the cellular mechanisms mediating CIPN remain to be determined, several lines of evidence support the notion that DNA damage caused by anticancer therapies could contribute to the neuropathy. DNA damage in sensory neurons after chemotherapy correlates with symptoms of CIPN. Augmenting apurinic/apyrimidinic endonuclease (APE)-1 function in the base excision repair pathway reverses this damage and the neurotoxicity caused by anticancer therapies. This neuronal protection is accomplished by either overexpressing APE1 or by using a first-generation targeted APE1 small molecule, E3330 [(2E)-2-[(4,5-dimethoxy-2-methyl-3,6-dioxo-1,4-cyclohexadien-1-yl)methylene]-undecanoic acid; also called APX3330]. Although E3330 has been approved for phase 1 clinical trials (Investigational New Drug application number IND125360), we synthesized novel, second-generation APE1-targeted molecules and determined whether they would be protective against neurotoxicity induced by cisplatin or oxaliplatin while not diminishing the platins' antitumor effect. We measured various endpoints of neurotoxicity using our ex vivo model of sensory neurons in culture, and we determined that APX2009is an effective small molecule that is neuroprotective against cisplatin and oxaliplatin-induced toxicity. APX2009 also demonstrated a strong tumor cell killing effect in tumor cells and the enhanced tumor cell killing was further substantiated in a more robust three-dimensional pancreatic tumor model. Together, these data suggest that the secondgeneration compound APX2009 is effective in preventing or reversing platinum-induced CIPN while not affecting the anticancer activity of platins.

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“…Currently, surgery, radiotherapy, and chemotherapy are still the main modalities in the treatment of cancer [2–4]. Chemotherapy, as one of the basic treatment strategies, is applied in most cancer therapies.…”

Section: Introductionmentioning

confidence: 99%

The emerging roles and therapeutic potential of cyclin-dependent kinase 11 (CDK11) in human cancer

et al. 2016

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Overexpression and/or hyperactivation of cyclin-dependent kinases (CDKs) are common features of most cancer types. CDKs have been shown to play important roles in tumor cell proliferation and growth by controlling cell cycle, transcription, and RNA splicing. CDK4/6 inhibitor palbociclib has been recently approved by the FDA for the treatment of breast cancer. CDK11 is a serine/threonine protein kinase in the CDK family and recent studies have shown that CDK11 also plays critical roles in cancer cell growth and proliferation. A variety of genetic and epigenetic events may cause universal overexpression of CDK11 in human cancers. Inhibition of CDK11 has been shown to lead to cancer cell death and apoptosis. Significant evidence has suggested that CDK11 may be a novel and promising therapeutic target for the treatment of cancers. This review will focus on the emerging roles of CDK11 in human cancers, and provide a proof-of-principle for continued efforts toward targeting CDK11 for effective cancer treatment.

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Cancer-treatment-induced neurotoxicity—focus on newer treatments

Cited by 209 publications

References 139 publications

Peripheral nervous system involvement in lymphomas

Peripheral nervous system involvement in lymphomas

Identification and Characterization of New Chemical Entities Targeting Apurinic/Apyrimidinic Endonuclease 1 for the Prevention of Chemotherapy-Induced Peripheral Neuropathy

The emerging roles and therapeutic potential of cyclin-dependent kinase 11 (CDK11) in human cancer

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