Chemotherapy‐induced peripheral neuropathy: A current review

Staff, Nathan P.; Grisold, Anna; Grisold, Wolfgang; Windebank, Anthony J.

doi:10.1002/ana.24951

Cited by 585 publications

(494 citation statements)

References 117 publications

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“…However, it is similar to reported levels in adult patients with other CDP-treated cancers, who are more prone to this side effect (24,25). Approximately one-third of patients experienced 1 or more episodes of nephrotoxicity, mostly G1, but in 1 case dialysis was required.…”

Section: Discussionsupporting

confidence: 84%

EURO-B.O.S.S.: A European study on chemotherapy in bone-sarcoma patients aged over 40: Outcome in primary high-grade osteosarcoma

Ferrari

Bielack

Smeland

et al. 2018

Tumori

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Introduction: The EUROpean Bone Over 40 Sarcoma Study (EURO-B.O.S.S.) was the first prospective internationalstudy for patients 41-65 years old with high-grade bone sarcoma treated with an intensive chemotherapy regimen derived from protocols for younger patients with high-grade skeletal osteosarcoma. Methods: Chemotherapy based on doxorubicin, cisplatin, ifosfamide, and methotrexate was suggested, but patients treated with other regimens at the investigators' choice were also eligible for the study. Results: The present report focuses on the subgroup of 218 patients with primary high-grade osteosarcoma. With a median follow-up of 47 months, the 5-year probability of overall survival (OS) was 66% in patients with localized disease and 22% in case of synchronous metastases. The 5-year OS in patients with localized disease was 29% in pelvic tumors, and 70% and 73% for extremity or craniofacial locations, respectively. In primary chemotherapy, tumor necrosis ≥90% was reported in 21% of the patients. There were no toxic deaths; however, hematological toxicity was considerable with 32% of patients experiencing 1 or more episodes of neutropenic fever. The incidence of nephrotoxicity and neurotoxicity (mainly peripheral) was 28% and 24%, respectively. After methotrexate, 23% of patients experienced delayed excretion, in 4 cases with nephrotoxicity.

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Section: Discussionsupporting

confidence: 84%

EURO-B.O.S.S.: A European study on chemotherapy in bone-sarcoma patients aged over 40: Outcome in primary high-grade osteosarcoma

Ferrari

Bielack

Smeland

et al. 2018

Tumori

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“…ATAXIN-3 aggregates cause degeneration of cells in the hindbrain [85]. iNSCs provide a valuable in vitro model of chemotherapy-induced peripheral neuropathy (CIPN), a complication often seen in cancer patients, in which treatment causes axon dieback and nerve degeneration [87]. More recently, Thier et al established an iNSC-based in vitro model for human congenital insensitivity to pain (CIP).…”

Section: Functional Characterization Of Insc-derived Neuronsmentioning

confidence: 99%

Take the shortcut – direct conversion of somatic cells into induced neural stem cells and their biomedical applications

et al. 2019

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Second-generation reprogramming of somatic cells directly into the cell type of interest avoids induction of pluripotency and subsequent cumbersome differentiation procedures. Several recent studies have reported direct conversion of human somatic cells into stably proliferating induced neural stem cells (iNSCs). Importantly, iNSCs are easier, faster, and more cost-efficient to generate than induced pluripotent stem cells (iPSCs), and also have a higher level of clinical safety. Stably, self-renewing iNSCs can be derived from different cellular sources, such as skin fibroblasts and peripheral blood mononuclear cells, and readily differentiate into neuronal and glial lineages that are indistinguishable from their iPSC-derived counterparts or from NSCs isolated from primary tissues. This review focuses on the derivation and characterization of iNSCs and their biomedical applications. We first outline different approaches to generate iNSCs and then discuss the underlying molecular mechanisms. Finally, we summarize the preclinical validation of iNSCs to highlight that these cells are promising targets for disease modeling, autologous cell therapy, and precision medicine. Take the shortcut: from iPSC to iNSCForced expression of lineage-specific transcription factors (TFs) has been shown to reprogram the developmental potential of various somatic cell types e.g. by inducing pluripotency [1]. The seminal breakthrough of fibroblast reprogramming into iPSCs offers a novel experimental tool to generate patient-specific cells for developmental studies and diverse biomedical applications, such as disease modeling and cell therapy. Since then, efficiency and robustness of reprogramming protocols have been substantially improved, but the derivation of patient-specific iPSCs remains a lengthy and cumbersome procedure. Moreover, clinical applications require subsequent redifferentiation of iPSCs into the cell type of interest, which is inefficient and risky because transplanted undifferentiated iPSCs are tumorigenic. In the shadow of iPSC-type reprogramming, second-generation reprogramming paradigms have been developed to bypass the pluripotency state Abbreviations

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“…However, worsening of neuropathic symptoms after cessation of therapy called “coasting phenomenon” must be considered (e.g., paclitaxel). Coasting phenomenon is explained by drugs persisting in nerve axons after finishing therapy that lead to ongoing toxicity [8]. It should be acknowledged that there is considerable variability of symptoms depending on the agent used and the individual risk factors of the patient.…”

Section: Assessment and Diagnosis Of Cipnmentioning

confidence: 99%

Prevention and Management of Chemotherapy-Induced Polyneuropathy

et al. 2019

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Chemotherapy-induced peripheral neurotoxicity (CIPN) is a severe and common side effect caused by a variety of antineoplastic agents. Approximately 30–40% of patients treated with agents such as taxanes, vinca alkaloids, or platinum derivatives will develop CIPN. CIPN presents predominantly as a sensory axonal neuro(no)pathy with occasional motor and autonomic dysfunction exhibiting considerable variability of clinical symptoms ranging from mild tingling sensation to severe neuropathic pain. Typical symptoms include numbness (“minus symptom”), weakness, and abnormal gait as well as paresthesia and pain (“positive symptoms”). As CIPN symptoms potentially lead to long-term morbidity and can even aggravate after cessation of therapy, patients’ quality of life can be tremendously affected. In view of improved breast cancer survival outcomes, the late effects of CIPN are an unmet need in these patients. Therefore, early detection and assessment of first symptoms is important to effectively prevent severe CIPN. Therapeutic options for patients with CIPN are still limited, and pharmacological treatment focuses primarily on reduction or relief of neuropathic pain. CIPN is usually acutely managed by dose reduction or discontinuation of causative chemotherapy, potentially compromising treatment outcome. Currently, there is no causative proven therapy for the prevention of CIPN.

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Chemotherapy‐induced peripheral neuropathy: A current review

Cited by 585 publications

References 117 publications

EURO-B.O.S.S.: A European study on chemotherapy in bone-sarcoma patients aged over 40: Outcome in primary high-grade osteosarcoma

EURO-B.O.S.S.: A European study on chemotherapy in bone-sarcoma patients aged over 40: Outcome in primary high-grade osteosarcoma

Take the shortcut – direct conversion of somatic cells into induced neural stem cells and their biomedical applications

Prevention and Management of Chemotherapy-Induced Polyneuropathy

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