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Eldridge, S. Chemotherapy-Induced Peripheral Neuropathy (CIPN). Encyclopedia. Available online: https://encyclopedia.pub/entry/18153 (accessed on 23 July 2024).
Eldridge S. Chemotherapy-Induced Peripheral Neuropathy (CIPN). Encyclopedia. Available at: https://encyclopedia.pub/entry/18153. Accessed July 23, 2024.
Eldridge, Sandy. "Chemotherapy-Induced Peripheral Neuropathy (CIPN)" Encyclopedia, https://encyclopedia.pub/entry/18153 (accessed July 23, 2024).
Eldridge, S. (2022, January 12). Chemotherapy-Induced Peripheral Neuropathy (CIPN). In Encyclopedia. https://encyclopedia.pub/entry/18153
Eldridge, Sandy. "Chemotherapy-Induced Peripheral Neuropathy (CIPN)." Encyclopedia. Web. 12 January, 2022.
Chemotherapy-Induced Peripheral Neuropathy (CIPN)
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This entry is adapted from the peer-reviewed paper 10.3390/toxics9110300

Chemotherapy-induced peripheral neuropathy (CIPN) is widely recognized as a potentially severe toxicity that often leads to dose reduction or discontinuation of cancer treatment. Symptoms may persist despite discontinuation of chemotherapy and quality of life can be severely compromised. The clinical symptoms of CIPN, and the cellular and molecular targets involved in CIPN, are just as diverse as the wide variety of anticancer agents that cause peripheral neurotoxicity.

chemotherapy-induced peripheral neuropathy (CIPN)

1. Introduction

Chemotherapy-induced peripheral neuropathy (CIPN) is an adverse consequence of a wide variety of commonly used anticancer agents [1][2][3][4][5][6][7][8][9] and there are no gold standard therapeutics recommended for the prevention or treatment of CIPN [10]. CIPN frequently leads to dose reduction or discontinuation of therapy [4][11][12]. Clinical symptoms can persist long after completion of chemotherapy and severely diminish the quality of life of patients [1][13]. The pathophysiology of CIPN is complex and compounded by the fact that the various neurotoxic events culminating in CIPN are not necessarily related to the anticancer mechanisms of action for the agents that cause CIPN [9][14]. However, several lines of evidence point toward interactions involving various target components of the peripheral nervous system (PNS), including dorsal root ganglion (DRG), myelin, microtubules, mitochondria, ion channels, blood vessels, and nerve terminals [5][9][15][16][17][18]. A common pathology in CIPN is a “dying back” axon degeneration of distal nerve endings [9][19]. 

2. Anticancer Agents That Cause CIPN

CIPN is a debilitating adverse effect with a prevalence ranging from 19% to over 85% [8] and caused by a spectrum of classes of widely used anticancer therapeutics including platinum-based agents, microtubule disruptors (taxanes and vinca alkaloids), proteasome, and angiogenesis inhibitors (Table 1) [1][2][3][4][5][7][8][9][20][21][22]. Clinically, CIPN symptoms may be acute, worsen with cumulative drug dosing, or emerge late during the course of treatment, even long after cessation of treatment [18]. Although many genetic and clinical risk factors have been identified, CIPN surveillance during and post-chemotherapy is needed as well as further study to better understand the pathophysiology of CIPN [8][18].
Table 1. Anticancer agents known to cause CIPN and their proposed mechanisms and target sites of CIPN toxicity [1][2][3][4][5][7][8][9][20][21][22].
Class Agents Proposed Mechanism Main Target of CIPN Toxicity
Taxanes Paclitaxel
Docetaxel
Ixabepilone		 Microtubule disruption Dorsal root ganglion; axons; distal nerve terminals
Platinum-based Cisplatin
Carboplatin
Oxaliplatin		 DNA adducts Dorsal root ganglion
Alkylating agents Cyclophosphamide
Hexamethylmelamine
Ifosphamide
Procarbazine		 Covalently bind to DNA Dorsal root ganglion
Vinca alkaloids Vincristine
Vinblastine
Vinorelbine
Vindesine		 Dysfunction of mitochondria and endoplasmic reticulum; microtubule disruption Dorsal root ganglion; distal nerve terminals
Proteasome inhibitors Bortezomib
Carfilzomib
Ixazomib		 Binds proteasome complex; mitochondrial disturbance; microtubule disruption Dorsal root ganglion and peripheral nerves
Immunomodulatory Thalidomide
Lenalidomide
Pomalidomide		 Antiangiogenesis Dorsal root ganglion; distal nerve terminals
Among commonly used classes of cancer therapies for many blood and solid tumors, platinum analogs (e.g., cisplatin and oxaliplatin), proteasome inhibitors (e.g., bortezomib), immunomodulatory/antiangiogenic (e.g., thalidomide), and taxanes (e.g., paclitaxel) have markedly different chemical structures and mechanisms of actions. However, they all share a common adverse side effect: CIPN [16]. Clinically, CIPN involves the PNS that predominately leads to sensory axonal peripheral neuropathy characterized by a “stocking and glove” distribution of a plethora of potentially debilitating sensory effects [5][17]. Although the proposed pathogenesis of CIPN involves the cell bodies of the DRG concomitant with dying back axonal damage, the exact pathophysiology remains elusive [19][22]. Evidence suggests that neurotoxic chemotherapy drugs may involve various cellular components in the PNS by (1) forming DNA adducts, DNA damage, and alterations in DNA repair; (2) stabilization/disruption of microtubules; (3) targeting mitochondria; (4) functionally impairing ion channels; (5) production of oxidative stress; (6) dysregulation of calcium signaling; (7) altering cell signaling events; and/or (8) triggering immunological mechanisms through activation of satellite glial cells [9][14][15][16][17][18]. Development of an in vitro human peripheral neuronal cell model in which these various cellular components can be investigated will provide an urgently needed tool to dissect the cellular and molecular effects of potentially neurotoxic compounds.
The DRG of the PNS is vulnerable to neurotoxic damage since it is less protected by the blood–nerve barrier than the CNS [23][24]. This may partially explain the predominance of sensory involvement in patients with CIPN [9]. Platinum compounds form DNA adducts that can accumulate in the DRG [25][26], potentially leading to sensory neuronal cell death [27][28]. Paclitaxel has been reported to accumulate in the DRG through transmembrane transport mediated specifically by organic anion transporting polypeptide 1B (OATP1B) [29].
Central to the transport of proteins from the nerve cell body, down the length of the axon are microtubules [3]. A commonly used class of anticancer agents, taxanes, are microtubule binding agents, which produce polymerization that interferes with normal microtubule dynamics linked to disruption of axonal transport [21][30][31]. Another class of chemotherapy agents that cause CIPN are vinca alkaloids (vincristine, vinblastine, vinorelbine, and vinderine) that also bind tubulin and inhibit microtubule dynamics, leading to interference with the mitotic spindle [32]. A proteasome inhibitor, bortezomib, also affects microtubule polymerization independent of its mechanism as an anticancer agent [9][33].
Damage to the mitochondria that impairs mitochondrial function may play a pivotal role in CIPN [9][34]. For example, paclitaxel has been reported to cause functional impairment in axonal mitochondria [35]. Additionally, bortezomib has also been shown to cause accumulation of ubiquitin-conjugated proteins, mitochondrial dysfunction in peripheral sensory neurons (PNS) including Schwann cells, and endoplasmic reticulum stress particularly in Schwann cells [9][36][37][38].
There is reported evidence for direct toxicity to the distal axon terminals associated with peripheral neuropathy following cancer treatment with paclitaxel [39], thalidomide [40], and vincristine [41]. Oxaliplatin may affect the function of voltage-gated sodium (Na+) ion channels, inducing an acute peripheral neuropathy manifested by hyperexcitability [42][43][44].
Thalidomide is also associated with peripheral neuropathy through different proposed mechanisms [45]. Thalidomide-induced peripheral neuropathy is proposed to be mediated by its antiangiogenic effects [46]. Notably, attempts to establish a thalidomide rodent model both in vivo and in vitro have not been successful [9][47][48].
Although the underlying mechanisms responsible for the development of CIPN remain elusive and are further complicated by the diversity of anticancer agents that cause CIPN, there may be common degenerative pathways triggered when normal cellular processes and energy delivery mechanisms of the PNS become disrupted [9]. It is important to appreciate that mechanisms of CIPN may be shared by different classes of chemotherapeutic agents independent of their anticancer properties [3][4][5][6][7][8][9][12]. Some pathways, such as those activated by the mitogen-activated protein kinase (MAPK) family members and by mechanistic target of rapamycin (mTOR), could represent a common core of CIPN pathophysiology, as they have been demonstrated to be closely related to hyperalgesia and more in general to pain, a hallmark of CIPN [49][50][51][52][53]. The activation of MAPKs, and in particular of p38, has been observed to have a pivotal role in CIPN induced by different chemotherapeutic agents, such as paclitaxel, oxaliplatin, cisplatin, and vincristine [50][51][52][53] through their relation with toll-like receptor (TLR4) and nuclear factor kappa B (NF-kB) signaling pathways, not only in DRG neurons, but also in glial cells [49][50].

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