Biological predictors of chemotherapy-induced peripheral neuropathy (CIPN): MASCC neurological complications working group overview

Abstract

Chemotherapy-induced peripheral neuropathy (CIPN) is a common and debilitating condition associated with a number of chemotherapeutic agents. Drugs commonly implicated in the development of CIPN include platinum agents, taxanes, vinca alkaloids, bortezomib, and thalidomide analogues. As a drug response can vary between individuals, it is hypothesized that an individual's specific genetic variants could impact the regulation of genes involved in drug pharmacokinetics, ion channel functioning, neurotoxicity, and DNA repair, which in turn affect CIPN development and severity. Variations of other molecular markers may also affect the incidence and severity of CIPN. Hence, the objective of this review was to summarize the known biological (molecular and genomic) predictors of CIPN and discuss the means to facilitate progress in this field.

Keywords: CIPN; Chemotherapy-induced peripheral neuropathy; Neuropathy.

Figure 1:. Molecular Targets and Pathways of CIPN

Affected neurons: dorsal root ganglion (∗); sensory neurons (∇); motor neurons (⊕); central projections of primary afferent neurons (σ). Abbreviations: VDAC – voltage-dependent anion channels; Ca²⁺ - calcium ions; TRP – transient receptor potential.