A review of novel biomarkers and imaging techniques for assessing the severity of chemotherapy-induced peripheral neuropathy

ABSTRACT

Introduction

Chemotherapy-induced peripheral neuropathy (CIPN) is a potentially persistent late toxicity of most common anticancer regimens. There is still a huge lack in CIPN assessment in clinical trials; therefore, biomarkers, both neuroimagery and molecular, could fill this gap.

Areas covered

In this review the first applications of high-resolution ultrasound (HRUS), magnetic resonance imaging (MRI) are discussed; different molecular biomarkers first report in CIPN are also addressed, broadening the spectrum of potential molecular candidates beyond pharmacogenomics.

Expert opinion

At the present moment, neuroimaging and biomarkers are not yet part of the clinical practice for CIPN management, but they deserved to be tested since they could be a valuable surrogate endpoint in a clinical trial. To ascertain the appropriateness of (a) potential biomarker(s), it is crucial to design a clinical trial based on sound design and taking advantage of international, multidisciplinary initiatives, such as the Toxic Neuropathy Consortium.

KEYWORDS:

• Biomarkers
• chemotherapy induced peripheral neuropathy
• chemotherapy induced peripheral neurotoxicity
• neuroimaging
• mrn
• hrsu

Article highlights

• There is no consensus on the gold standard measure(s) in CIPN assessment and biomarkers could fill this huge gap becoming, eventually, a surrogate endpoint.

• HRUS are quite convenient given they can be performed rapidly and with little discomfort for patients. A few studies showed promising HRUS application in CIPN, but - to verify their appropriateness - further studies are warranted.

• MRI can give precious information on peripheral nerves/DRG or demonstrate alterations of the CNS in consequence of CIPN. It is far more time consuming than HRUS and requires an expensive equipment, but it can give insights on pathogenetic mechanisms in vivo. So far, applications were limited in number and on small cohorts. Larger studies are still warranted.

• Molecular biomarkers are rather promising in CIPN; the most promising ones are type 2 biomarkers that test modifications/levels of molecular components that can be specifically altered in consequence of CIPN specific pathogenetic mechanisms and be elected as a surrogate clinical endpoint.

Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Disclosure

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This paper was not funded.