Problems with chemotherapy-induced peripheral neuropathy (CIPN), which can be caused by potentially neurotoxic chemotherapy, are becoming more and more important in oncological treatments that aim to cure and treat cancer. When acute CIPN develops during chemotherapy, the dose may need to be lowered or stopped, which might have a negative effect on survival. After completing chemotherapy, over 30% of patients would still have CIPN after a year or more. Long-established medications like platinum agents (such as oxaliplatin), vinca alkaloids (such as vincristine), and taxanes have been linked to peripheral neuropathy (e.g. paclitaxel). However, newer, more focused medications including ixabepilone, bortezomib, and eribulin are also linked to a considerable prevalence of peripheral neuropathy. These chemotherapeutic agents all exert their anti-mitotic actions through various ways (e.g. perturbation of microtubule dynamics, DNA cross-linking, proteasome inhibition).
It is hypothesized that an individual's particular genetic variations may affect the regulation of genes involved in drug pharmacokinetics, ion channel functioning, neurotoxicity, and DNA repair, which in turn affect CIPN development and severity. This is because response to the same drug can vary between individuals. The incidence and severity of CIPN may be impacted by variations in other molecular markers. In order to summarize the known biology (molecular and genetic) predictors of CIPN, examine the effects of the various chemotherapeutic agents, and comprehend the prevalence linked with distinct risk factors, this retrospective analysis paper will also discuss the effects of chemotherapeutic agents.
Melissa Sheehan, Grade 11, Natick High School