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Chemotherapy-induced peripheral neuropathy (CIPN) is a common side effect of many types of chemotherapy treatment. CIPN affects up to 80-90% of patients treated with the chemotherapeutic agent paclitaxel. Vincristine causes CIPN in~ 20% of patients and, the prevalence of bortezomibinduced peripheral neuropathy is~ 47%(1). Patients with CIPN often experience pain, numbness and a burning sensation in hands and feet, that makes every-day life challenging and painful. The severity and symptoms of CIPN vary greatly among patients, depending on the type of chemotherapy used in their treatment, cumulative-dose, and genetic factors (2). This makes it challenging for clinicians and health personal to properly diagnose and grade patients with CIPN while maintaining an effective treatment towards the cancer. Today, common tools used to grade neuropathy are subjective and have limited sensitivity. Currently, there are no effective treatment for CIPN and understanding the molecular mechanisms and changes behind CIPN, can hopefully aid development of preventive tools and/or new treatment strategies. Additionally, an objective and sensitive biomarker would help improve patient-treatment-course and maybe reduce adverse events in patients with increased risk of developing CIPN. In the end, this could better patient health and quality-of-life worldwide.

The idea behind this thesis is to dig into the molecular mechanisms behind CIPN. More specifically, paclitaxel-, vincristine-and bortezomib-induced peripheral neuropathy. Until now, the majority of CIPN research has focused on sensory neurons that are involved in the disease …