Chemotherapy induced peripheral neuropathy (CIPN) commonly occurs following platinum-based chemotherapy (e.g. cisplatin).  A typical adverse effect is a delayed but lasting chronic pain, that remains into adulthood.  Such a complication is prevalent in about 50% of childhood cancer survivors and it decreases quality of life.  Presently, there are no preventative treatments and no condition-tailored analgesia.  Being dose-dependent, a major concern is that this may negatively impact on chemotherapy treatment, preventing the administration of chemotherapy at the optimal effective doses and premature discontinuation of therapy.  Exposing dorsal root ganglion (DRG) sensory neurons to platinum-based chemotherapy such as cisplatin, sensory neurodegeneration is exhibited.  In previous studies, 24hr cisplatin treatment of 50B11s (an immortalised nociceptive sensory neuronal cell line) resulted in inhibited neurite outgrowth and increased cleaved caspase 3 (CC3) expression [Vencappa et al., 2015].  In rodent models, however, following exposure to cisplatin early in life and subsequent washout, aberrant nociceptor intraepidermal sensory nerve fibre (IENF) growth is induced, a hallmark of chronic pain and putatively mediated by Tropomyosin receptor kinase A (TrkA) [Hathway et al., 2018].  In this study, the hallmarks of CIPN and TrkA dependent signalling were investigated.  SH-SY5Y cells and DRGs underwent 24hr treatment with varying concentrations of cisplatin (0-10μg/ml).  Cisplatin-induced neurodegeneration occurred in a dose-dependent manner (****P<0.0001, *P<0.05 One Way ANOVA) alongside increased phosphorylation of DNA damage markers, p53 and Histone H2A.X.  TrkA expression remained unchanged following treatment with cisplatin.  TrkA mediated aberrant sensory nerve fibre growth following CIPN is believed to be nerve growth factor (NGF) driven.  SH-SY5Y cells treated with NGF (1nM) showed increased phosphorylated TrkA expressions.  All experimental procedures involving animals were performed in accordance with the UK Home office animals (Scientific procedures) Act 1986 and reviewed by Nottingham Trent University Animal Welfare and Ethics Review Boards.  Male Wistar rats (~250g) intraplantar injected (under recover gaseous isoflurane anaesthetic ~2% O2) with NGF (1μM) showed increased PGP9.5+ve IENF growth in the plantar skin (*P<0.05 Mann Whitney Test n=3 per group) and increased mechanical sensitivity (*P<0.05 Two Way ANOVA; n=6 per group) up to 5hrs post-treatment versus the vehicle control group.  In addition, Wistar rats injected with NGF (1μM) and accompanied with either TrkA inhibitor, GW441756 (intraperitoneal 2mg/kg) or NGF neutralising antibody (intraperitoneal 1mg/kg) presented no mechanical behaviour sensitization (*P<0.05 Two Way ANOVA) when compared to NGF+vehicle (n=3 all groups).  It appears that the NGF-TrkA pathway can sensitize nociceptor sensory neurons, thus potentially causing cisplatin-induced survivorship pain.