Oxaliplatin rechallenge in metastatic colorectal cancer patients with clinically significant oxaliplatin‐induced peripheral neurotoxicity

Abstract

We investigated whether rechallenge with oxaliplatin (OXA) can worsen the preexisting oxaliplatin-induced peripheral neurotoxicity (OXAIPN) in metastatic colorectal cancer (mCRC) patients. Patients previously treated with OXA, having clinically significant grade 1 or 2 OXAIPN were assessed, after receiving rechallenge with OXA, using the clinical version of the Total Neuropathy Score (TNSc). Peripheral neuropathy was assessed at the end of first OXA exposure and at completion of OXA rechallenge. The first line OXA-based chemotherapy was completed at least 9 months earlier (OXA-free interval). We studied 25 mCRC patients, 14 males and 11 females, with a median age of 63 (35-77) years. After their first exposure to OXA-based chemotherapy, 9 (36%) patients developed grade 1 OXAIPN and 16 patients grade 2 (64%) neurotoxicity. OXA reintroduction with a median of 10 (8-14) cycles led to

Evaluating combined bevacizumab and XELOX in advanced colorectal cancer: Serum markers carcinoembryonic antigen, carbohydrate antigen 125, carbohydrate antigen 199 analysis

“…Currently, mCRC can be treated with the XELOX regimen, which can inhibit cancer cell proliferation and prolong patient survival time[ 28 , 29 ]. However, oxaliplatin in the XELOX regimen has certain toxicity and cannot be used for a long time, so the significance of taking low-intensity and low-toxicity drugs for treatment is even greater[ 30 ].…”

Prospectively assessing serum neurofilament light chain levels as a biomarker of paclitaxel‐induced peripheral neurotoxicity in breast cancer patients

“…25 Additionally, it remains to be explained the reasons behind the decision of Kim et al 24 to test sNfL as a valid biomarker for OXAIPN regardless of its various neurotoxic mechanisms, including mitochondrial dysfunction, effects on nerve cell vascularization, and ion channel dysfunction, rather than axonal degeneration. 37,38 That said, we might suggest that sNfL might not be a relevant biomarker for any type of CIPN and should ideally be used in typical toxic axonopathies with evidence of axonal degeneration, such as PIPN, 4,29 or neurotoxicity after exposure to bortezomib 39 and vinca alkaloids. 40 Nonetheless, our results contradict those previously reported by Sumitani et al, 23 which measured, using an ELISA technique, serum phosphorylated neurofilament heavy subunit (pNF-H) levels as a potential systemic biomarker of CIPN in 71 patients with early breast cancer, treated with various chemotherapeutic regimens.…”

“…In addition, NCI‐CTC scores generally underestimate CIPN severity when compared to a patients' reported outcome (PRO) measure, like the EORTC CIPN20 25 . Additionally, it remains to be explained the reasons behind the decision of Kim et al 24 to test sNfL as a valid biomarker for OXAIPN regardless of its various neurotoxic mechanisms, including mitochondrial dysfunction, effects on nerve cell vascularization, and ion channel dysfunction, rather than axonal degeneration 37,38 . That said, we might suggest that sNfL might not be a relevant biomarker for any type of CIPN and should ideally be used in typical toxic axonopathies with evidence of axonal degeneration, such as PIPN, 4,29 or neurotoxicity after exposure to bortezomib 39 and vinca alkaloids 40 …”

The Combination of Zinc and Melatonin Enhanced Neuroprotection and Attenuated Neuropathy in Oxaliplatin-Induced Neurotoxicity

“… 5 , 6 Peripheral neurotoxicity induced by OXL may continue even after finishing the treatment for more than 5 years in 25–30% of the patients including psychological problems and depression. 7 , 8 The anticipated unwanted responses of OXA have been reported as the clinical use of OXA has grown. These OXA side effects may result in the termination of treatment plans, as well as a reduction in treatment compliance of the patients.…”