Blood biomarkers for neuroaxonal injury and astrocytic activation in chemotherapy-induced peripheral neuropathy.


Journal

Acta oncologica (Stockholm, Sweden)
ISSN: 1651-226X
Titre abrégé: Acta Oncol
Pays: Sweden
ID NLM: 8709065

Informations de publication

Date de publication:
05 Aug 2024
Historique:
received: 21 01 2024
accepted: 21 06 2024
medline: 5 8 2024
pubmed: 5 8 2024
entrez: 5 8 2024
Statut: epublish

Résumé

Chemotherapy-induced peripheral neuropathy (CIPN) is a troublesome side effect in patients exposed to taxanes in the treatment of cancer and may affect quality of life dramatically. Here we assessed whether serum levels of neurofilament light (NfL) and tau (two neuroaxonal injury biomarkers) and glial fibrillary acidic protein (GFAP, a biomarker for astrocytic activation) correlate with the development of CIPN in the adjuvant setting of early breast cancer. Using ultrasensitive single molecule array technology, serum levels of NfL, GFAP, and tau were measured before and every 3 weeks in 10 women receiving adjuvant EC (epirubicin 90 mg/m² and cyclophosphamide 600 mg/m²) every 3 weeks × 3, followed by weekly paclitaxel 80 mg/m² × 9-12 weeks after surgery due to early breast cancer. CIPN was graded according to the NCI Common Terminology Criteria for Adverse Events (CTCAE v5.0) and the questionnaire EORTC QLQ CIPN-20. Serum levels of GFAP increased successively during cycles of EC. NfL increased instead in response to the treatment of paclitaxel. NfL and GFAP continued to rise throughout exposure of cumulatively higher doses of paclitaxel and were reduced 3 months after the end of chemotherapy. Serums levels of tau were marginally affected by exposure to chemotherapy. Women with worse symptoms of CIPN had higher concentrations of NfL than women with mild symptoms of CIPN. NfL and GFAP are promising biomarkers to identify women at risk of developing CIPN. Larger prospective studies are now needed.

Sections du résumé

BACKGROUND AND PURPOSE OBJECTIVE
Chemotherapy-induced peripheral neuropathy (CIPN) is a troublesome side effect in patients exposed to taxanes in the treatment of cancer and may affect quality of life dramatically. Here we assessed whether serum levels of neurofilament light (NfL) and tau (two neuroaxonal injury biomarkers) and glial fibrillary acidic protein (GFAP, a biomarker for astrocytic activation) correlate with the development of CIPN in the adjuvant setting of early breast cancer.
MATERIALS AND METHODS METHODS
Using ultrasensitive single molecule array technology, serum levels of NfL, GFAP, and tau were measured before and every 3 weeks in 10 women receiving adjuvant EC (epirubicin 90 mg/m² and cyclophosphamide 600 mg/m²) every 3 weeks × 3, followed by weekly paclitaxel 80 mg/m² × 9-12 weeks after surgery due to early breast cancer. CIPN was graded according to the NCI Common Terminology Criteria for Adverse Events (CTCAE v5.0) and the questionnaire EORTC QLQ CIPN-20.
RESULTS RESULTS
Serum levels of GFAP increased successively during cycles of EC. NfL increased instead in response to the treatment of paclitaxel. NfL and GFAP continued to rise throughout exposure of cumulatively higher doses of paclitaxel and were reduced 3 months after the end of chemotherapy. Serums levels of tau were marginally affected by exposure to chemotherapy. Women with worse symptoms of CIPN had higher concentrations of NfL than women with mild symptoms of CIPN.
INTERPRETATION CONCLUSIONS
NfL and GFAP are promising biomarkers to identify women at risk of developing CIPN. Larger prospective studies are now needed.

Identifiants

pubmed: 39099324
doi: 10.2340/1651-226X.2024.39895
doi:

Substances chimiques

Neurofilament Proteins 0
neurofilament protein L 0
Glial Fibrillary Acidic Protein 0
Paclitaxel P88XT4IS4D
tau Proteins 0
Biomarkers 0
Epirubicin 3Z8479ZZ5X
Cyclophosphamide 8N3DW7272P
GFAP protein, human 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

636-641

Auteurs

Jamila Adra (J)

Department of Oncology, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Sweden; Department of Oncology, Sahlgrenska University Hospital, Gothenburg, Sweden. jamila.adra@regionhalland.se.

Daniel Giglio (D)

Department of Oncology, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Sweden; Department of Oncology, Sahlgrenska University Hospital, Gothenburg, Sweden.

Per Karlsson (P)

Department of Oncology, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Sweden; Department of Oncology, Sahlgrenska University Hospital, Gothenburg, Sweden.

Henrik Zetterberg (H)

Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden; Department of Neurodegenerative Disease, UCL Institute of Neurology, Queen Square, London, UK; UK Dementia Research Institute at UCL, London, UK; Hong Kong Center for Neurodegenerative Diseases, Clear Water Bay, Hong Kong, China; Wisconsin Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, USA.

Zakaria Einbeigi (Z)

Department of Oncology, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Sweden; Department of Medicine and Oncology, Södra Älvsborgs Hospital, Borås, Sweden.

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Classifications MeSH