Aim Glioblastoma multiforme is the most prevalent brain tumour, with a high recurrence rate due to the lack of quality and cost-effective imaging techniques. Thus, our study aims to explore application of biosensors as a potential non-invasive, low-cost and highly specific means of identifying GBM cells intraoperatively utilising differences in refractive indices of tissue imprints obtained. Method A literature search was performed on Medline OVID, PubMed and Google Scholar with keywords including ‘glioblastoma’, ‘biosensor’, ‘refractive index’ and ‘glutamate’. Conclusions Splicing pattern alterations and downregulation of canonical isoforms of Glial Fibrillary Acidic Protein (GFAP) are pivotal in glioma progression. Glutamate dysregulation in glioblastoma (GBM) is emphasised by GLAST (glutamate aspartate transporter) activity. GLAST, vital for extracellular glutamate homeostasis, is dependent on the Na+/K+-ATPase electrochemical gradient. GBM cells exhibit compromised glutamate uptake due to GLT-1 absence, influenced by oncogenes such as AEG-16, and aberrant GLAST localization in the nucleus. Neurophotonics and spectroscopy methods show promise in distinguishing between GBM and healthy brain parenchyma, however they are limited by cost. A prospective study revealed high specificity with gold imprinting biosensors in identifying GBM tissue with refractive index 1.350, warranting investigation into the differences in the interaction of GFAP and GLAST proteins with light via spectroscopic techniques which could provide better intraoperative guidance. A potential methodology could involve refractive index sensing with “label-free optical sensors to detect biomolecular interactions” with GFAP and GLAST proteins using transmitted diffraction patterns.
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Balaji et al. (2024) studied this question.
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