AI Article Synopsis

  • Glioblastoma (GB) is a highly lethal brain cancer, with patients typically surviving only 15-18 months after diagnosis, underlining the urgent need for effective biomarkers for treatment and monitoring.
  • The study examined proteins MMP-2, MMP-9, YKL40, and VEGFA in GB patients, finding that high VEGFA levels were linked to better progression-free survival following treatment with bevacizumab, making it a potential biomarker for response to this therapy.
  • Conversely, VEGFA didn’t correlate with outcomes from another treatment, temozolomide, while YKL40 also showed some relevance to bevacizumab treatment effectiveness, emphasizing the importance of researching protein expressions in GB for future clinical

Article Abstract

Glioblastoma (GB) is one of the deadliest human cancers. Many GB patients do not respond to treatment, and inevitably die within a median of 15-18 months post-diagnosis, highlighting the need for reliable biomarkers to aid clinical management and treatment evaluation. The GB microenvironment holds tremendous potential as a source of biomarkers; several proteins such as MMP-2, MMP-9, YKL40, and VEGFA have been identified as being differentially expressed in GB patient samples. Still to date, none of these proteins have been translated into relevant clinical biomarkers. This study evaluated the expression of MMP-2, MMP-9, YKL40, and VEGFA in a series of GBs and their impact on patient outcome. High levels of VEGFA expression were significantly associated with improved progression-free survival after bevacizumab treatment, thus having potential as a tissue biomarker for predicting patients' response to bevacizumab. Noteworthily, VEGFA expression was not associated with patient outcome after temozolomide treatment. To a lesser extent, YKL40 also provided significant information regarding the extent of bevacizumab treatment. This study highlights the importance of studying secretome-associated proteins as GB biomarkers and identifies VEGFA as a promising marker for predicting response to bevacizumab.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10136662PMC
http://dx.doi.org/10.3390/cancers15082196DOI Listing

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