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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http://dx.doi.org/10.3390/cancers15082196 | DOI Listing |
J Cell Mol Med
January 2025
Department of Ophthalmology, Muğla Training and Research Hospital, Mugla, Turkey.
Nowadays, the use of monoclonal antibodies to target angiogenic signalling pathways is common, but, unfortunately, the clinical activity of these agents is limited. Thus, the development of approaches targeting multiple pathways for anti-angiogenic effect will lead to increase the clinical benefit. For this purpose, oleuropein, hesperidin, piperine, proanthocyanidins and retinoic acid, which have previously been proven to be bioactive components, anti-angiogenic performances were experimentally tested in retinal pigment epithelial cells.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Icahn School of Medicine at Mount Sinai Medical Center, New York, NY, USA.
Background: Presenilin1 (PS1)/γ-secretase cleaves within the transmembrane domain of numerous receptor substrates. Mutations in PS1 have implications on the catalytic subunit of γ-secretase decreasing its activity and becoming a potential causative factor for Familial Alzheimer's Disease (FAD). This work studies the role of PS1/γ-secretase on the processing, angiogenic signaling, and functions of VEGFR2 and the effects of PS1 FAD mutants on the γ-secretase-mediated epsilon cleavage of VEGFR2.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Emory University School of Medicine, Atlanta, GA, USA.
Background: Circular RNA represents a distinctive form of noncoding RNA resulting from back-splicing of exons and introns in mRNA. CircRNA has been shown play important roles in neurological diseases, such as Alzheimer's disease (AD). Some recent studies also have demonstrated circRNA is enriched in the mammal brain and differentially altered during AD.
View Article and Find Full Text PDFFront Mol Biosci
December 2024
Department of Microbiology, Biochemistry and Immunology, Morehouse School of Medicine, Atlanta, GA, United States.
Introduction: Sickle cell disease (SCD) is a genetic blood disorder caused by a mutation in the HBB gene, which encodes the beta-globin subunit of hemoglobin. This mutation leads to the production of abnormal hemoglobin S (HbS), causing red blood cells to deform into a sickle shape. These deformed cells can block blood flow, leading to complications like chronic hemolysis, anemia, severe pain episodes, and organ damage.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Cardiovascular Surgery, Nihon University Hospital, Itabashi-ku, Tokyo, Japan.
We investigated the influence of false lumen (FL) status on the systemic inflammatory response triggered by acute aortic dissection (AAD) using cytokine profiling. The study included 44 patients with AAD. Patients were divided between those with a thrombosed FL (Group T, n = 21) and those with a non-thrombosed FL (Group P, n = 23).
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