ArticleMolecular cancer2018
Shedding of bevacizumab in tumour cells-derived extracellular vesicles as a new therapeutic escape mechanism in glioblastoma.
Article in Molecular cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.
- Pooled it
- Rituximab Binding Endows CD20+ Extracellular Vesicles With NK Cell-Activating Properties in B Cell Lymphoma.Journal of extracellular vesicles · 2026Article
- Exosomal biomarkers and therapeutics in lung cancer: a narrative review on their role in early detection and targeted treatment.Translational lung cancer research · 2025Review
- Enabling mechanistic studies of EVs in vivo: a protocol for isolation and cell-specific labelling in larval zebrafish.Cell communication and signaling : CCS · 2025Article
- Research landscape of glioma and inflammation over the past two decades.Frontiers in immunology · 2025Article
- Extracellular vesicle-bound VEGF in oral squamous cell carcinoma and its role in resistance to Bevacizumab Therapy.Cancer cell international · 2024Article
- The Role of Intracellular and Extracellular Vesicles in the Development of Therapy Resistance in Cancer.Current pharmaceutical design · 2024Review
- PEDF-Enriched Extracellular Vesicle for Vessel Normalization to Potentiate Immune Checkpoint Blockade Therapy.Biomaterials research · 2024Article
- The emerging role of the exosomal proteins in neuroblastoma.Frontiers in oncology · 2024Review
- Insight into extracellular vesicles in vascular diseases: intercellular communication role and clinical application potential.Cell communication and signaling : CCS · 2023Review
- The role of extracellular vesicles in the development of nasopharyngeal carcinoma and potential clinical applications.Cancer medicine · 2023Review
- Extracellular vesicles in tumor angiogenesis and resistance to anti-angiogenic therapy.Cancer science · 2023Review
- Review
- Extracellular Vesicles in Cancer Drug Resistance: Roles, Mechanisms, and Implications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Review
- Article
- Glioblastoma Microenvironment and Cellular Interactions.Cancers · 2022Review
- The Role of Exosomal Non-Coding RNAs in Colorectal Cancer Drug Resistance.International journal of molecular sciences · 2022Review
- Dynamic Intercell Communication between Glioblastoma and Microenvironment through Extracellular Vesicles.Biomedicines · 2022Review
- Definition of an Inflammatory Biomarker Signature in Plasma-Derived Extracellular Vesicles of Glioblastoma Patients.Biomedicines · 2022Article
- Facilitating drug delivery in the central nervous system by opening the blood-cerebrospinal fluid barrier with a single low energy shockwave pulse.Fluids and barriers of the CNS · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Glioblastoma (GBM) is the most aggressive type of primary brain tumours. Anti-angiogenic therapies (AAT), such as bevacizumab, have been developed to target the tumour blood supply. However, GBM presents mechanisms of escape from AAT activity, including a speculated direct effect of AAT on GBM cells. Furthermore, bevacizumab can alter the intercellular communication of GBM cells with their direct microenvironment. Extracellular vesicles (EVs) have been recently described as main acts in the GBM microenvironment, allowing tumour and stromal cells to exchange genetic and proteomic material. Herein, we examined and described the alterations in the EVs produced by GBM cells following bevacizumab treatment. Interestingly, bevacizumab that is able to neutralise GBM cells-derived VEGF-A, was found to be directly captured by GBM cells and eventually sorted at the surface of the respective EVs. We also identified early endosomes as potential pathways involved in the bevacizumab internalisation by GBM cells. Via MS analysis, we observed that treatment with bevacizumab induces changes in the EVs proteomic content, which are associated with tumour progression and therapeutic resistance. Accordingly, inhibition of EVs production by GBM cells improved the anti-tumour effect of bevacizumab. Together, this data suggests of a potential new mechanism of GBM escape from bevacizumab activity.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.