ArticleActa neuropathologica communications2022
Soluble CD146, a biomarker and a target for preventing resistance to anti-angiogenic therapy in glioblastoma.
Article in Acta neuropathologica communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Biological properties of soluble CD146 and its role and mechanisms in disease progression.Frontiers in immunology · 2026Review
- CD146Theranostics · 2026Article
- The multifaceted roles of MCAM in development, homeostasis, pathological conditions, and cancer.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Navigating the blood-brain barrier to blood-brain tumor barrier transition: microvascular P-glycoprotein and CD146 potentially contribute to glioma grading.Fluids and barriers of the CNS · 2025Article
- CD146: a promising target in respiratory diseases.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Treatment mechanism and research progress of bevacizumab for glioblastoma.American journal of cancer research · 2025Review
- CD146, a therapeutic target involved in cell plasticity.Science China. Life sciences · 2024Review
- Plasma nanoDSF Denaturation Profile at Baseline Is Predictive of Glioblastoma EGFR Status.Cancers · 2023Article
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
rationaleGlioblastoma multiforme (GBM) is a primary brain tumor with poor prognosis. The U.S. food and drug administration approved the use of the anti-VEGF antibody bevacizumab in recurrent GBM. However, resistance to this treatment is frequent and fails to enhance the overall survival of patients. In this study, we aimed to identify novel mechanism(s) responsible for bevacizumab-resistance in CD146-positive glioblastoma.
methodsThe study was performed using sera from GBM patients and human GBM cell lines in culture or xenografted in nude mice.
resultsWe found that an increase in sCD146 concentration in sera of GBM patients after the first cycle of bevacizumab treatment was significantly associated with poor progression free survival and shorter overall survival. Accordingly, in vitro treatment of CD146-positive glioblastoma cells with bevacizumab led to a high sCD146 secretion, inducing cell invasion. These effects were mediated through integrin αvβ3 and were blocked by mucizumab, a novel humanized anti-sCD146 antibody. In vivo, the combination of bevacizumab with mucizumab impeded CD146 + glioblastoma growth and reduced tumor cell dissemination to an extent significantly higher than that observed with bevacizumab alone.
conclusionWe propose sCD146 to be 1/ an early biomarker to predict and 2/ a potential target to prevent bevacizumab resistance in patients with glioblastoma.
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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 OpenQuestion graph.