ArticleCell cycle (Georgetown, Tex.)2021
Perspective: targeting VEGF-A and YKL-40 in glioblastoma - matter matters.
Article in Cell cycle (Georgetown, Tex.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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
9 citing papers in PubMed, 13 citations in OpenAlex.
- Chitinase-3-like protein 1 depletion in glioma cells alters tumor microenvironment and normalizes neovasculature in human glioma xenografts.Cell communication and signaling : CCS · 2026Article
- Targeting of YKL-40 as a Protumor in Personalized Medicine: A New Dimension in Disease Understanding.Current gene therapy · 2026Review
- Angiogenesis and Resistance Mechanisms in Glioblastoma: Targeting Alternative Vascularization Pathways to Overcome Therapy Resistance.Current pharmaceutical design · 2026Review
- Understanding Neovascularization in Glioblastoma: Insights from the Current Literature.International journal of molecular sciences · 2025Review
- YKL-40 inhibits melanoma progression and metastasis by inducing immune cell infiltration in a mouse model.Scientific reports · 2025Article
- Article
- Functional analysis of the short splicing variant encoded by CHI3L1/YKL-40 in glioblastoma.Frontiers in oncology · 2022Article
- New Angiogenic Regulators Produced by TAMs: Perspective for Targeting Tumor Angiogenesis.Cancers · 2021Review
- Plasma IL-8 and ICOSLG as prognostic biomarkers in glioblastoma.Neuro-oncology advancesArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastomas (GBM) are heterogeneous highly vascular brain tumors exploiting the unique microenvironment in the brain to resist treatment and anti-tumor responses. Anti-angiogenic agents, immunotherapy, and targeted therapy have been studied extensively in GBM patients over a number of decades with minimal success. Despite maximal efforts, prognosis remains dismal with an overall survival of approximately 15 months.Bevacizumab, a humanized anti-vascular endothelial growth factor (VEGF) antibody, underwent accelerated approval by the U.S. Food and Drug Administration in 2009 for the treatment of recurrent GBM based on promising preclinical and early clinical studies. Unfortunately, subsequent clinical trials did not find overall survival benefit. Pursuing pleiotropic targets and leaning toward multitarget strategies may be a key to more effective therapeutic intervention in GBM, but preclinical evaluation requires careful consideration of model choices. In this study, we discuss bevacizumab resistance, dual targeting of pro-angiogenic modulators VEGF and YKL-40 in the context of brain tumor microenvironment, and how model choice impacts study conclusions and its translational significance.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.