ArticleBMC cancer2017
Transcriptional changes induced by bevacizumab combination therapy in responding and non-responding recurrent glioblastoma patients.
Article in BMC cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Circulating galectin-1 delineates response to bevacizumab in melanoma patients and reprograms endothelial cell biology.Proceedings of the National Academy of Sciences of the United States of America · 2023Trial
- Neoadjuvant anti-PD-1 immunotherapy promotes a survival benefit with intratumoral and systemic immune responses in recurrent glioblastoma.Nature medicine · 2019Trial
- Anti-VEGF vascular remodeling drives germinal center B cell-rich tertiary lymphoid structures during antibody-toxin and anti-CD40 combination therapy in glioblastoma.Research square · 2026Article
- Pan-cancer landscape of cellular senescence heterogeneity reveals associations with prognosis and therapy response.Scientific reports · 2025Article
- Repeated responders to bevacizumab combination treatment in recurrent glioblastoma: a retrospective case study.Journal of neuro-oncology · 2025Article
- Transcriptomic analysis identifies a potential target for bevacizumab resistant glioblastoma.Scientific reports · 2025Article
- A tumor microenvironment model for glioma diagnosis and therapeutic evaluation based on the analysis of tissues and biological fluids.iScience · 2025Article
- The PARPscore system using poly (ADP-ribose) polymerase (PARP) family features and tumor immune microenvironment in glioma.Discover oncology · 2024Article
- Single-cell RNA sequencing identifies a subtype of FN1 + tumor-associated macrophages associated with glioma recurrence and as a biomarker for immunotherapy.Biomarker research · 2024Article
- Article
- Single-cell RNA-seq reveals T cell exhaustion and immune response landscape in osteosarcoma.Frontiers in immunology · 2024Article
- Polymorphism at codon 31 of CDKN1A (p21) as a predictive factor for bevacizumab therapy in glioblastoma multiforme.BMC cancer · 2023Article
- A programmed cell death-related model based on machine learning for predicting prognosis and immunotherapy responses in patients with lung adenocarcinoma.Frontiers in immunology · 2023Article
- Inhibitor of differentiation 1 in U87MG glioblastoma cells promotes HUVEC sprouting through endothelin-1.Oncology letters · 2022Article
- Perspective: targeting VEGF-A and YKL-40 in glioblastoma - matter matters.Cell cycle (Georgetown, Tex.) · 2021Article
- Article
- Angiotensinogen promoter methylation predicts bevacizumab treatment response of patients with recurrent glioblastoma.Molecular oncology · 2020Article
- A Six-lncRNA Signature for Immunophenotype Prediction of Glioblastoma Multiforme.Frontiers in genetics · 2020Article
- Hypoxia Regulated Gene Network in Glioblastoma Has Special Algebraic Topology Structures and Revealed Communications Involving Warburg Effect and Immune Regulation.Cellular and molecular neurobiology · 2019Article
- Article
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBevacizumab combined with chemotherapy produces clinical durable response in 25-30% of recurrent glioblastoma patients. This group of patients has shown improved survival and quality of life. The aim of this study was to investigate changes in gene expression associated with response and resistance to bevacizumab combination therapy.
methodsRecurrent glioblastoma patients who had biomarker-accessible tumor tissue surgically removed both before bevacizumab treatment and at time of progression were included. Patients were grouped into responders (n = 7) and non-responders (n = 14). Gene expression profiling of formalin-fixed paraffin-embedded tumor tissue was performed using RNA-sequencing.
resultsBy comparing pretreatment samples of responders with those of non-responders no significant difference was observed. In a paired comparison analysis of pre- and posttreatment samples of non-responders 1 gene was significantly differentially expressed. In responders, this approach revealed 256 significantly differentially expressed genes (72 down- and 184 up-regulated genes at the time of progression). Genes differentially expressed in responders revealed a shift towards a more proneural and less mesenchymal phenotype at the time of progression.
conclusionsBevacizumab combination treatment demonstrated a significant impact on the transcriptional changes in responders; but only minimal changes in non-responders. This suggests that non-responding glioblastomas progress chaotically without following distinct gene expression changes while responding tumors adaptively respond or progress by means of the same transcriptional changes. In conclusion, we hypothesize that the identified gene expression changes of responding tumors are associated to bevacizumab response or resistance mechanisms.
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