ReviewTranslational oncology2017
Vascular Mimicry: A Novel Neovascularization Mechanism Driving Anti-Angiogenic Therapy (AAT) Resistance in Glioblastoma.
Review in Translational oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 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
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.
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Who cites it
78 citing papers in PubMed, 138 citations in OpenAlex.
- Aminated fullerene-based nanoplatform enables synergistic VEGFR2-targeted anti-angiogenesis and tumor immunotherapy.Bioactive materials · 2026Article
- PKM2 Lactylation Promotes Colorectal Cancer Vasculogenic Mimicry and Bevacizumab Resistance by Facilitating FOSL1 Super-enhancer Formation.Cancer research · 2026Article
- Endothelial plasticity as a continuum in the tumor microenvironment.Vascular biology (Bristol, England) · 2026Article
- Angiogenesis and Resistance Mechanisms in Glioblastoma: Targeting Alternative Vascularization Pathways to Overcome Therapy Resistance.Current pharmaceutical design · 2026Review
- Targeting focal adhesion kinase inhibits cell migration and non-angiogenic vascularization in malignant breast cancer.Breast cancer (Tokyo, Japan) · 2026Article
- NLRC5 expression within tumor cells is critical to activate adaptive and innate antitumor immune responses.Immunotherapy advances · 2026Article
- Vascular mimicry and mosaic vessels in parathyroid tumours: a new diagnostic approach?Journal of clinical pathology · 2025Article
- Murine Cell Line Models for Vascular Mimicry: The Role of YAP/TAZ Signaling.International journal of molecular sciences · 2025Article
- Energy stress and adaptation strategy of tumor cells in different microenvironments: from primary tumors to distant metastases.Acta biochimica et biophysica Sinica · 2025Review
- Role and Mechanisms of Angiogenesis in Tumours.Biology · 2025Review
- Understanding Neovascularization in Glioblastoma: Insights from the Current Literature.International journal of molecular sciences · 2025Review
- Dihydroartemisinin inhibits EphA2/PI3K/Akt pathway-mediated malignant behaviors and vasculogenic mimicry in glioma stem cells.Heliyon · 2025Article
- Establishment and validation of a prognostic model based on vasculogenic mimicry-related gene clustering in ovarian cancer.Frontiers in oncology · 2025Article
- Deciphering molecular pathways driving cancer invasion and metastasis: advances and therapeutic prospects.Frontiers in oncology · 2025Review
- The Role of HDAC6 in Glioblastoma Multiforme: A New Avenue to Therapeutic Interventions?Biomedicines · 2024Review
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- Vascular mimicry in zebrafish fin regeneration: how macrophages build new blood vessels.Angiogenesis · 2024Article
- HNRNPA2B1 stabilizes NFATC3 levels to potentiate its combined actions with FOSL1 to mediate vasculogenic mimicry in GBM cells.Cell biology and toxicology · 2024Article
- A 3D Bioprinted Human Neurovascular Unit Model of Glioblastoma Tumor Growth.Advanced healthcare materials · 2024Article
18 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Glioblastoma (GBM) is a hypervascular neoplasia of the central nervous system with an extremely high rate of mortality. Owing to its hypervascularity, anti-angiogenic therapies (AAT) have been used as an adjuvant to the traditional surgical resection, chemotherapy, and radiation. The benefits of AAT have been transient and the tumors were shown to relapse faster and demonstrated particularly high rates of AAT therapy resistance. Alternative neovascularization mechanisms were shown to be at work in these resilient tumors to counter the AAT therapy insult. Vascular Mimicry (VM) is the uncanny ability of tumor cells to acquire endothelial-like properties and lay down vascular patterned networks reminiscent of host endothelial blood vessels. The VM channels served as an irrigation system for the tumors to meet with the increasing metabolic and nutrient demands of the tumor in the event of the ensuing hypoxia resulting from AAT. In our previous studies, we have demonstrated that AAT accelerates VM in GBM. In this review, we will focus on the origins of VM, visualizing VM in AAT-treated tumors and the development of VM as a resistance mechanism to AAT.
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.