Malignant astrocytic glioma: genetics, biology, and paths to treatment
Open accessAbstract
Malignant astrocytic gliomas such as glioblastoma are the most common and lethal intracranial tumors. These cancers exhibit a relentless malignant progression characterized by widespread invasion throughout the brain, resistance to traditional and newer targeted therapeutic approaches, destruction of normal brain tissue, and certain death. The recent confluence of advances in stem cell biology, cell signaling, genome and computational science and genetic model systems have revolutionized our understanding of the mechanisms underlying the genetics, biology and clinical behavior of glioblastoma. This progress is fueling new opportunities for understanding the fundamental basis for development of this devastating disease and also novel therapies that, for the first time, portend meaningful clinical responses.
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EGFR amplification and EGFRvIII activating mutation are the most common oncogenes promoting PI3K signaling in GBM.
“EGFR amplification, and EGFRvIII activating mutation are the most common oncogenes promoting PI3K signaling in GBM (1, 6).”
From An LXR Agonist Promotes Glioblastoma Cell Death through Inhibition of an EGFR/AKT/SREBP-1/LDLR–Dependent Pathway (2011) · cites this paper as [1]
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Antagonistic Effects of Endogenous Nitric Oxide in a Glioblastoma Photodynamic Therapy Model
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- Authors
- Furnari, F. B., Fenton, T., Bachoo, R. M., Mukasa, A., Stommel, J. M., Stegh, A., Hahn, W. C., Ligon, K. L., Louis, D. N., Brennan, C., Chin, L., DePinho, R. A., & Cavenee, W. K.
- Affiliations
- University of California San Diego (US)
- The University of Texas Southwestern Medical Center (US)
- Harvard University (US)
- Brigham and Women's Hospital (US)
- Memorial Sloan Kettering Cancer Center (US)
- ORCID
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2007-11-01
- Volume
- 21
- Issue
- 21
- Pages
- 2683-2710
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- OpenAlex
- W2151335185
- Cited by
- 2,316
- References
- 22
- Citations by year
- 2026: 32 · 2025: 55 · 2024: 67 · 2023: 77 · 2022: 79 · 2021: 133 · 2020: 122 · 2019: 129 · 2018: 157 · 2017: 150 · 2016: 148 · 2015: 189 · 2014: 158 · 2013: 173 · 2012: 154
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Genes & Development (publishedVersion)
- PubMed (publishedVersion)
- Kent Academic Repository (University of Kent) (acceptedVersion)
- ePrints Soton (University of Southampton) (submittedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- Ellison Medical Foundation
- V Foundation for Cancer Research
- National Foundation for Cancer Research
- National Cancer Institute (CA 95616, R01CA099041, P01CA095616, CA099041)
- Topics
- Health Sciences › Medicine › Genetics › Glioma Diagnosis and Treatment
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cancer Mechanisms and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
- Keywords
- glioblastoma, cancer genetics, tumor biology, tumor invasion, drug resistance, targeted therapy, stem cell biology, signal transduction, new drugs
- MeSH terms
- Animals, Antineoplastic Combined Chemotherapy Protocols, Astrocytoma, Brain Neoplasms, Disease Models, Animal, Humans, Models, Biological, Necrosis, Neoplasm Invasiveness, Neoplasm Staging, Neovascularization, Pathologic, Animals, Genetically Modified, Gene Regulatory Networks
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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