Related Experiment Video
Updated: Jul 20, 2026
09:33
Preparation Of Neovascular Tissues from Human Glioma Tissues for Quantitative Proteomics Analysis of Tumor Angiogenesis
Published on: March 20, 2026
Malignant glioma progression and nitric oxide
Dora Lam-Himlin1, Michael G Espey, George Perry
1Department of Pathology, University of Maryland, 22 South Greene Street, Baltimore, MD 21201, USA.
Neurochemistry International
|September 15, 2006
Summary
Nitric oxide metabolism plays a complex role in glioblastoma, influencing tumor growth and treatment. Its dual neuroprotective and neurotoxic effects in brain tumors remain under investigation.
Area of Science:
- Neuroscience
- Oncology
- Biochemistry
Background:
- Glioblastoma multiforme is an aggressive brain tumor with poor prognosis.
- Nitric oxide (NO) has diverse physiological and pathophysiological roles.
- The role of NO in glioblastoma is not well understood.
Purpose of the Study:
- To review the multifaceted roles of nitric oxide in glioblastoma.
- To explore NO's involvement in neoplastic transformation and tumor progression.
- To discuss NO's impact on glioblastoma treatment efficacy.
Main Methods:
- Literature review of nitric oxide metabolism in gliomas.
- Analysis of NO's physiological and pathophysiological functions.
- Discussion of NO's dual role in neuroprotection and neurotoxicity.
Main Results:
- Nitric oxide is implicated in key glioblastoma processes like neovascularization and apoptosis.
- NO exhibits both beneficial and detrimental effects in the context of brain tumors.
- Its influence on chemotherapeutic efficacy is complex and unresolved.
Conclusions:
- Nitric oxide metabolism is intimately associated with glioblastoma progression.
- Further research is needed to clarify NO's precise role and therapeutic potential in glioblastoma.
- Understanding NO's dual nature is crucial for developing effective glioblastoma treatments.
Related Concept Videos
01:28Nitric Oxide Signaling Pathway
Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure to...
02:07Tumor Progression
Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
02:07Tumor Progression
Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
01:24Regulation of Angiogenesis and Blood Supply
Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits. Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...