[Intracranial stereotaxic external radiation using a linear accelerator].

K Watne; K Tverå; B Hager; H Nornes; H Hirschberg

Home/Archive/PubMed

PubMed · 2501907

[Intracranial stereotaxic external radiation using a linear accelerator].

K Watne·K Tverå·B Hager·H Nornes·H Hirschberg

View original source ↗Export metadata ↓

Abstract

The article describes a method making it possible to give high radiation doses to a localized volume of the brain while sparing normal surrounding brain tissue. The treatment consists of sending multiple narrow radiation beams from different directions to the volume of tissue to be treated by rotating the radiation source and the patient table in relation to each other. Mega-voltage radiation from a linear accelerator is used. A non-invasive stereotactic frame is mounted on the patient and a CT scan of the brain is performed to localize the center and extent of the tissue to be treated. The radiation treatment is then given by using the coordinates on the frame to assure that the center of rotation of the treatment table and the linear accelerator pass through the center of the volume of tissue. The method has been used to give radiation boosts after external radiation to brain tumours, and to treat patients with recurrent tumours. Small localized benign intracranial tumours and AV-malformations have also been treated.

Explore related subjects

Brain Neoplasms Humans Intracranial Arteriovenous Malformations Radiotherapy, High-Energy Stereotaxic Techniques English Abstract Journal Article

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

K Watne, K Tverå, B Hager, H Nornes, H Hirschberg. 1989-06-30. [Intracranial stereotaxic external radiation using a linear accelerator].. https://pubmed.ncbi.nlm.nih.gov/2501907/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2026

Leveraging single-cell and spatial omics for brain tumour insights to improve therapeutic strategies.

Single-cell and spatial omics (SPOs) technologies have advanced how healthcare physicians characterise brain tumours by enabling detailed understanding of their cellular architecture, functional states, and microenvironmental dynamics. These approaches provide high-resolution detection of tumour heterogeneity and allow precise analysis of the brain tumour microenvironment. Their application has also led to the discovery of novel biomarkers used for early brain tumour detection, prognosis, and improved tumour stratification. Furthermore, integrative multi-omic analyses have revealed new therapeutic targets, clarified mechanisms of drug resistance, and uncovered molecular pathways underpinning treatment failure. By bridging cellular-level insights with spatial context, SPOs hold significant promise for advancing personalised diagnostics, predicting therapeutic response, and guiding the development of targeted interventions for brain tumours. Despite these advances, several limitations constrain the full translational potential of SPOs, including high experimental costs, substantial computational demands, lack of standardised protocols, and challenges in data integration and reproducibility. Addressing these barriers through scalable bioinformatic pipelines, consensus experimental frameworks, and cost-effective platforms remains critical for broadening accessibility and enabling clinical adoption.

Brain Neoplasms↗

PubMed2026

Identification of Critical Genes Related to Breast Cancer with Brain Metastasis Through Bioinformatics Analysis.

INTRODUCTION: Distant metastasis accounts for the majority of Breast Cancer (BC)-related mortality. The brain is one of the most common regions of metastasis. However, the underlying molecular mechanisms remain uncertain. METHODS: In this study, gene expression profiles were downloaded from the Gene Expression Omnibus (GEO) database. Datasets GSE100534 and GSE52604, containing 16 primary brain tumor samples and 38 breast cancer brain metastasis samples, were used to identify the Differentially Expressed Genes (DEGs). The Metascape database was used to analyze enriched Gene Ontology (GO) entries and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway entries in DEGs. The STRING database was then used to construct a Protein-Protein Interaction (PPI) network, and the Cytoscape platform was employed to visualize the network. Furthermore, the Kaplan-Meier curve was used to analyze the Relapse-Free Survival (RFS) among the hub genes. Finally, the iRegulon plugin was used to construct a regulatory network to find the transcription factors (TFs) that regulate the expression of the hub genes. RESULTS: A total of 344 DEGs, including 182 up-regulated and 162 down-regulated genes, were identified by using the limma package in R. A module with 18 nodes and 9 hub genes was selected from the PPI network by using the plugins MCODE and Cyto- Hubba, respectively. KEGG pathway analysis demonstrated that brain metastasis in BC was closely related to the oocyte cell cycle. The Kaplan-Meier curve showed that high expression of these 9 hub genes was associated with poor RFS in BC patients. TFs' analysis showed that E2F4, SIN3A, FOXM1, and TFDP1 interacted with these hub genes. DISCUSSION: This study revealed that Breast Cancer Brain Metastasis (BCBM) may have a promoting effect on the cell cycle of oocytes and affect the maturation and division of oocytes through the KEGG and GO analyses of 344 DEGs. The selected 9 hub genes (ASPM, BUB1, BUB1B, CCNA2, CCNB1, CDK1, NDC80, NCAPG, and TOP2A) and 4 transcription factors (E2F4, SIN3A, FOXM1, TFDP1) may play a critical role in brain metastasis of BC. CONCLUSION: The results of this study may aid in the early diagnosis and suggest potential targets for the treatment of BCBM.

Brain Neoplasms↗

PubMed2024

Simultaneous targeting of peripheral and brain tumors with a therapeutic nanoparticle to disrupt metabolic adaptability at both sites.

Brain metastasis of advanced breast cancer often results in deleterious consequences. Metastases to the brain lead to significant challenges in treatment options, as the blood-brain barrier (BBB) prevents conventional therapy. Thus, we hypothesized that creation of a nanoparticle (NP) that distributes to both primary tumor site and across the BBB for secondary brain tumor can be extremely beneficial. Here, we report a simple targeting strategy to attack both the primary breast and secondary brain tumors utilizing a single NP platform. The nature of these mitochondrion-targeted, BBB-penetrating NPs allow for simultaneous targeting and drug delivery to the hyperpolarized mitochondrial membrane of the extracranial primary tumor site in addition to tumors at the brain. By utilizing a combination of such dual anatomical distributing NPs loaded with therapeutics, we demonstrate a proof-of-concept idea to combat the increased metabolic plasticity of brain metastases by lowering two major energy sources, oxidative phosphorylation (OXPHOS) and glycolysis. By utilizing complementary studies and genomic analyses, we demonstrate the utility of a chemotherapeutic prodrug to decrease OXPHOS and glycolysis by pairing with a NP loaded with pyruvate dehydrogenase kinase 1 inhibitor. Decreasing glycolysis aims to combat the metabolic flexibility of both primary and secondary tumors for therapeutic outcome. We also address the in vivo safety parameters by addressing peripheral neuropathy and neurobehavior outcomes. Our results also demonstrate that this combination therapeutic approach utilizes mitochondrial genome targeting strategy to overcome DNA repair-based chemoresistance mechanisms.

Brain Neoplasms↗