ArticleCurrent neuropharmacology2015
Neurodegeneration and the Brain Tumor Microenvironment. [corrected].
Article in Current neuropharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 22 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.
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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
- Review
- TREM2 in neurodegeneration and diseases.Molecular psychiatry · 2026Review
- Role of Glutamate Excitotoxicity in Glioblastoma Growth and Its Implications in Treatment.Cell biology international · 2025Review
- Seizures in brain tumors: pathogenesis, risk factors and management (Review).International journal of molecular medicine · 2025Review
- Utilizing human cerebral organoids to model breast cancer brain metastasis in culture.Breast cancer research : BCR · 2024Article
- Elucidating Cancer Subtypes by Using the Relationship between DNA Methylation and Gene Expression.Genes · 2024Article
- Glioblastoma Therapy: Past, Present and Future.International journal of molecular sciences · 2024Review
- Amyloids and brain cancer: molecular linkages and crossovers.Bioscience reports · 2023Review
- Therapeutic Potential of Nanomedicine in Management of Alzheimer's Disease and Glioma.International journal of nanomedicine · 2023Review
- Ferroptosis and PPAR-gamma in the limelight of brain tumors and edema.Frontiers in oncology · 2023Review
- The Role of SLC7A11 in Cancer: Friend or Foe?Cancers · 2022Review
- In vivo compression and imaging in mouse brain to measure the effects of solid stress.Nature protocols · 2020Article
- Molecular crosstalk between cancer and neurodegenerative diseases.Cellular and molecular life sciences : CMLS · 2020Review
- Glioblastoma cells vampirize WNT from neurons and trigger a JNK/MMP signaling loop that enhances glioblastoma progression and neurodegeneration.PLoS biology · 2019Article
- In silico characterization of residues essential for substrate binding of human cystine transporter, xCT.Journal of molecular modeling · 2019Article
- Bidirectional Microglia-Neuron Communication in Health and Disease.Frontiers in cellular neuroscience · 2018Review
- ATF4 promotes angiogenesis and neuronal cell death and confers ferroptosis in a xCT-dependent manner.Oncogene · 2017Article
- Article
- The oxido-metabolic driver ATF4 enhances temozolamide chemo-resistance in human gliomas.Oncotarget · 2017Article
- Temozolomide toxicity operates in a xCT/SLC7a11 dependent manner and is fostered by ferroptosis.Oncotarget · 2016Article
Corrections and comments
- Erratum issuedERRATUM.2015
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Malignant brain tumors are characterized by destructive growth and neuronal cell death making them one of the most devastating diseases. Neurodegenerative actions of malignant gliomas resemble mechanisms also found in many neurodegenerative diseases such as Alzheimer's and Parkinson's diseases and amyotrophic lateral sclerosis. Recent data demonstrate that gliomas seize neuronal glutamate signaling for their own growth advantage. Excessive glutamate release via the glutamate/cystine antiporter xCT (system xc-, SLC7a11) renders cancer cells resistant to chemotherapeutics and create the tumor microenvironment toxic for neurons. In particular the glutamate/cystine antiporter xCT takes center stage in neurodegenerative processes and sets this transporter a potential prime target for cancer therapy. Noteworthy is the finding, that reactive oxygen species (ROS) activate transient receptor potential (TRP) channels and thereby TRP channels can potentiate glutamate release. Yet another important biological feature of the xCT/glutamate system is its modulatory effect on the tumor microenvironment with impact on host cells and the cancer stem cell niche. The EMA and FDA-approved drug sulfasalazine (SAS) presents a lead compound for xCT inhibition, although so far clinical trials on glioblastomas with SAS were ambiguous. Here, we critically analyze the mechanisms of action of xCT antiporter on malignant gliomas and in the tumor microenvironment. Deciphering the impact of xCT and glutamate and its relation to TRP channels in brain tumors pave the way for developing important cancer microenvironmental modulators and drugable lead targets.
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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.