ArticleJournal of neuro-oncology2012
GBM secretome induces transient transformation of human neural precursor cells.
Article in Journal of neuro-oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 26 citations in OpenAlex.
- Characterization, Preconditioning, Safety, and Other Issues of MSC-Derived EVs and Secretome.International journal of molecular sciences · 2026Review
- Safety and Regenerative Properties of Immortalized Human Mesenchymal Stromal Cell Secretome.International journal of molecular sciences · 2025Article
- Isolation and Culture of Human Neural Stem Cells.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Dynamic profiling of medulloblastoma surfaceome.Acta neuropathologica communications · 2023Article
- An effective kinase inhibition strategy for metastatic recurrent childhood medulloblastoma.Journal of neuro-oncology · 2023Article
- Metabolism-based targeting of MYC via MPC-SOD2 axis-mediated oxidation promotes cellular differentiation in group 3 medulloblastoma.Nature communications · 2023Article
- Derivation and culturing of neural stem cells from human embryonic brain tissue.STAR protocols · 2022Article
- Potential Neurotoxic Effects of Glioblastoma-Derived Exosomes in Primary Cultures of Cerebellar Neurons via Oxidant Stress and Glutathione Depletion.Antioxidants (Basel, Switzerland) · 2022Article
- The Relevance of Circadian Clocks to Stem Cell Differentiation and Cancer Progression.NeuroSci · 2022Review
- Article
- Temporal profiling of therapy resistance in human medulloblastoma identifies novel targetable drivers of recurrence.Science advances · 2021Article
- BMI1 is a therapeutic target in recurrent medulloblastoma.Oncogene · 2019Article
- From glioblastoma to endothelial cells through extracellular vesicles: messages for angiogenesis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- TrkB-containing exosomes promote the transfer of glioblastoma aggressiveness to YKL-40-inactivated glioblastoma cells.Oncotarget · 2016Article
- Epidermal growth factor signaling in transformed cells.International review of cell and molecular biology · 2015Review
- Inflammatory cytokines, interleukin-1 beta and tumor necrosis factor-alpha, upregulated in glioblastoma multiforme, raise the levels of CRYAB in exosomes secreted by U373 glioma cells.Biochemical and biophysical research communications · 2014Article
- Transfer of malignant trait to immortalized human cells following exposure to human cancer serum.Journal of experimental & clinical cancer research : CR · 2014Article
- Interleukin-1-induced changes in the glioblastoma secretome suggest its role in tumor progression.Journal of proteomics · 2014Article
- Proteomic profiling of the tumor microenvironment: recent insights and the search for biomarkers.Genome medicine · 2014Article
- Disulfiram, a drug widely used to control alcoholism, suppresses the self-renewal of glioblastoma and over-rides resistance to temozolomide.Oncotarget · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) is the most aggressive primary brain tumor in humans, with a uniformly poor prognosis. The tumor microenvironment is composed of both supportive cellular substrates and exogenous factors. We hypothesize that exogenous factors secreted by brain tumor initiating cells (BTICs) could predispose normal neural precursor cells (NPCs) to transformation. When NPCs are grown in GBM-conditioned media, and designated as "tumor-conditioned NPCs" (tcNPCs), they become highly proliferative and exhibit increased stem cell self-renewal, or the unique ability of stem cells to asymmetrically generate another stem cell and a daughter cell. tcNPCs also show an increased transcript level of stem cell markers such as CD133 and ALDH and growth factor receptors such as VEGFR1, VEGFR2, EGFR and PDGFRα. Media analysis by ELISA of GBM-conditioned media reveals an elevated secretion of growth factors such as EGF, VEGF and PDGF-AA when compared to normal neural stem cell-conditioned media. We also demonstrate that tcNPCs require prolonged or continuous exposure to the GBM secretome in vitro to retain GBM BTIC characteristics. Our in vivo studies reveal that tcNPCs are unable to form tumors, confirming that irreversible transformation events may require sustained or prolonged presence of the GBM secretome. Analysis of GBM-conditioned media by mass spectrometry reveals the presence of secreted proteins Chitinase-3-like 1 (CHI3L1) and H2A histone family member H2AX. Collectively, our data suggest that GBM-secreted factors are capable of transiently altering normal NPCs, although for retention of the transformed phenotype, sustained or prolonged secretome exposure or additional transformation events are likely necessary.
Indexed as
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.