ArticleEBioMedicine2018
Cells isolated from residual intracranial tumors after treatment express iPSC genes and possess neural lineage differentiation plasticity.
Article in EBioMedicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Biomaterial-based strategies for postoperative residual tumors: From margin clearance to immune control and tissue repair.Materials today. Bio · 2026Review
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- Is modulation of immune checkpoints on glioblastoma-infiltrating myeloid cells a viable therapeutic strategy?Neuro-oncology · 2025Review
- Glioblastoma Standard of Care: Effects on Tumor Evolution and Reverse Translation in Preclinical Models.Cancers · 2024Review
- Antipsychotics possess anti-glioblastoma activity by disrupting lysosomal function and inhibiting oncogenic signaling by stabilizing PTEN.Cell death & disease · 2024Article
- Glioblastoma stem cells deliver ABCB4 transcribed by ATF3 via exosomes conferring glioblastoma resistance to temozolomide.Cell death & disease · 2024Article
- miRNA-194-3p represses NF-κB in gliomas to attenuate iPSC genes and proneural to mesenchymal transition.iScience · 2024Article
- Knock-Down of CD24 in Astrocytes Aggravates Oxyhemoglobin-Induced Hippocampal Neuron Impairment.Neurochemical research · 2022Article
- Prospects of antibodies targeting CD47 or CD24 in the treatment of glioblastoma.CNS neuroscience & therapeutics · 2021Review
- Targeting AGTR1/NF-κB/CXCR4 axis by miR-155 attenuates oncogenesis in glioblastoma.Neoplasia (New York, N.Y.) · 2020Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe goal of this study is to identify and characterize treatment resistant tumor initiating cells (TRTICs) using orthotopic xenografts.
methodsTRTICs were enriched from GBM cell lines using mouse xenografts treated with fractionated doses of radiation and temozolomide. TRTICs were characterized by neurosphere clonogenicity and self-renewal, serial xenotransplantation, differentiation potential, and mRNA & miRNA transcriptomic profiling. We use an unbiased approach to identify antigens encoding TRTIC and glioma stem cells (GSC) populations. Co-culture experiments of TRTIC and differentiated cells were conducted to evaluate the reliance of TRTIC differentiation on the secretome of differentiated cells.
findingsTRTICs acquire stem-like gene expression signatures and increased side population staining resulting from the activation of multi-drug resistance genes. Genetic and functional characterization of TRTICs shows a striking resemblance with GSCs. TRTICs can differentiate towards specific progeny in the neural stem cell lineage. TRTIC-derived tumors display all the histological hallmarks of glioblastoma (GBM) and exhibit a miRNA-transcript and mRNA-transcriptomic profile associated with aggressiveness. We report that CD24+/CD44+ antigens are expressed in TRTICs and patient-derived GSCs. Double positive CD24+/CD44+ exhibit treatment resistance and enhanced tumorigenicity. Interestingly, co-culture experiments with TRTICs and differentiated cells indicated that the regulation of TRTIC differentiation could rely on the secretome in the tumor niche.
interpretationRadiation and temozolomide treatment enriches a population of cells that have increased iPSC gene expression. As few as 500 cells produced aggressive intracranial tumors resembling patient GBM. CD24+/CD44+ antigens are increased in TRTICs and patient-derived GSCs. The enrichment for TRTICs may result in part from the secretome of differentiated cells. FUND: NIH/NCI 1RC2CA148190, 1R01CA108633, 1R01CA188228, and The Ohio State University Comprehensive Cancer Center.
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