ArticleCancer research2012
Definition of genetic events directing the development of distinct types of brain tumors from postnatal neural stem/progenitor cells.
Article in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Pericytes orchestrate a tumor-restraining microenvironment in glioblastoma.Nature communications · 2025Article
- SMARCB1-related schwannomatosis and other SMARCB1-associated phenotypes: clinical spectrum and molecular pathogenesis.Familial cancer · 2025Review
- SMARCB1-deficient poorly differentiated testicular carcinoma: a case report.Frontiers in oncology · 2025Article
- The unfolded protein response machinery in glioblastoma genesis, chemoresistance and as a druggable target.CNS neuroscience & therapeutics · 2024Review
- Drug screening with a novel tumor-derived cell line identified alternative therapeutic options for patients with atypical teratoid/rhabdoid tumor.Human cell · 2021Article
- Targeting proteostasis and autophagy in SMARCB1-deficient malignancies: where next?Oncotarget · 2019Article
- The putative tumor suppressor gene EphA7 is a novel BMI-1 target.Oncotarget · 2016Article
- Overview of Transgenic Glioblastoma and Oligoastrocytoma CNS Models and Their Utility in Drug Discovery.Current protocols in pharmacology · 2016Review
- Renal cell carcinoma with rhabdoid-like features lack intracytoplasmic inclusion bodies and show aggressive behavior.Virchows Archiv : an international journal of pathology · 2016Article
- Contribution of tumor heterogeneity in a new animal model of CNS tumors.Molecular cancer research : MCR · 2014Article
- NCoR controls glioblastoma tumor cell characteristics.Neuro-oncology · 2014Article
- Sources of CNS tumor heterogeneity.Oncoscience · 2014Article
- The unfolded protein response in glioblastomas: passing the stress test.CNS oncology · 2013Article
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 3 countries.
Funding
Abstract
Although brain tumors are classified and treated based upon their histology, the molecular factors involved in the development of various tumor types remain unknown. In this study, we show that the type and order of genetic events directs the development of gliomas, central nervous system primitive neuroectodermal tumors, and atypical teratoid/rhabdoid-like tumors from postnatal mouse neural stem/progenitor cells (NSC/NPC). We found that the overexpression of specific genes led to the development of these three different brain tumors from NSC/NPCs, and manipulation of the order of genetic events was able to convert one established tumor type into another. In addition, loss of the nuclear chromatin-remodeling factor SMARCB1 in rhabdoid tumors led to increased phosphorylation of eIF2α, a central cytoplasmic unfolded protein response (UPR) component, suggesting a role for the UPR in these tumors. Consistent with this, application of the proteasome inhibitor bortezomib led to an increase in apoptosis of human cells with reduced SMARCB1 levels. Taken together, our findings indicate that the order of genetic events determines the phenotypes of brain tumors derived from a common precursor cell pool, and suggest that the UPR may represent a therapeutic target in atypical teratoid/rhabdoid tumors.
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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.