ArticleNeoplasia (New York, N.Y.)2012
Alternative splicing of CHEK2 and codeletion with NF2 promote chromosomal instability in meningioma.
Article in Neoplasia (New York, N.Y.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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Who cites it
28 citing papers in PubMed.
- Multi-omics and Mendelian randomization study explores potential therapeutic targets for meningiomas.Discover oncology · 2025Article
- Exploring the genetic correlation and causal relationships between breast cancer and meningioma using bidirectional Mendelian randomization.Scientific reports · 2025Article
- RNA splicing as a biomarker and phenotypic driver of meningioma DNA-methylation groups.Neuro-oncology · 2024Article
- Meningioma: International Consortium on Meningiomas consensus review on scientific advances and treatment paradigms for clinicians, researchers, and patients.Neuro-oncology · 2024Review
- Splicing modulators impair DNA damage response and induce killing of cohesin-mutant MDS and AML.Science translational medicine · 2024Article
- Domestic Animal Models of Central Nervous System Tumors: Focus on Meningiomas.Life (Basel, Switzerland) · 2023Review
- Two unrelated cases with biallelic CHEK2 variants:a novel condition with constitutional chromosomal instability?European journal of human genetics : EJHG · 2023Article
- Article
- Brain Invasion and Trends in Molecular Research on Meningioma.Brain tumor research and treatment · 2023Review
- Alternative RNA splicing defects in pediatric cancers: new insights in tumorigenesis and potential therapeutic vulnerabilities.Annals of oncology : official journal of the European Society for Medical Oncology · 2022Review
- Discovering the Molecular Landscape of Meningioma: The Struggle to Find New Therapeutic Targets.Diagnostics (Basel, Switzerland) · 2021Review
- Molecular Profiling of 22 Primary Atypical Meningiomas Shows the Prognostic Significance of 18q Heterozygous Loss andCancers · 2021Article
- Molecular characteristics of meningiomas.Journal of pathology and translational medicine · 2020Review
- Emerging Medical Treatments for Meningioma in the Molecular Era.Biomedicines · 2018Review
- Article
- Global Proteome and Phospho-proteome Analysis of Merlin-deficient Meningioma and Schwannoma Identifies PDLIM2 as a Novel Therapeutic Target.EBioMedicine · 2017Article
- Pleomorphism and drug resistant cancer stem cells are characteristic of aggressive primary meningioma cell lines.Cancer cell international · 2017Article
- Genomic landscape of high-grade meningiomas.NPJ genomic medicine · 2017Article
- Inhibiting p21-Activated Kinase Induces Cell Death in Vestibular Schwannoma and Meningioma via Mitotic Catastrophe.Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology · 2017Article
- Molecular Genetics of Intracranial Meningiomas with Emphasis on Canonical Wnt Signalling.Cancers · 2016Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Mutations of the NF2 gene on chromosome 22q are thought to initiate tumorigenesis in nearly 50% of meningiomas, and 22q deletion is the earliest and most frequent large-scale chromosomal abnormality observed in these tumors. In aggressive meningiomas, 22q deletions are generally accompanied by the presence of large-scale segmental abnormalities involving other chromosomes, but the reasons for this association are unknown. We find that large-scale chromosomal alterations accumulate during meningioma progression primarily in tumors harboring 22q deletions, suggesting 22q-associated chromosomal instability. Here we show frequent codeletion of the DNA repair and tumor suppressor gene, CHEK2, in combination with NF2 on chromosome 22q in a majority of aggressive meningiomas. In addition, tumor-specific splicing of CHEK2 in meningioma leads to decreased functional Chk2 protein expression. We show that enforced Chk2 knockdown in meningioma cells decreases DNA repair. Furthermore, Chk2 depletion increases centrosome amplification, thereby promoting chromosomal instability. Taken together, these data indicate that alternative splicing and frequent codeletion of CHEK2 and NF2 contribute to the genomic instability and associated development of aggressive biologic behavior in meningiomas.
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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.