ArticleHuman pathology2007
Evaluation of NF2 gene deletion in sporadic schwannomas, meningiomas, and ependymomas by chromogenic in situ hybridization.
Article in Human pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 39 citations in OpenAlex.
- Merlin immunoreactivity fails to predict neurofibromatosis type 2 mutations in human meningiomas.Journal of neuropathology and experimental neurology · 2025Article
- The Hippo pathway in cancer: YAP/TAZ and TEAD as therapeutic targets in cancer.Clinical science (London, England : 1979) · 2022Review
- Article
- Neurofibromatosis type 2 gene mutation and progesterone receptor messenger RNA expression in the pathogenesis of sporadic orbitocranial meningioma.International journal of ophthalmology · 2019Article
- Low Merlin expression and high Survivin labeling index are indicators for poor prognosis in patients with malignant pleural mesothelioma.Molecular oncology · 2016Article
- Expression of merlin, NDRG2, ERBB2, and c-MYC in meningiomas: relationship with tumor grade and recurrence.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2016Article
- Expression alterations define unique molecular characteristics of spinal ependymomas.Oncotarget · 2015Article
- Schwannomas and their pathogenesis.Brain pathology (Zurich, Switzerland) · 2014Review
- Using the neurofibromatosis tumor predisposition syndromes to understand normal nervous system development.Scientifica · 2014Review
- Nf2/Merlin controls spinal cord neural progenitor function in a Rac1/ErbB2-dependent manner.PloS one · 2014Article
- Loss of tumor suppressor Merlin in advanced breast cancer is due to post-translational regulation.The Journal of biological chemistry · 2011Article
- The genetic and epigenetic basis of ependymoma.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2009Review
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Fluorescence in situ hybridization, loss of heterozygosity testing, and comparative genomic hybridization have been used to detect NF2 gene alterations in both sporadic and neurofibromatosis type 2 (NF2)-associated central nervous system tumors. In this study, we performed chromogenic in situ hybridization (CISH) and immunohistochemistry to evaluate for NF2 gene deletion in a group of sporadic meningiomas, schwannomas, and ependymomas. Twenty-two sporadic tumors, including 9 ependymomas, 10 meningiomas, and 3 schwannomas, were studied. CISH and immunohistochemistry were performed using the NF2 gene deletion probe and NF2 polyclonal antibody. Deletion of the NF2 gene was identified in 11 (50%) tumors, including 60% (6/10) of meningiomas, 33% (3/9) of ependymomas, and 67% (2/3) of schwannomas. The remaining 11 (50%) cases were diploid. Overall, immunoexpression of NF2 protein was observed in 50% (11/22) tumors, and concordance between CISH and immunohistochemistry was observed in 73% of cases. Our results support previous observations that schwannomas and meningiomas, and to a lesser degree, ependymomas, express a high incidence of NF2 gene deletion, which supports the hypothesis that NF2 gene plays an important role in their tumorigenesis. In addition, we have validated CISH as an efficient, economic, and reliable method for routinely assessing NF2 gene deletion in these tumors.
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