ArticleJournal of neuro-oncology2005
Cyclin D1 is overexpressed in atypical teratoid/rhabdoid tumor with hSNF5/INI1 gene inactivation.
Article in Journal of neuro-oncology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 42 citations in OpenAlex.
- Rhabdoid Tumor of the Kidney and Soft Tissues: Results from National Wilms Tumor Study-5 and Children's Oncology Group Study AREN0321.Pediatric blood & cancer · 2025Article
- Functional screening reveals genetic dependencies and diverging cell cycle control in atypical teratoid rhabdoid tumors.Genome biology · 2024Article
- Molecular targeted therapies for pediatric atypical teratoid/rhabdoid tumors.Pediatric investigation · 2022Review
- Characterization of molecular signatures of supratentorial ependymomas.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2020Article
- Atypical Teratoid Rhabdoid Tumour : From Tumours to Therapies.Journal of Korean Neurosurgical Society · 2018Review
- Atypical teratoid/rhabdoid tumors-current concepts, advances in biology, and potential future therapies.Neuro-oncology · 2016Review
- Biology and Treatment of Rhabdoid Tumor.Critical reviews in oncogenesis · 2015Review
- Profiling pathway-specific novel therapeutics in preclinical assessment for central nervous system atypical teratoid rhabdoid tumors (CNS ATRT): favorable activity of targeting EGFR- ErbB2 signaling with lapatinib.Molecular oncology · 2013Article
- Inhibition of EZH2 suppresses self-renewal and induces radiation sensitivity in atypical rhabdoid teratoid tumor cells.Neuro-oncology · 2013Article
- Targeting Aurora Kinase A enhances radiation sensitivity of atypical teratoid rhabdoid tumor cells.Journal of neuro-oncology · 2012Article
- Histone deacetylase inhibition decreases proliferation and potentiates the effect of ionizing radiation in atypical teratoid/rhabdoid tumor cells.Neuro-oncology · 2012Article
- p16INK4A and p14ARF tumor suppressor pathways are deregulated in malignant rhabdoid tumors.Journal of neuropathology and experimental neurology · 2011Article
- Therapeutically targeting cyclin D1 in primary tumors arising from loss of Ini1.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- The role of SMARCB1/INI1 in development of rhabdoid tumor.Cancer biology & therapy · 2009Review
- Loss of the epigenetic tumor suppressor SNF5 leads to cancer without genomic instability.Molecular and cellular biology · 2008Article
- Mutation of the INI1 gene in composite rhabdoid tumor of the endometrium.Human pathology · 2007Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectAlthough atypical teratoid/rhabdoid tumor (AT/RT) is known to generate through inactivation of the hSNF5/INI1 gene on chromosome 22q, the downstream molecular mechanism remains unclear. We histologically and molecularly reviewed our pediatric brain tumors for unrecognized AT/RTs and evaluated the role of cyclin D1, a potential molecular target of hSNF5/INI1.
methodsWe analyzed 16 tumors under three years of age: seven medulloblastomas, three anaplastic ependymomas (E IIIs), two each of supratentorial primitive neuroectodermal tumors (sPNETs) and choroid plexus carcinomas (CPCs), and one each of neuroblastoma and pineoblastoma. Immunohistochemistry for glial fibrillary acidic protein, vimentin, epithelial membrane antigen, smooth muscle actin and cyclin D1 was performed. Polymerase chain reaction (PCR)-single-strand conformation polymorphism analysis with direct sequencing, differential PCR and microsatellite analysis were conducted for hSNF5/INI1mutation, homozygous deletion and loss of heterozygosity (LOH) on 22q, respectively. Because of the presence of rhabdoid cells and the polyimmunophenotypic features, the diagnosis was revised to AT/RT in five (31%) tumors, namely, two E IIIs and one each of medulloblastoma, CPC and pineoblastoma. Three of them harbored such hSNF5/INI1 aberrations as germline single base deletion (492/6 delC) and missense mutation (C157T) together with LOH 22q or homozygous deletion. Cyclin D1 was overexpressed in those three tumors but not in the two that lacked hSNF5/INI1 inactivation.
conclusionAT/RT can be misdiagnosed as a variety of tumors, including ependymoma that potentially harbors LOH 22q. Our data indicate that cyclin D1 is a target of hSNF5/INI1in primary tumors.
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