ArticleChild's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery2004
Chromosomal imbalances detected by comparative genomic hybridisation in atypical teratoid/rhabdoid tumours.
Article in Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 24 citations in OpenAlex.
- Epigenetic modification after inhibition of IGF-1R signaling in human central nervous system atypical teratoid rhabdoid tumor (AT/RT).Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2013Article
- A complex karyotype in an atypical teratoid/rhabdoid tumor: case report and review of the literature.Journal of neuro-oncology · 2011Review
- Congenital anomalies and rhabdoid tumor associated with 22q11 germline deletion and somatic inactivation of the SMARCB1 tumor suppressor.Genes, chromosomes & cancer · 2011Article
- Renal medullary-like carcinoma in an adult without sickle cell hemoglobinopathy.Nature reviews. Urology · 2010Article
- Loss of the epigenetic tumor suppressor SNF5 leads to cancer without genomic instability.Molecular and cellular biology · 2008Article
- Article
- Cancer-associated mutations in chromatin remodeler hSNF5 promote chromosomal instability by compromising the mitotic checkpoint.Genes & development · 2005Article
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2 authors at 1 institution in 1 country.
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Abstract
introductionAtypical teratoid/rhabdoid tumours (AT/RT) are highly malignant embryonal tumours of the brain composed of rhabdoid cells. Inactivating mutations of the hSNF5/INI-1 gene located in the chromosomal region 22q11.2 are regarded as a crucial step in their molecular pathogenesis. Apart from monosomy or deletions of chromosome 22 not much data exists on additional chromosomal aberrations.
methodsWe investigated seven primary AT/RT by comparative genomic hybridisation (CGH) and found DNA copy number changes in each case.
resultsThese consisted of loss of 22q in 7 out of 7 (100%) and loss of 19 in 3 out of 7 (43%) patients. In 4/7 AT/RT (57%), loss of chromosome 22q was the sole aberration whereas one patient showed additional losses of 16p, 17p and 20q.
conclusionsOur CGH data suggest that apart from monosomy 22 additional genetic pathways may seem feasible for a subset of AT/RT that is yet to be defined. Furthermore, this study also emphasises the potential practical value of loss of chromosome 22 as a diagnostic marker for AT/RT.
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