ArticleHuman genetics1992
Molecular characterization of a 17q11.2 translocation in a malignant schwannoma cell line.
Article in Human genetics, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 42 citations in OpenAlex.
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- Establishment and characterization of a novel human malignant peripheral nerve sheath tumor cell line, FMS-1, that overexpresses epidermal growth factor receptor and cyclooxygenase-2.Virchows Archiv : an international journal of pathology · 2009Article
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- Varicella-zoster virus glycoprotein I is essential for growth of virus in Vero cells.Journal of virology · 1997Article
- Varicella-zoster virus (VZV) open reading frame 10 protein, the homolog of the essential herpes simplex virus protein VP16, is dispensable for VZV replication in vitro.Journal of virology · 1994Article
- The cellular transcription factor USF cooperates with varicella-zoster virus immediate-early protein 62 to symmetrically activate a bidirectional viral promoter.Molecular and cellular biology · 1994Article
- Neurofibromin can inhibit Ras-dependent growth by a mechanism independent of its GTPase-accelerating function.Molecular and cellular biology · 1994Article
- Molecular characterization of a 17q11.2 translocation in a malignant schwannoma cell line.Human genetics · 1992Article
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Authors and funding
6 authors at 3 institutions in 1 country.
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Abstract
Malignant schwannomas are soft-tissue neoplasms that occur at increased frequency with germline alterations of the neurofibromatosis-1 (NF1) gene at 17q11.2. We report molecular and cytogenetic characterization of a malignant schwannoma cell line established from an individual affected with NF1. This cell line has a complex hyperdiploid karyotype with two cytogenetically identical der(13)t(13;17)(p11,q11.2) chromosomes. Using somatic cell hybrids, we mapped twelve chromosome-17 probes to either the der(13)t(13;17) chromosome or a small der(17) chromosome. Two chromosome-17p loci, including the p53 tumor suppressor gene, were present in the schwannoma cell line, but did not map to either of these chromosomes. Loss of heterozygosity studies indicated that the two der(13)t(13;17) chromosomes arose by duplication, presumably after the translocation event. The 17q11.2 translocation break-point maps distal to the NF1 gene, and may not disrupt its functioning. Although NF1 mRNA was detected in this cell line by polymerase chain reaction, Northern blot analysis revealed very little or none of the 13-kb mature NF1 transcript. This suggests that the single remaining allele of the NF1 gene contains a mutation that results in either greatly reduced transcription or message instability.
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