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Article: Combined molecular genetic studies of chromosome 22q and the neurofibromatosis type 2 gene in central nervous system tumors

TitleCombined molecular genetic studies of chromosome 22q and the neurofibromatosis type 2 gene in central nervous system tumors
Authors
KeywordsChromosome 22q
Meningiomas
Neurofibromatosis type 2 gene
Issue Date1995
Citation
Neurosurgery, 1995, v. 37, n. 4, p. 764-773 How to Cite?
AbstractMONOSOMY OF CHROMOSOME 22 or deletions of 22q have been described in meningiomas and astrocytic tumors, the incidence of which is increased in Type 2 neurofibromatosis. Recently, the gene for neurofibromatosis Type 2 (NF2) has been identified at Chromosome 22q12, and a tumor suppression role has been suggested. Because there have been only a few studies of the NF2 gene on central nervous system tumors other than vestibular schwannomas, we investigated the potential role of NF2 as a tumor suppressor gene in a group of sporadic meningiomas and astrocytomas. Forty-four tumors (26 meningiomas and 18 astrocytic tumors of different grades) were screened for NF2 mutations for the entire 17 exons by the polymerase chain reaction-single-strand conformation polymorphism method. In addition, 37 tumors and their respective constitutional deoxyribonucleic acid were analyzed for loss of heterozygosity of 22q alleles by four polymorphic microsatellite markers. Seven inactivating mutations were found in Exons 4, 5, 6, and 10 in 7 of 26 (27%) meningiomas, but none were found in astrocytic tumors. Altogether, 69% of meningiomas and 20% of astrocytic tumors revealed a loss of heterozygosity of 22q markers. All tumors with NF2 mutations showed concurrent loss of alleles on 22q, thus fulfilling Knudson's criteria for tumor suppressor genes in meningiomas. We conclude that inactivation of the NF2 gene is involved in the pathogenesis of a proportion of meningiomas but not in astrocytic tumors. Because many meningiomas and some astrocytic tumors had allelic loss of 22q but intact NF2, there is a possibility that other tumor suppressor genes exist on 22q and may be involved in the pathogenesis of central nervous system tumors. © by the Congress of Neurological Surgeons.
Persistent Identifierhttp://hdl.handle.net/10722/324990
ISSN
2023 Impact Factor: 3.9
2023 SCImago Journal Rankings: 1.313
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorNg, Ho Keung-
dc.contributor.authorLau, Kin Mang-
dc.contributor.authorTse, Jenny Y.M.-
dc.contributor.authorLo, Kwok Wai-
dc.contributor.authorWong, Joseph H.C.-
dc.contributor.authorPoon, Wai Sang-
dc.contributor.authorHuang, Dolly P.-
dc.date.accessioned2023-02-27T07:28:48Z-
dc.date.available2023-02-27T07:28:48Z-
dc.date.issued1995-
dc.identifier.citationNeurosurgery, 1995, v. 37, n. 4, p. 764-773-
dc.identifier.issn0148-396X-
dc.identifier.urihttp://hdl.handle.net/10722/324990-
dc.description.abstractMONOSOMY OF CHROMOSOME 22 or deletions of 22q have been described in meningiomas and astrocytic tumors, the incidence of which is increased in Type 2 neurofibromatosis. Recently, the gene for neurofibromatosis Type 2 (NF2) has been identified at Chromosome 22q12, and a tumor suppression role has been suggested. Because there have been only a few studies of the NF2 gene on central nervous system tumors other than vestibular schwannomas, we investigated the potential role of NF2 as a tumor suppressor gene in a group of sporadic meningiomas and astrocytomas. Forty-four tumors (26 meningiomas and 18 astrocytic tumors of different grades) were screened for NF2 mutations for the entire 17 exons by the polymerase chain reaction-single-strand conformation polymorphism method. In addition, 37 tumors and their respective constitutional deoxyribonucleic acid were analyzed for loss of heterozygosity of 22q alleles by four polymorphic microsatellite markers. Seven inactivating mutations were found in Exons 4, 5, 6, and 10 in 7 of 26 (27%) meningiomas, but none were found in astrocytic tumors. Altogether, 69% of meningiomas and 20% of astrocytic tumors revealed a loss of heterozygosity of 22q markers. All tumors with NF2 mutations showed concurrent loss of alleles on 22q, thus fulfilling Knudson's criteria for tumor suppressor genes in meningiomas. We conclude that inactivation of the NF2 gene is involved in the pathogenesis of a proportion of meningiomas but not in astrocytic tumors. Because many meningiomas and some astrocytic tumors had allelic loss of 22q but intact NF2, there is a possibility that other tumor suppressor genes exist on 22q and may be involved in the pathogenesis of central nervous system tumors. © by the Congress of Neurological Surgeons.-
dc.languageeng-
dc.relation.ispartofNeurosurgery-
dc.subjectChromosome 22q-
dc.subjectMeningiomas-
dc.subjectNeurofibromatosis type 2 gene-
dc.titleCombined molecular genetic studies of chromosome 22q and the neurofibromatosis type 2 gene in central nervous system tumors-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1227/00006123-199510000-00022-
dc.identifier.pmid8559307-
dc.identifier.scopuseid_2-s2.0-0029097158-
dc.identifier.volume37-
dc.identifier.issue4-
dc.identifier.spage764-
dc.identifier.epage773-
dc.identifier.eissn1524-4040-
dc.identifier.isiWOS:A1995RY96800067-

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