Literature DB >> 8640707

Cytogenetic analysis of aggressive meningiomas: possible diagnostic and prognostic implications.

A Perry1, R B Jenkins, R J Dahl, C A Moertel, B W Scheithauer.   

Abstract

BACKGROUND: Published karyotypes from aggressive (atypical and malignant) meningiomas are few, but suggest clonal evolution from benign tumors with monosomy 22 to aggressive forms with additional abnormalities. The goal of this study was to identify the most frequent karyotypic abnormalities associated with aggressive histopathology and biologic behavior.
METHODS: Eight intracranial meningiomas exhibiting histologically atypical features at the time of intraoperative diagnosis were chosen for cytogenetic analysis. The study set was comprised entirely of histologically atypical meningiomas. Four were considered malignant; three on the basis of brain invasion and one due to extracranial metastases. None was histologically anaplastic.
RESULTS: Chromosomal abnormalities were demonstrated in 6 cases (75%), 5 of which were complex (63%). Loss of chromosome 22 was identified in two cases, both of which were associated with additional aberrations. Abnormalities most frequently involved chromosomes 1 (63%), 3 (50%), and 6 (63%). Four cases (50%) had dicentric or ring chromosomes. An additional 47 previously reported karyotypes from atypical and malignant meningiomas were reviewed. Comparison with published karyotypes of 200 histologically benign meningiomas served to underscore the increased frequency of complex karyotypes, chromosome 1, 3, and 6 abnormalities, and telomeric associations in the aggressive tumors. Apparently normal karyotypes as well as monosomy 22 alone were more frequently associated with benign, nonatypical histopathology.
CONCLUSIONS: These findings suggest a possible role for cytogenetic analysis in determining the prognosis and perhaps in refining the diagnosis of atypical or aggressive meningiomas. Further studies are necessary to determine the significance of complex karyotypes, chromosome 1, 3, and 6 abnormalities, and telomeric associations, particularly whether they portend a more aggressive clinical course in meningiomas lacking features of histologic atypia.

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Year:  1996        PMID: 8640707     DOI: 10.1002/(SICI)1097-0142(19960615)77:12<2567::AID-CNCR21>3.0.CO;2-P

Source DB:  PubMed          Journal:  Cancer        ISSN: 0008-543X            Impact factor:   6.860


  11 in total

1.  Comparative genomic hybridization analysis of genetic alterations associated with malignant progression of meningioma.

Authors:  S Ozaki; T Nishizaki; H Ito; K Sasaki
Journal:  J Neurooncol       Date:  1999-01       Impact factor: 4.130

2.  Expression of TGFalpha in meningiomas.

Authors:  J Halper; C Jung; A Perry; H Suliman; M P Hill; B Scheithauer
Journal:  J Neurooncol       Date:  1999       Impact factor: 4.130

3.  Intratumoral patterns of clonal evolution in meningiomas as defined by multicolor interphase fluorescence in situ hybridization (FISH): is there a relationship between histopathologically benign and atypical/anaplastic lesions?

Authors:  José María Sayagués; María Dolores Tabernero; Angel Maíllo; Ana Espinosa; Ana Rasillo; Pedro Díaz; Juana Ciudad; Antonio López; Marta Merino; Jesús María Gonçalves; Angel Santos-Briz; Francisco Morales; Alberto Orfao
Journal:  J Mol Diagn       Date:  2004-11       Impact factor: 5.568

4.  Oncogenic role of p53 is suppressed by si-RNA bicistronic construct of uPA, uPAR and cathepsin-B in meningiomas both in vitro and in vivo.

Authors:  Reshu Gupta; Venkateswara Rao Gogineni; Arun Kumar Nalla; Chandramu Chetty; Jeffrey D Klopfenstein; Andrew J Tsung; Sanjeeva Mohanam; Jasti S Rao
Journal:  Int J Oncol       Date:  2011-02-02       Impact factor: 5.650

5.  Chromosome 1p36 and 22qter deletions in paraffin block sections of intracranial meningiomas.

Authors:  Zerrin Yilmaz; Feride Iffet Sahin; Basar Atalay; Ozlem Ozen; Hakan Caner; Murad Bavbek; Beyhan Demirhan; Nur Altinörs
Journal:  Pathol Oncol Res       Date:  2005-12-31       Impact factor: 3.201

6.  Genetic profiling by single-nucleotide polymorphism-based array analysis defines three distinct subtypes of orbital meningioma.

Authors:  Cheng-Ying Ho; Stacy Mosier; Janice Safneck; Diva R Salomao; Neil R Miller; Charles G Eberhart; Christopher D Gocke; Denise A S Batista; Fausto J Rodriguez
Journal:  Brain Pathol       Date:  2014-05-21       Impact factor: 6.508

7.  Diagnostic impact of ornithine decarboxylase in meningiomas.

Authors:  Werner Stenzel; Gabriele Röhn; Hrvoje Miletic; Herbert Radner; Martina Deckert; Ralf-Ingo Ernestus
Journal:  J Neurooncol       Date:  2004-01       Impact factor: 4.130

8.  Matrix metalloproteinase-2 and matrix metalloproteinase-9 expressions correlate with the recurrence of intracranial meningiomas.

Authors:  Masaki Okada; Keisuke Miyake; Yoshihito Matsumoto; Nobuyuki Kawai; Katsuzo Kunishio; Seigo Nagao
Journal:  J Neurooncol       Date:  2004-01       Impact factor: 4.130

9.  Molecular biological determinations of meningioma progression and recurrence.

Authors:  Stefan Linsler; Dennis Kraemer; Christina Driess; Joachim Oertel; Kai Kammers; Jörg Rahnenführer; Ralf Ketter; Steffi Urbschat
Journal:  PLoS One       Date:  2014-04-10       Impact factor: 3.240

10.  Anaplastic Meningioma Presenting as a Left Parietal Mass: A Case Report.

Authors:  Marwan W Najjar; Nour H Abdul Halim; Fares R Sukhon; Bassem Youssef; Hazem I Assi
Journal:  Am J Case Rep       Date:  2017-11-04
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