Gains of chromosome 22 by fluorescence in situ hybridization in the context of an hyperdiploid karyotype are associated with aggressive clinical features in meningioma patients

Citation
A. Maillo et al., Gains of chromosome 22 by fluorescence in situ hybridization in the context of an hyperdiploid karyotype are associated with aggressive clinical features in meningioma patients, CANCER, 92(2), 2001, pp. 377-385
Citations number
61
Categorie Soggetti
Oncology,"Onconogenesis & Cancer Research
Journal title
CANCER
ISSN journal
0008543X → ACNP
Volume
92
Issue
2
Year of publication
2001
Pages
377 - 385
Database
ISI
SICI code
0008-543X(20010715)92:2<377:GOC2BF>2.0.ZU;2-A
Abstract
BACKGROUND. Meningiomas usually are considered to be benign tumors; however , 10-20% of cases recur. Few disease characteristics have proved to have pr ognostic impact for predicting disease free survival. The objective of the current study was to explore the prognostic value of numeric abnormalities of chromosome 22 for meningioma patients. METHODS. In this study, the authors prospectively analyzed the incidence of numeric chromosome abnormalities of chromosome 22 by interphase fluorescen ce in situ hybridization, using a specific probe for the bcr gene located i n chromosome 22q11.2, on a total of 88 consecutive meningioma patients. The authors also analyzed its correlation with both the clinicobiologic charac teristics at presentation and the patient's outcome. RESULTS. The authors' results show that monosomy 22 was present in 49% of t he cases and that this numeric chromosomal abnormality is not associated wi th other prognostic features of the disease. In contrast, gains (trisomy/te trasomy) of chromosome 22 were detected in 8 (9%) cases who simultaneously showed gains for other chromosomes and represent an adverse prognostic fact or regarding disease free survival (P = 0.001); in addition, trisomy/tetras omy 22 was more frequently related to younger patients (P = 0.001), aggress ive histopathologic features (P < 0.000), a greater incidence of DNA aneupl oidy (P = 0.006), and a higher proportion of S-phase tumor cells (P = 0.02) . CONCLUSIONS, In summary, the authors conclude that loss of a copy of chromo some 22 is a frequent finding in meningioma tumors, but it does not affect the clinical outcome of these patients. In contrast, gains (trisomy/tetraso my) of chromosome 22, in the context of an hyperdiploid karyotype, although much less frequent, are associated with a more aggressive disease course. (C) 2001 American Cancer Society.