Artikel
Hyperdiploidy defines a distinct cytogenetic entity of aggressive meningiomas
Hyperdiploidy definiert eine eigenständige Gruppe von aggressiven Meningeomen
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Autoren
Veröffentlicht: | 4. Mai 2005 |
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Gliederung
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Objective
The most common chromosomal aberration found in meningiomas of all grades is monosomy 22. Progression and recurrence of meningiomas is usually associated with stronger hypodiploidy, i.e., monosomy of further autosomes and, most frequently, heterozygous loss of chromosome 1p. Rarely, however, hyperdiploid karyotypes occur; the objective of this study was to explore the cytogenetic and histopathologic patterns as well as the clinical significance of hyperdiploidy in meningiomas.
Methods
A consecutive series of over 400 meningiomas were cultured in vitro and cytogenetically characterized using standard banding techniques and, in one structurally aberrant case, spectral karyotyping (SKY). In patients with hyperdiploid meningiomas, clinical and histomorphological data as well as results of long-term postoperative survey were compared with data from patients with cytogenetically typical meningiomas.
Results
We identified a subgroup comprising about 4 % of all meningiomas that do not display the common chromosome losses but instead a strikingly uniform pattern of hyperdiploidy. Mostly in the absence of structural chromosome rearrangements, these meningiomas each have between 49 and 56 chromosomes, with trisomy 12 (14/16 cases), trisomy 20 (13/16 cases), trisomy 5 (12/16 cases), and trisomy 17 (10/16 cases), along with variable trisomies of all other autosomes except #1, #2, and #21. Chromosome losses are rare, affecting #22 in 2/16, and #7 and Y each in only 1/16 cases. Histomorphologically, the hyperdiploid meningiomas show intermediate differentiation with patternless growth and/ or microcystic degeneration. However, a loss of chromosome 22 may be associated with a persistent fibrous growth pattern. The proliferative potential in terms of increased mitotic activity and Ki-67 labelling index is significantly elevated; all investigated hyperdiploid meningiomas were assigned to WHO grade II. 14 patients in whom tumor resections were determined to be simpson grade I or II and 2 patients with simpson grade III could be followed up after tumor extirpation. In 2 patients recurrences were documented and 3 patients died during the period of observation.
Conclusions
We conclude that hyperdiploidy constitutes a small but clinically relevant entity of biologically aggressive, histopathologically atypical meningiomas (WHO grade II), which are cytogenetically distinguishable from the majority of common-type meningiomas.