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

Abstract

BACKGROUND Meningiomas usually are considered to be benign tumors; however, 10–20% of cases recur. Few disease characteristics have proved to have prognostic 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 fluorescence in situ hybridization, using a specific probe for the bcr gene located in chromosome 22q11.2, on a total of 88 consecutive meningioma patients. The authors also analyzed its correlation with both the clinicobiologic characteristics at presentation and the patient's outcome. RESULTS The authors' results show that monosomy 22 was present in 49% of the cases and that this numeric chromosomal abnormality is not associated with other prognostic features of the disease. In contrast, gains (trisomy/tetrasomy) of chromosome 22 were detected in 8 (9%) cases who simultaneously showed gains for other chromosomes and represent an adverse prognostic factor regarding disease free survival (P = 0.001); in addition, trisomy/tetrasomy 22 was more frequently related to younger patients (P = 0.001), aggressive histopathologic features (P < 0.000), a greater incidence of DNA aneuploidy (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 chromosome 22 is a frequent finding in meningioma tumors, but it does not affect the clinical outcome of these patients. In contrast, gains (trisomy/tetrasomy) of chromosome 22, in the context of an hyperdiploid karyotype, although much less frequent, are associated with a more aggressive disease course. Cancer 2001;92:377–85. © 2001 American Cancer Society.

Global epigenetic profiling identifies methylation subgroups associated with recurrence-free survival in meningioma

“…These findings were generally supported by our analyses with more complex karyotypes clustering in the MM-UNFAV subgroup [17]. Interestingly in our cohort several tumors showed gains of 22q and in support of the published literature when present, they were more likely categorized as of unfavorable clinical course (MM-UNFAV) [44,63,46,75] (Figures 1 and 2). However, on survival analysis this was not significant (Online resource 4).…”

Patterns of BCR/ABL gene rearrangements by interphase fluorescence in situ hybridization (FISH) in BCR/ABL+ leukemias: incidence and underlying genetic abnormalities

“…Hybridization with fluorochrome-labelled FISH probes was performed according to the recommendation of the manufacturers with slight modifications. 19 For the biotinylated probe, appropriate immunologic detection of hybridization was performed using avidin-FITC. 7 Fluorescence signals were evaluated using a BX60 fluorescence microscope (Olympus, Hamburg, Germany) and a  100 oil objective.…”

Hyperdiploidy defines a distinct cytogenetic entity of meningiomas

“…Beyond these anecdotal reports of karyotypes, hyperdiploidy in meningiomas has been demonstrated so far mainly through FISH with probes for single chromosomes, such as # 6, 7, 10, 17, 20, 22, and X [9][10][11]. While gains of chromosome 22 have been shown to be associated with aggressive clinical features of meningiomas [12,13], no conclusive data is at hand so far on the overall pattern of chromosome gains in hyperdiploid meningiomas.…”