Allelic loss on chromosomes 1p32, 9p21, 13q14, 16q22, 17p, and 22q12 in meningiomas associated with meningioangiomatosis and pure meningioangiomatosis

Abstract

Meningioangiomatosis (MA) is a rare lesion appearing sporadically or as a part of neurofibromatosis 2. The occurrences of meningiomas arising from MA (MA-M) have raised doubts about the traditional concept of a hamartomatous origin for MA. Cytogenetic or molecular studies on MA, with or without meningiomas, are limited because of the rarity of MA. The current study was to evaluate the loss of heterozygosity (LOH) in seven cases of MA-M and two cases of pure MA. LOH on six chromosomes (1p32, 9p21, 13q14, 16q22, 17p, and 22q12) were investigated using 13 sets of microsatellite markers, including D1S193, D1S463, D22S193, D22S929, D22S282, TP53, D17S796, D16S421, D16S512, D13S118, D13S153, D9S162, and D9S104. PCR was performed using each marker and polymorphic analysis was accomplished by silver staining. Immunohistochemical stain for Ki-67 was carried out and labeling index was measured by using a semiquantitative manual counting method. The meningioma portions of MA-Ms showed LOH for loci on chromosomes 22q12, 9p21, and 1p32 in 57.1% (4/7), 28.6% (2/7), and 28.6% (2/7) of cases, respectively. The MA portions of MA-M had a LOH for loci on 22q12 in 28.6% (2/7) of cases, whereas each pure MA harbored one LOH on either chromosome 22q12 or 9p21. The proliferation indices of MA-Ms were significantly higher in the meningioma than in the MA components. Our data suggest that both the meningioma and the MA undergo the same overlapping clonal process, with the MA-M while undergoing additional genetic alterations that confer a greater proliferative potential.