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early cell cultures the presence of SV 40 related T antigens was described (Weiss et a1., 1975;<br />
Scherneck et aI., 1979; Krieg et aI., 1981). However, these findings were not confirmed by<br />
others (Merletti et a1., 1975).<br />
4.6 Cytogenetic and molecular genetic studies of meningiomas<br />
As early as 1967, cytogenetic studies showed non-random loss of one G-group chromosome<br />
in meningiomas. This was the first specific chromosomal aberration observed in solid tumors<br />
(Zang and Singer, 1967). The subsequent development of banding techniques and molecular<br />
genetic studies revealed that monosomy of chromosome 22 is the hallmark for these tumors<br />
(Zang, 1982; Seizinger et a1., 1987a; Dumanski et aI., 1990a). In a considerable number of<br />
tumors loss of chromosome 22 is the only cytogenetically visible chromosomal alteration (AI<br />
Saadi et a1., 1987; Maltby et a1., 1988; Vagner-Capodano et aI., 1993). These results<br />
indicate that loss of genetic material from this chromosome is a primary and specific event<br />
in the development of these tumors, which is reminiscent of the involvement of a tumor<br />
suppressor gene(s) as is mentioned in section 2. In addition, other less common non random<br />
chromosomal changes occur. The most frequent ones are loss or rearrangements of<br />
chromosomes 1, 7, 14, 18 and 19 and these are thought to playa role in tumor progression<br />
(Katsuyama et aI., 1986; AI Saadi et aI., 1987; Maltby et aI., 1988; Rey et aI., 1988;<br />
Casalone et aI., 1990). The karyotypic evolution observed in meningiomas appears to be<br />
associated with more anaplastic features (Vagner-Capodano et aI., 1993).<br />
As mentioned earlier the majority of meningiomas are sporadic cases but they are also<br />
found in patients with NF2 or in familial or multiple meningioma patients. Genetic linkage<br />
studies in NF2 families, tumor deletion mapping in both sporadic and hereditary meningioma<br />
cases resulted in the identification of at least three different loci on the long arm of<br />
chromosome 22, which might be involved in the pathogenesis of meningioma. In figure 3 the<br />
three chromosome 22 loci are depicted.<br />
Evidence for the involvement of the most proximal locus in band 22q 11 came from<br />
cytogenetic and molecular genetic findings in two independent patients with meningiomas.<br />
The meningioma from the first patient revealed a reciprocal t(4;22)(pI6;qll), which resulted<br />
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