Mj. Bello et al., CHROMOSOME-22 HETEROZYGOSITY IS RETAINED IN MOST HYPERDIPLOID AND PSEUDODIPLOID MENINGIOMAS, Cancer genetics and cytogenetics, 66(2), 1993, pp. 117-119
Hyperdiploid or pseudodiploid modal chromosome numbers were found char
acterizing six human meningiomas, and all six tumors were disomic for
chromosome 22, The scarce previous reports on the subject suggest that
, in these cytogenetic subgroups of meningiomas, duplication of the re
tained chromosome 22 occurs after the loss of the other member of the
pair, thus correlating well with the main characteristic of meningioma
s, that is, losses of 22. To verify this question, molecular genetic a
nalyses were performed on DNA pairs from blood and tumoral samples of
all six cases, using polymorphic markers for chromosome 22. Restrictio
n fragment length polymorphism studies failed to show any loss of hete
rozygosity for markers located on this chromosome in all six cases, su
ggesting that a different mechanism to that previously proposed might
take place in the hyperdiploid or pseudodiploid meningiomas; perhaps a
submicroscopic involvement (microdeletions or inactivating mutations)
of the meningioma locus (both alleles) may result in an effect simila
r to that produced by monosomy 22 (which probably unmasks recessive mu
tations on the retained allele), enhancing the development of meningio
mas.