Within the confines of this study, it is concluded that: 1) the estrogen receptor is generally absent in meningioma tissue, and 2) the progesterone receptor is mainly absent in the nuclear compartment, leading to the conclusion that the cytosolic progesterone receptor may be an inactive form.
The high number of SS receptors found in meningiomas is therefore unlikely to be regulated by an autocrine SS production from the meningioma tissue itself but rather from another, unknown distant SS source.
Within the confines of this study, it is concluded that: 1) the estrogen receptor is generally absent in meningioma tissue, and 2) the progesterone receptor is mainly absent in the nuclear compartment, leading to the conclusion that the cytosolic progesterone receptor may be an inactive form.
The localization of breakpoints in these 9 cases with deletions suggests that a meningioma locus is localized distal to myoglobin locus, within 22q12.3-qter.
The minimal deletion common to 81 meningiomas, and thus the position of the tentative meningioma tumour suppressor gene (TSG), has been determined to lie distal to the myoglobin locus on the long arm of chromosome 22, corresponding to the region 22q12.3-qter.
A deletion in an Alu repetitive sequence in the fifth intron of the c-sis gene of meningioma patients was previously described (M. Smidt et al., J. Clin.Invest., 86:1151-1157, 1990).
A consecutive series of six meningiomas and one meningioma/neurofibroma derived from a patient with neurofibromatosis type 2 was investigated and it was found that the growth of all seven tumours in response to mitotic stimuli (fetal bovine serum or epidermal growth factor) is strongly inhibited by IFN-alpha.
These data suggest that progesterone receptor mRNA and protein is expressed in meningiomas and support the concept that progesterone may play an important role in meningioma growth.
The presence of ER variants missing exon 4, which is probably not able to bind heat shock protein 90 and therefore may be constitutively active, might explain the autonomous expression of PR in meningioma.
Northern analysis of RNA from four meningiomas showed IGF-II mRNA of 6.0, 4.8, and 2.2 kb, and in situ hybridization revealed that meningioma tumor cells contained IGF-II mRNA.
In the last set of experiments, the functionality of the PDGF-beta-R was determined by examining the induction of the proto-oncogene c-fos by PDGF-BB in meningioma cell cultures.
A 140 kb homozygous deletion from 22q12 in one meningioma directed us towards the cloning and characterization of a new member of the human beta-adaptin gene family (named BAM22).