Results showed a high frequency of NF2 gene mutations (40%), increased 22q LOH as aggressiveness increased, frequent losses and gains by MLPA in benign meningiomas, and gene expression silencing by hypermethylation.
The immunoprofile was similar to normal cap cells with one exception; whereas normal cells were uniformly negative forPR, nuclear positivity was seen in 64% of hyperplasias, a frequency similar to that of benign meningiomas.
We also compared the average change in expression level of the three genes (CCNB1, CDC2, and MKI67) in atypical/anaplastic versus benign meningiomas; the difference between the groups was highly significant (P<0.001).
One anaplastic meningioma, three atypical meningiomas, and one benign meningioma without a demonstrated homozygous deletion or mutation of CDKN2A, p14(ARF), or CDKN2B lacked detectable transcripts from at least one of these genes.
In order to investigate the disruption of the p53 function in a patient presenting this mutation and the TP53Arg72Pro polymorphism who had so far suffered five malignant tumors and a benign meningioma, we tested her fibroblasts in response to DNA damage by evaluating the proliferation rate, apoptosis, and disruption of the TP53 pathway.
All cases of atypical and anaplastic meningiomas were positive for c-myc protein and mRNA by immunohistochemistry and in situ hybridisation, respectively, while all 10 benign meningiomas were negative for c-myc immunostaining, with only one benign tumour positive for c-myc mRNA.
No p53 positive cells were recognized in atypical meningiomas, and several cells were weakly stained in only two of 52 benign meningiomas. p53 staining index and immunoblot analysis indicated increasing amounts of p53 protein associated with subsequent recurrences of anaplastic meningiomas.
We found methylation of p14(ARF) gene in five of 58 cases of benign meningiomas (8.6%), two of 10 cases of atypical meningiomas (20%), and two of four cases of anaplastic meningiomas (50%).
C-Myc mRNA and protein levels were not grade-related, but validated subdivision of the 36 benign meningiomas into two groups, Groups IA and IB, based on histological and clinical features (Ki-67-proliferative index, absence or presence of mitoses, rate of recurrence and incidence of perilesional edema).
IGF-II mRNA is present in higher amounts in benign meningiomas than in malignant glioblastomas and astrocytomas, whereas the content of immunoreactive IGF-II is similar.
The present study investigates the role and regulatory mechanism of IL-1β, one of the most important pro-inflammatory cytokines, in the methylation of NF2 in benign meningioma.
Further validation methods for gene expression included quantitative PCR (qPCR), western blot and immunohistochemistry analysis, and these methods confirmed that RIZ1 is significantly downregulated in malignant meningioma tissues, as compared with benign meningiomas.
Western blot analyses showed expression of phosphorylated P1 (45 kD) and P2 (47 kD) Cx43 as well as the unphosphorylated form (42 kD) in 11 of 14 (79%) benign meningiomas.
We have studied the role of micro-RNA 145 (miR-145) in meningiomas and detected significantly reduced miR-145 expression in atypical and anaplastic tumors as compared with benign meningiomas.
Seventy-one percent of the atypical meningiomas exhibited a low level of staining intensity for the galectin-3-binding sites as compared to only 36% of the benign meningiomas (P=0.007).
In this study, we aimed to evaluate the patterns of expression of 23 MMPs, 4 TIMPs, 8 ADAMs, selective growth factors and their receptors in 17 benign meningiomas using a quantitative real-time polymerase chain reaction (qPCR).
In 56 cases, immunostaining for proliferating cell nuclear antigen showed higher proliferating cell fraction in atypical and malignant meningiomas than that in benign meningiomas (p < 0.05).