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.
Additionally, we found significant upregulation of CCNB1 and MKI67 in recurrent tumors in comparison with primary tumors of benign meningiomas (P<0.05).
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.
ELISA analysis showed that patients with benign meningiomas and ovarian cancers had the highest serum levels of EGFL6 (mean concentration: 672 pg/ml for benign meningiomas, and 616 pg/ml for ovarian cancers).
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.
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).
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.
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).
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.
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.