The average DDX3X immunostaining score was significantly higher in meningiomas than non-neoplastic brain tissues and significantly higher in atypical meningiomas than in various subtypes of benign meningiomas.
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.
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).
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.
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.
Together with histological grade, increased co-expression of MIF and MMP9 in tumor might be a valuable predictor for recurrence, especially for benign meningiomas.
Together with histological grade, increased co-expression of MIF and MMP9 in tumor might be a valuable predictor for recurrence, especially for benign meningiomas.
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).
Additionally, we found significant upregulation of CCNB1 and MKI67 in recurrent tumors in comparison with primary tumors of benign meningiomas (P<0.05).
We performed direct sodium bisulfite sequencing in a series of 50 meningiomas, including 27 benign meningiomas [World Health Organization (WHO) grade I], 11 atypical meningiomas (WHO grade II) and 12 anaplastic meningiomas (WHO grade III), and found hypermethylation of TIMP3 in 67% of anaplastic meningiomas, but only 22% of atypical and 17% of 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).
We examined by immunohistochemistry the expression of HGF/SF and its cMET receptor in a group of patients with benign meningioma with or without recurrence (n = 17 and n = 25, respectively), after a minimal follow-up of least 6 years.
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.
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).
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.
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).
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.
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).
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%).
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.