Multi-Omics Analysis in Initiation and Progression of Meningiomas: From Pathogenesis to Diagnosis

Abstract

Meningiomas are common intracranial tumors that can be cured by surgical resection in most cases. However, the most disconcerting is high-grade meningiomas, which frequently recur despite initial successful treatment, eventually conferring poor prognosis. Therefore, the early diagnosis and classification of meningioma is necessary for the subsequent intervention and an improved prognosis. A growing body of evidence demonstrates the potential of multi-omics study (including genomics, transcriptomics, epigenomics, proteomics) for meningioma diagnosis and mechanistic links to potential pathological mechanism. This thesis addresses a neglected aspect of recent advances in the field of meningiomas at multiple omics levels, highlighting that the integration of multi-omics can reveal the mechanism of meningiomas, which provides a timely and necessary scientific basis for the treatment of meningiomas.

ITF2357 Induces Cell Cycle Arrest and Apoptosis in Meningioma Cells

“…Its treatment includes surgical resection combined with radiotherapy and chemotherapy. However, its frequent recurrence can lead to a poor prognosis [19]. Therefore, research into new approaches to meningioma treatment has become urgent.…”

DNA methylation meningioma biomarkers: attributes and limitations

“…RIC8A is a protein-coding gene that plays a role in the regulation of G protein signaling, which is involved in various physiological processes such as vision, smell, and the response to hormones and neurotransmitters. The RIC8A DNA methylation is associated with pathological phenotypes in meningioma ( Liu et al, 2020 ).…”

“…DNA methylation of NF2, MN1, ARID1B, Semaphorin 4D ( SEMA4D ) , and MUC2 have been implicated in the development of meningiomas. The combined analysis of DNA methylation markers has shown promise in classifying meningiomas into different subtypes and identifying unique molecular and clinical characteristics of meningioma ( Liu et al, 2020 ). AT-rich interactive domain-containing protein 1B (ARID1B) mutations found in the cranial ( Huntoon et al, 2022 ).…”

Unveiling a Biomarker Signature of Meningioma: the Need for a Panel of Genomic, Epigenetic, Proteomic, and RNA Biomarkers to Advance Diagnosis and Prognosis

“…In this study, meningiomas were segregated into Merlin-intact meningiomas (34%, best clinical outcomes and response to cytotoxic drugs, owing to the apoptotic function of the intact Merlin protein), immune-enriched meningiomas (38%, have intermediate prognosis, are distinguished by immune cell infiltration, HLA expression, and lymphatic vessels, and have 22q loss and inactivation of NF2), and hypermitotic meningiomas (28%, have the worst prognosis, high aneuploidy with frequent chromosomal losses, loss of CDKN2A/B, hypermethylation, and resistance to cytotoxic drugs) [62]. Comparative genome hybridization was also used for the identification of chromosome 1p loss in radiation-induced meningiomas, a less prevalent late danger of cranial irradiation, which has a higher recurrence rate and pathologically malignant characteristics than sporadic meningiomas [130]. A study of 31 meningioma cases, using exome, epigenome, and RNA-seq analyses, revealed the presence of NF2 rearrangements in radiation-induced meningiomas, and this may be utilized to differentiate this type of meningioma from sporadic ones [131].…”