Meningioma: Signaling pathways and tumor growth

Burnett, Brian; Womeldorff, Matthew Robert; Jensen, Randy L.

doi:10.1016/b978-0-12-804280-9.00009-3

Cited by 10 publications

(17 citation statements)

References 56 publications

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“…Notably, it has been reported that both MAPK and PI3K/Akt pathways are activated in benign and malignant meningiomas [31]. Activation of PI3K/Akt signaling might be responsive to the aggressive behavior of malignant meningiomas, whereas MAPK activation contributes to their proliferation and apoptosis [32]. And co-targeting PI3K/Akt/mTOR and MAPK pathways improved cell proliferation inhibition in comparison to the target of each pathway alone [33].…”

Section: Discussionmentioning

confidence: 99%

Identification of key genes of anti-programmed death ligand 1 for meningioma immunotherapy by bioinformatic analysis

Zhang

Wang

Tan

et al. 2022

Preprint

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Meningioma is one of the most common primary tumors in the central nervous system (CNS). A deeper understanding of its molecular characterization could provide potential therapeutic targets to reduce recurrence. In this study, we attempted to identify specific gene mutations in meningioma for immunotherapy. One GSE43290 dataset was obtained from the Gene Expression Omnibus (GEO) database to find differentially expressed genes (DEGs) between meningioma tissues and normal meninges. In total, 420 DEGs were identified, including 15 up-regulated and 405 down-regulated genes. Functional enrichment analysis showed that these DEGs were mainly enriched in PI3K-Akt signaling pathway, Focal adhesion, and MAPK signaling pathway. We identified 20 hub genes by protein-protein interaction (PPI) analysis. Among the hub genes, the expression of FLT1, CXCL8, JUN, THBS1, FECAM1, CD34, and FGF13 were negatively correlated with Programmed Death Ligand-1 (PD-L1). Additionally, the expression of those genes was co-regulated by miR-155‐5p. The findings suggest that miR-155-5p play an important role in the pathogenesis of meningioma and may represent potential therapeutic targets for its anti-PD-L1 immunotherapy.

show abstract

Section: Discussionmentioning

confidence: 99%

Identification of key genes of anti-programmed death ligand 1 for meningioma immunotherapy by bioinformatic analysis

Zhang

Wang

Tan

et al. 2022

Preprint

View full text Add to dashboard Cite

show abstract

“…Notably, it has been reported that both MAPK and PI3K/Akt pathways are activated in benign and malignant meningiomas [ 28 ]. Activation of PI3K/Akt signaling might be responsive to the aggressive behavior of malignant meningiomas, whereas MAPK activation contributes to their proliferation and apoptosis [ 29 ]. And co-targeting PI3K/Akt/mTOR and MAPK pathways improved cell proliferation inhibition in comparison to the target of each pathway alone [ 30 ].…”

Section: Discussionmentioning

confidence: 99%

Identification of key genes of anti-programmed death ligand 1 for meningioma immunotherapy by bioinformatic analysis

et al. 2022

View full text Add to dashboard Cite

Meningioma is one of the most common primary tumors in the central nervous system (CNS). A deeper understanding of its molecular characterization could provide potential therapeutic targets to reduce recurrence. In this study, we attempted to identify specific gene mutations in meningioma for immunotherapy. One GSE43290 dataset was obtained from the Gene Expression Omnibus (GEO) database to find differentially expressed genes (DEGs) between meningioma tissues and normal meninges. In total, 420 DEGs were identified, including 15 up-regulated and 405 down-regulated genes. Functional enrichment analysis showed that these DEGs were mainly enriched in PI3K-Akt signaling pathway, Focal adhesion, and MAPK signaling pathway. We identified 20 hub genes by protein–protein interaction (PPI) analysis. Among the hub genes, the expression of FLT1, CXCL8, JUN, THBS1, FECAM1, CD34, and FGF13 were negatively correlated with Programmed Death Ligand-1 (PD-L1). Additionally, the expression of those genes was co-regulated by miR‐155‐5p. The findings suggest that miR-155-5p play an important role in the pathogenesis of meningioma and may represent potential therapeutic targets for its anti-PD-L1 immunotherapy.

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“…When analyzed as a general population, the expression of EGFR in MN ranges between 50% and 89% [93]. Even though EGFR is a potentially targetable molecule, its significance in meningioma might not be prognostic [94]. Caltabiano et al analyzed MN samples using immunohistochemistry and FISH.…”

Section: Epidermal Growth Factor Receptor (Egfr) Inhibitorsmentioning

confidence: 99%

High Grade Meningiomas: Current Therapy Based on Tumor Biology

García-Robledo¹,

Ordóñez-Reyes²,

Ruíz-Patiño³

et al. 2022

Brain Tumors

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Atypical (WHO grade II) and malignant meningiomas (WHO Grade III) are a rare subset of primary intracranial tumors. Due to the high recurrence rate after surgical resection and radiotherapy, there has been a recent interest in exploring other systemic treatment options for these refractory tumors. Recent advances in molecular sequencing of tumors have elucidated new pathways and drug targets currently being studied. This article provides a thorough overview of novel investigational therapeutics, including targeted therapy, immunotherapy, and new technological modalities for atypical and malignant meningiomas. There is encouraging preclinical evidence regarding the efficacy of the emerging treatments discussed in this chapter. Several clinical trials are currently recruiting patients to translate targeted molecular therapy for recurrent and high-grade meningiomas.

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Meningioma: Signaling pathways and tumor growth

Cited by 10 publications

References 56 publications

Identification of key genes of anti-programmed death ligand 1 for meningioma immunotherapy by bioinformatic analysis

Identification of key genes of anti-programmed death ligand 1 for meningioma immunotherapy by bioinformatic analysis

Identification of key genes of anti-programmed death ligand 1 for meningioma immunotherapy by bioinformatic analysis

High Grade Meningiomas: Current Therapy Based on Tumor Biology

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