TERT Promoter Alterations in Glioblastoma: A Systematic Review

Olympios, Nathalie; Gilard, Vianney; Marguet, Florent; Clatot, Florian; Fiore, Frédéric Di

doi:10.3390/cancers13051147

Cited by 44 publications

(35 citation statements)

References 123 publications

(120 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Its dysfunction also causes immense genomic instability. This alteration is present in 44% of GBM [204].…”

Section: Rb Signal Alterationmentioning

confidence: 94%

Tracing the Origins of Glioblastoma by Investigating the Role of Gliogenic and Related Neurogenic Genes/Signaling Pathways in GBM Development: A Systematic Review

Shafi

Siddiqui

2022

Preprint

View full text Add to dashboard Cite

Background: Glioblastoma is one of the most aggressive tumors. The etiology and the factors determining its onset are not yet entirely known. This study investigates the origins of GBM and for this purpose it focuses primarily on developmental gliogenic processes. It also focuses on impact of the related neurogenic developmental processes in glioblastoma oncogenesis. It also addresses why glial cells are at more risk of tumor development compared to neurons.Methods: Databases including PubMed, MEDLINE and Google Scholar were searched for published articles without any date restrictions, involving glioblastoma, gliogenesis, neurogenesis, stemness, neural stem cells, gliogenic signaling and pathways, neurogenic signaling and pathways, astrocytogenic genes. Results: The origin of GBM is dependent on dysregulation in multiple genes and pathways that accumulatively converge the cells towards oncogenesis. There are multiple layers of steps in glioblastoma oncogenesis including the failure of cell fate specific genes to keep the cells differentiated in their specific cell type such as p300, BMP, HOPX, NRSF/REST and others. There are genes and signaling pathways that are involved in differentiation and also contribute to GBM such as FGFR3, JAK-STAT, hey1 and others. The genes that contribute to differentiation processes but also contribute to stemness in GBM include notch, Sox9, Sox4, c-myc gene overrides p300 and then GFAP, leading to upregulation of nestin, SHH, NF-κB and others. GBM mutations pathologically impact the cell circuitry such as the interaction between Sox2 and JAK-STAT pathway, resulting in GBM development and progression.Conclusion: Glioblastoma originates when the gene expression of key gliogenic genes and signaling pathways become dysregulated. This study identifies key gliogenic genes having the ability to control oncogenesis in glioblastoma cells, including p300, BMP, PAX6, HOPX, NRSF/REST, LIF, TGF beta. It also identifies key neurogenic genes having the ability to control oncogenesis including PAX6, neurogenins including Ngn1, NeuroD1, NeuroD4, Numb, NKX6-1 Ebf, Myt1, ASCL1 and others. This study also postulates how aging contributes to the onset of glioblastoma by dysregulating the gene expression of NF-κB, REST/NRSF, ERK, AKT, EGFR and others.

show abstract

“…Its dysfunction also causes immense genomic instability. This alteration is present in 44% of GBM [204].…”

Section: Rb Signal Alterationmentioning

confidence: 94%

Tracing the Origins of Glioblastoma by Investigating the Role of Gliogenic and Related Neurogenic Genes/Signaling Pathways in GBM Development: A Systematic Review

Shafi

Siddiqui

2022

Preprint

View full text Add to dashboard Cite

show abstract

“…Since multiple molecular pathways lead to telomerase activation, there are several targeting strategies including vaccines and immunotherapies [ 44 ]. To date, there are no approved TERT promoter glioblastoma therapies.…”

Section: Diffuse Gliomamentioning

confidence: 99%

Imaging diagnosis and treatment selection for brain tumors in the era of molecular therapeutics

et al. 2022

View full text Add to dashboard Cite

Currently, most CNS tumors require tissue sampling to discern their molecular/genomic landscape. However, growing research has shown the powerful role imaging can play in non-invasively and accurately detecting the molecular signature of these tumors. The overarching theme of this review article is to provide neuroradiologists and neurooncologists with a framework of several important molecular markers, their associated imaging features and the accuracy of those features. A particular emphasis is placed on those tumors and mutations that have specific or promising imaging correlates as well as their respective therapeutic potentials.

show abstract

“…Mutations in the promoter of telomerase reverse transcriptase (TERT) are the most common mutations found in GBM, in up to 86% (46,47). Two mutually exclusive hotspots are located -124bp and -146bp upstream of the transcription start site (TSS) and both are C>T transitions, which create DNA consensus sites enabling binding of transcription factors and increased expression of the gene (46,48). TERT promoter mutations as well as TP53, EGFR, and PTEN mutations are believed to occur early during gliomagenesis because they were found in matched GBM tissue samples and the distant subventricular zone (SVZ), which is believed to be the place of origin of gliomas (49).…”

Section: Tert Mutationsmentioning

confidence: 99%

Biomarkers In Brain Tumors With Focus On Glioblastoma

Łysiak

2022

Linköping University Medical Dissertations

View full text Add to dashboard Cite

TERT Promoter Alterations in Glioblastoma: A Systematic Review

Cited by 44 publications

References 123 publications

Tracing the Origins of Glioblastoma by Investigating the Role of Gliogenic and Related Neurogenic Genes/Signaling Pathways in GBM Development: A Systematic Review

Tracing the Origins of Glioblastoma by Investigating the Role of Gliogenic and Related Neurogenic Genes/Signaling Pathways in GBM Development: A Systematic Review

Imaging diagnosis and treatment selection for brain tumors in the era of molecular therapeutics

Biomarkers In Brain Tumors With Focus On Glioblastoma

Contact Info

Product

Resources

About