Glioblastoma: pathology, molecular mechanisms and markers
Abstract
Recent advances in genomic technology have led to a better understanding of key molecular alterations that underlie glioblastoma (GBM). The current WHO-based classification of GBM is mainly based on histologic features of the tumor, which frequently do not reflect the molecular differences that describe the diversity in the biology of these lesions. The current WHO definition of GBM relies on the presence of high-grade astrocytic neoplasm with the presence of either microvascular proliferation and/or tumor necrosis. High-throughput analyses have identified molecular subtypes and have led to progress in more accurate classification of GBM. These findings, in turn, would result in development of more effective patient stratification, targeted therapeutics, and prediction of patient outcome. While consensus has not been reached on the precise nature and means to sub-classify GBM, it is clear that IDH-mutant GBMs are clearly distinct from GBMs without IDH1/2 mutation with respect to molecular and clinical features, including prognosis. In addition, recent findings in pediatric GBMs regarding mutations in the histone H3F3A gene suggest that these tumors may represent a 3rd major category of GBM, separate from adult primary (IDH1/2 wt), and secondary (IDH1/2 mut) GBMs. In this review, we describe major clinically relevant genetic and epigenetic abnormalities in GBM-such as mutations in IDH1/2, EGFR, PDGFRA, and NF1 genes-altered methylation of MGMT gene promoter, and mutations in h…
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The histological organization of the neoplasms is reminiscent of glioblastoma.
“This histological organization is reminiscent of GBM [23].”
From MiR-338-3p regulates neuronal maturation and suppresses glioblastoma proliferation. (2017) · cites this paper as [23]
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- Authors
- Aldape, K., Zadeh, G., Mansouri, S., Reifenberger, G., & von Deimling, A.
- Venue
- Acta Neuropathologica
- Published
- 2015-05-06
- Volume
- 129
- Issue
- 6
- Pages
- 829-848
- ISSN
- 0001-6322
- 1432-0533
- Cited by
- 621
- References
- 11
- Language
- en
- Licence
- www.springer.com/tdm (tdm)
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