Glioblastoma

Hans Georg Wirsching, Evanthia Galanis, Michael Weller

Research output: Chapter in Book/Report/Conference proceedingConference contribution

26 Citations (Scopus)

Abstract

Glioblastoma is the most common and aggressive primary brain tumor in adults. Defining histopathologic features are necrosis and endothelial proliferation, resulting in the assignment of grade IV, the highest grade in the World Health Organization (WHO) classification of brain tumors. The classic clinical term "secondary glioblastoma" refers to a minority of glioblastomas that evolve from previously diagnosed WHO grade II or grade III gliomas. Specific point mutations of the genes encoding isocitrate dehydrogenase (IDH) 1 or 2 appear to define molecularly these tumors that are associated with younger age and more favorable outcome; the vast majority of glioblastomas are IDH wild-type. Typical molecular changes in glioblastoma include mutations in genes regulating receptor tyrosine kinase (RTK)/rat sarcoma (RAS)/phosphoinositide 3-kinase (PI3K), p53, and retinoblastoma protein (RB) signaling. Standard treatment of glioblastoma includes surgery, radiotherapy, and alkylating chemotherapy. Promoter methylation of the gene encoding the DNA repair protein, O6-methylguanyl DNA methyltransferase (MGMT), predicts benefit from alkylating chemotherapy with temozolomide and guides choice of first-line treatment in elderly patients. Current developments focus on targeting the molecular characteristics that drive the malignant phenotype, including altered signal transduction and angiogenesis, and more recently, various approaches of immunotherapy.

Original languageEnglish (US)
Title of host publicationGliomas, 2016
PublisherElsevier
Pages381-397
Number of pages17
Volume134
ISBN (Print)9780128029978
DOIs
StatePublished - 2016

Publication series

NameHandbook of Clinical Neurology
Volume134
ISSN (Print)00729752
ISSN (Electronic)22124152

Fingerprint

Glioblastoma
Isocitrate Dehydrogenase
temozolomide
Brain Neoplasms
Genes
Drug Therapy
Retinoblastoma Protein
1-Phosphatidylinositol 4-Kinase
Methyltransferases
Receptor Protein-Tyrosine Kinases
Point Mutation
Glioma
DNA Repair
Sarcoma
Immunotherapy
Methylation
Signal Transduction
Necrosis
Radiotherapy
Phenotype

Keywords

  • Angiogenesis
  • Glioblastoma
  • Glioma-initiating cell
  • Immunotherapy
  • Molecular subtype
  • Radiotherapy
  • Temozolomide

ASJC Scopus subject areas

  • Clinical Neurology
  • Neurology

Cite this

Wirsching, H. G., Galanis, E., & Weller, M. (2016). Glioblastoma. In Gliomas, 2016 (Vol. 134, pp. 381-397). (Handbook of Clinical Neurology; Vol. 134). Elsevier. https://doi.org/10.1016/B978-0-12-802997-8.00023-2

Glioblastoma. / Wirsching, Hans Georg; Galanis, Evanthia; Weller, Michael.

Gliomas, 2016. Vol. 134 Elsevier, 2016. p. 381-397 (Handbook of Clinical Neurology; Vol. 134).

Research output: Chapter in Book/Report/Conference proceedingConference contribution

Wirsching, HG, Galanis, E & Weller, M 2016, Glioblastoma. in Gliomas, 2016. vol. 134, Handbook of Clinical Neurology, vol. 134, Elsevier, pp. 381-397. https://doi.org/10.1016/B978-0-12-802997-8.00023-2
Wirsching HG, Galanis E, Weller M. Glioblastoma. In Gliomas, 2016. Vol. 134. Elsevier. 2016. p. 381-397. (Handbook of Clinical Neurology). https://doi.org/10.1016/B978-0-12-802997-8.00023-2
Wirsching, Hans Georg ; Galanis, Evanthia ; Weller, Michael. / Glioblastoma. Gliomas, 2016. Vol. 134 Elsevier, 2016. pp. 381-397 (Handbook of Clinical Neurology).
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