User Tools

Site Tools




Neurosurgery Service, Alicante University General Hospital, Alicante Institute for Health and Biomedical Research (ISABIAL - FISABIO Foundation), Alicante, Spain.


During the early 19th century, glioblastoma was considered of mesenchymal origin and was defined as a sarcoma. In 1863, Rudolf Ludwig Karl Virchow demonstrated its glial origin 1) , and in 1914 Mallory proposed the term glioblastoma multiforme. However, it was not until 1925 that Globus and Strass presented a complete description of the neoplasm, at which point the most common term became spongioblastoma multiforme. Finally, in 1926, Bailey and Cushing successfully reintroduced the term originally proposed by Mallory: glioblastoma multiforme.


see Glioblastoma multiforme epidemiology.

Prior malignancies in patients harboring glioblastoma

Patients who develop GBM following a prior malignancy constitute ~8% of patients with GBM. Despite significant molecular differences these two cohorts appear to have a similar overall prognosis and clinical course. Thus, whether or not a patient harbors a malignancy prior to diagnosis of GBM should not exclude him or her from aggressive treatment or for consideration of novel investigational therapies 2).



They are comprised of a heterogeneous population of tumor cells, immune cells, and extracellular matrix.

Interactions among these different cell types and pro-/anti-inflammatory cytokines may promote tumor development and progression.

Histologically, they are characterized by hypercellularity, nuclear pleomorphism, microvascular proliferation, and pseudopalisading necrosis.

Glioblastomas are among the most vascularized tumors in humans. There is also an abnormal vascular remodeling process that leads to microvascular proliferation that is a histopathological hallmark of glioblastoma.

In these tumors, angiogenesis appears to be triggered by expression of vascular endothelial growth factor, an important regulator of tumor blood vessel permeability 3)



Genomic alterations


Other types



Clinical Features

It generally presents with epilepsy, cognitive decline, headache, dysphasia, or progressive hemiparesis. 4).

Seizures as the presenting symptom of glioblastoma predicted longer survival in adults younger than 60 years. The IDH1 R132H mutation and p53 overexpression (>40%) were associated with seizures at presentation. Seizures showed no relationship with the tumor size or proliferation parameters 5).


Diagnostic tools include computed tomography (CT or CAT scan) and magnetic resonance imaging (MRI).

Magnetic resonance imaging (MRI) is the most sensitive and best method of detecting brain tumors.

Magnetic resonance spectroscopy (MRS) is used to study the tumor’s chemical profile and determine the nature of the lesions seen on the MRI.

Positron emission tomography (PET scan) can help detect recurring brain tumors.

see Glioblastoma multiforme magnetic resonance imaging






Case series

Case reports

A 57-year-old man presented with seizures. Until the seizure onset, he had been treated for thyroid cancer and its metastasis to the thoracic vertebral body with the multi-receptor tyrosine kinase inhibitor (RTK) lenvatinib for 4 years. MRI revealed a slightly high intensity lesion in the left frontal base area on T2-weighted or fluid-attenuated inversion recovery (FLAIR) images, and the lesion showed only faint enhancement on T1-weighted images after gadolinium administration. Total resection was performed and the histopathological diagnosis was glioblastoma. However, grade IV histology was observed in only a limited area, and the majority of the specimen showed lower grade histology with moderate vascularization that lacked microvascular proliferation.

Lenvatinib, which is anti-angiogenic, might have affected the radiological characteristics, as well as the pathology of the tumor. Brain tumors arising during treatment with RTKs for other cancers could show atypical imaging findings 6).

Virchow R. Pathologie In Die Krankhaften Geschwülste. Berlin. 1864-1865.
Zacharia BE, DiStefano N, Mader MM, Chohan MO, Ogilvie S, Brennan C, Gutin P, Tabar V. Prior malignancies in patients harboring glioblastoma: an institutional case-study of 2164 patients. J Neurooncol. 2017 May 27. doi: 10.1007/s11060-017-2512-y. [Epub ahead of print] Review. PubMed PMID: 28551847.
Thomas AA, Omuro A. Current role of antiangiogenic strategies for glioblas- toma. Curr Treat Options Oncol. 2014;15:551–66.
Thomas DGT,Graham DI, McKeran RO,Thomas DGT. The clinical study of gliomas. In: Brain tumours: scientific basis, clinical investigation and current therapy. In: Thomas DGT, Graham DI eds. London: Butterworths, 1980:194–230.
Toledo M, Sarria-Estrada S, Quintana M, Maldonado X, Martinez-Ricarte F, Rodon J, Auger C, Aizpurua M, Salas-Puig J, Santamarina E, Martinez-Saez E. Epileptic features and survival in glioblastomas presenting with seizures. Epilepsy Res. 2016 Dec 26;130:1-6. doi: 10.1016/j.eplepsyres.2016.12.013. [Epub ahead of print] PubMed PMID: 28073027.
Arai N, Sasaki H, Tamura R, Obara K, Yoshida K. Unusual magnetic resonance imaging findings of a glioblastoma arising during treatment with lenvatinib for thyroid cancer. World Neurosurg. 2017 Aug 10. pii: S1878-8750(17)31314-1. doi: 10.1016/j.wneu.2017.08.017. [Epub ahead of print] PubMed PMID: 28804045.
glioblastoma.txt · Last modified: 2018/12/10 08:07 by administrador