Neurosurgery Service, Alicante University General Hospital, Alicante Institute for Health and Biomedical Research (ISABIAL - FISABIO Foundation), Alicante, Spain.
see Glioblastoma History.
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 1).
Glioblastomas are intrinsic brain tumors thought to originate from a neuroglial stem or progenitor cells. More than 90% of glioblastomas are isocitrate dehydrogenase (IDH)-wildtype tumors. Incidence increases with age, males are more often affected. Beyond rare instances of genetic predisposition and irradiation exposure, there are no known glioblastoma risk factors.
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.
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 4).
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 5).