Peritumoral brain edema in intracranial meningiomas: the emergence of vascular endothelial growth factor–directed therapy

Abstract

<jats:p>Meningioma is the second most common type of adult intracranial neoplasm. A substantial subset of patients present with peritumoral brain edema (PTBE), which can cause significant morbidity via mass effect, complicate surgical management, and impact the safety of stereotactic radiosurgery. Recent studies suggest a close relationship between vascular endothelial growth factor-A (VEGF-A) expression and PTBE development in meningiomas. The authors performed a systematic review of the literature on the pathogenesis of PTBE in meningiomas, the effectiveness of steroid therapy, the role played by VEGF-A, and the current clinical evidence for antiangiogenic therapy to treat peritumoral brain edema. Mounting evidence suggests VEGF-A is secreted directly by meningioma cells to induce angiogenesis and edemagenesis of tumoral as well as peritumoral brain tissue. The VEGF-A cascade results in recruitment of cerebral-pial vessels and disruption of the tumor-brain barrier, which appear to be requisite for VEGF-A to have an edemagenic effect. Results of preliminary clinical studies suggest VEGF-directed therapy has modest activity against recurrent and progressive meningioma growth but can alleviate PTBE in some patients. A comprehensive understanding of the VEGF-A pathway and its modulators may hold the key to an effective therapeutic approach to treating PTBE associated with meningiomas. Further clinical trials with larger patient cohorts and longer follow-up periods are warranted to confirm the efficacy of VEGF-directed therapy.</jats:p>

Mechanisms of Global Cerebral Edema Formation in Aneurysmal Subarachnoid Hemorrhage

“…71 Although originally studied in oncology for its role in angiogenesis, recent studies in the field of neuro-oncology have highlighted the important edemagenic role of VEGF in brain tumors. 72 As part of the angiogenic process, VEGF potently induces the formation of capillary fenestrations, allowing for leakage of fluid and large molecules. 73 Given that VEGF production in the brain is significantly upregulated following aSAH, VEGF-mediated blood-brain barrier disruption forms a highly plausible mechanism for edema formation following aSAH.…”

Pearls & Oy-sters: Persistent elevation of serum carcinoembryonic antigen in secretory meningioma

“…5 Secretion of proinflammatory and proangiogenic mediators such as histamine, serotonin, and vascular endothelial growth factor (VEGF) by mast cells can play a major role in the development of peritumoral edema in SM. 8,9 As noted above, pseudopsammoma bodies often stain positive for CEA when immunohistochemistry is performed in SM tissue samples. However, elevated serum CEA levels are only present in 50%-60% of patients with SM.…”

Intracranial Venous Sinuses Characteristics Prior To And Following Resection Of Brain Tumors

“…A significant brain edema characterizes mainly rapidly growing brain tumors (e.g. metastases and primary brain tumors), but can also be caused in cases of slowly growing benign brain tumors like meningiomas [18]. Another mechanism in which brain tumors can cause elevation in ICP is interference in the natural CSF drainage resulting in obstructive hydrocephalus [19,20].…”