The neurofibromatosis 2 tumor suppressor gene product, merlin, regulates human meningioma cell growth by signaling through YAP.
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Neurofibromatosis type 2 (NF2) is an autosomal dominant disorder characterized by the occurrence of schwannomas and meningiomas. Several studies have examined the ability of the NF2 gene product, merlin, to function as a tumor suppressor in diverse cell types; however, little is known about merlin growth regulation in meningiomas. In Drosophila, merlin controls cell proliferation and apoptosis by signaling through the Hippo pathway to inhibit the function of the transcriptional coactivator Yorkie. The Hippo pathway is conserved in mammals. On the basis of these observations, we developed human meningioma cell lines matched for merlin expression to evaluate merlin growth regulation and investigate the relationship between NF2 status and Yes-associated protein (YAP), the mammalian homolog of Yorkie. NF2 loss in meningioma cells was associated with loss of contact-dependent growth inhibition, enhanced anchorage-independent growth and increased cell proliferation due to increased S-phase entry. In addition, merlin loss in both meningioma cell lines and primary tumors resulted in increased YAP expression and nuclear localization. Finally, siRNA-mediated reduction of YAP in NF2-deficient meningioma cells rescued the effects of merlin loss on cell proliferation and S-phase entry. Collectively, these results represent the first demonstration that merlin regulates cell growth in human cancer cells by suppressing YAP. (+info)
Bilateral acute subdural hematomas with intracerebral hemorrhage without subarachnoid hemorrhage, caused by rupture of an internal carotid artery dorsal wall aneurysm. Case report.
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A 45-year-old man presented with bilateral acute subdural hematomas (ASDHs) without subarachnoid hemorrhage (SAH). He was found comatose in a parked car. Computed tomography showed left frontal intracerebral hemorrhage (ICH) and bilateral ASDHs but no signs of SAH. Magnetic resonance angiography demonstrated an internal carotid artery dorsal wall aneurysm. Emergent surgical intervention was performed. However, he died of cerebral herniation 6 days later. We inferred that massive intracranial bleeding might have ruptured through the cortex and lacerated the arachnoid membrane. Aneurysm rupture generally results in unilateral SDH, whereas trauma is the usual cause of bilateral ASDHs with ICH. Our case suggests that ruptured aneurysm should be considered in patients with non-traumatic bilateral ASDHs without SAH. (+info)
NF2/merlin is a novel negative regulator of mTOR complex 1, and activation of mTORC1 is associated with meningioma and schwannoma growth.
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Transethmoidal meningoencephalocele involving the olfactory bulb with enlarged foramina of the lamina cribrosa--case report.
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A 3-year-old girl presented with a transethmoidal meningoencephalocele manifesting as recurrent rhinorrhea. Initially, she developed meningitis, but after treatment she experienced rhinorrhea. Two months later, she again presented with rhinorrhea. Neuroimaging studies revealed a small protrusion (15 mm x 10 mm) at the roof of the ethmoidal sinus. Nasal endoscopy confirmed the diagnosis of meningoencephalocele. The operative findings revealed a small hole in the left olfactory bulb, which had descended into an enlarged foramen along with the arachnoid membrane. The left olfactory bulb was removed, and the enlarged foramina of the lamina cribrosa were covered with a frontal pericranial flap. The defect in the bone was very small, but contributed to the development of meningitis and leakage of the cerebrospinal fluid. Basal cephalocele should be considered in a patient with recurrent rhinorrhea and intracranial infections, even in the absence of any apparent anomaly. (+info)
Multiple meningeal cysts affecting the whole craniospinal axis. Case report.
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A 61-year-old female presented with multiple meningeal cysts arising along the whole craniospinal axis, manifesting as trigeminal neuralgia, truncal ataxia, and gradually aggravating headache persisting for 2 years. The patient had suspected Sjogren syndrome, but no other contributory medical history such as infection, subarachnoid hemorrhage, trauma, malignancies affecting the central nervous system, or habitual drug use. Cerebral magnetic resonance imaging revealed displaced trigeminal root and midbrain, distorted cerebellar hemisphere, and ventriculomegaly, which were relieved by microsurgical resection of the cyst wall. Histological examination confirmed the diagnosis of arachnoid cysts without concomitant meningeal inflammatory reactions. We thought that the multiple meningeal cysts might have originated from undetected meningitis or undetermined underlying mechanism associated with the autoimmune reactions occurring in the arachnoid membrane covering the central nervous system. (+info)
Spinal cord compression caused by idiopathic intradural arachnoid cysts of the spine: review of the literature and illustrated case.
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