Precursor B-lymphoblastic lymphoma mimicking: An acute subdural hematoma

Objective and importanceWe present the first case of a precursor acute subdural B-lymphoblastic lymphoma mimicking an acute subdural hematoma.Clinical presentationA 19 year old male presented with an acute onset of headache, nausea and vomiting. CT scan showed crescentic right-sided, frontoparietal subdural mass isointense with cortex and showing homogeneous enhancement after gadolinium.InterventionThe patient underwent a craniotomy and a gray subdural tumor with invasion of both dura and brain was observed. The invaded dura was resected and duraplasty performed. Histopathologically, the tumor was composed of small round cells infiltrating soft tissue. In some areas of the tumor, cells were arranged in a linear, “Indian file” fashion between collagen bundles. Their nuclei were generally uniform, round to ovoid in shape, small to medium in size, and featured delicate chromatin. Accompanying cytoplasm was scant. Necrosis was absent. On immunohistochemical analysis, the tumor cells were positive for CD79a, TdT, CD10 and CD34.ConclusionSubdural lymphoma can present as a neurosurgical emergency, and lymphoma should be considered as a rare but possible diagnosis before operation

Thymoquinone: An edible redox-active quinone for the pharmacotherapy of neurodegenerative conditions and glial brain tumors. A short review

There exist few efficient agents in the neurological and neurosurgical armamentarium for treatment of neurotrauma, refractory seizures and high grade glial tumors. Pathophysiological conditions of diverse neural injuries have converging common pathways including oxidative stress and apoptosis. Targeted therapies have been throughly investigated, but limited success has been achieved until now. Phytochemical drugs may provide easily achievable and cheap adjunctive sources. Thymoquinone is an edible quinone obtained from Nigella sativa seed oil and exerts powerful antiinflammatory, antioxidant and antitumor activities in experimental models. Recently emerging studies conducted with animal models suggest that thymoquinone - bearing a very simple molecular structure - significantly crosses the blood brain barrier and exerts neuromodulatory activities. Indeed, in animal studies, the following actions of thymoquinone were demonstrated: 1-Protection against ischemic brain damage. 2-Reduction of epileptic seizures and associated cerebral oxidative injury. 3-Reduction of morphine tolerance and associated oxidative brain damage. 4-Anxiolytic effects and reduction of immobility stress-associated cerebral oxidative injury. 5-Reduction of diabetes-induced cerebral oxidative stress, 6-Reduction of cerebral oxidative injuries induced by noxious exposures including toluene, lead and ionizing radiation. Substantial in vitro data suggest that thymoquinone may be beneficial in treatment of glial tumors. However, there is no clinical study investigating its antitumor effects. In fact, thymoquinone suppresses growth and invasion, and induces apoptosis of glial tumor cells via degrading tubulins and inhibiting 20S proteasome, telomerase, autophagy, FAK and metalloproteinases. A simple and easily available agent may be a promising adjunctive treatment option in neurological and neurosurgical practice. (C) 2016 Elsevier Masson SAS. All rights reserved

Long non-coding RNA MALAT1 as a key target in pathogenesis of glioblastoma. Janus faces or Achilles' heal?

Altinoz, Meric/0000-0001-7804-4087WOS: 000523630800011PubMed: 32119915Glioblastomas (GBMs) are primary brain tumors with extremely bad prognosis and therefore; discovery of novel regulators of their pathology is of immense importance. LncRNAs (long noncoding RNAs) regulate nuclear structure, embryonic pluripotency, cell differentiation, development and carcinogenesis. Many lncRNAs have weak evolutionary conservation; however, a nuclear lncRNA, MALAT1 (metastasis-associated lung adenocarcinoma transcript 1), is exceptionally conserved and is among the most abundant lncRNAs in benign tissues. the majority of cell culture studies and clinico-epidemiological studies demonstrated that MALAT1 acts a tumor promoter in GBMs and inhibition of MALAT1 suppressed tumor growth in various preclinical models of GBM. MALAT1 involves in stemness of GBM cells by regulating SOX2, nestin and members of WNT pathway. MALAT1 induces protective autophagy and suppresses apoptosis in GBM cells via sponging miRNA-101 and increases temozolomide chemoresistance via enhancing epithelial-mesenchymal transition, suppressing miR-203 and promoting thymidilate synthase. Moreover, knockdown of MALAT1 expression enhances blood-brain tumor barrier permeability via miR-140, which may provide a double benefit of MALAT1 suppression by increasing the delivery of chemotherapy agents into the GBM tissues. on the other hand, there also exist some cell culture and animal studies showing that MALAT1 acts as a tumor suppressor in GBMs by suppression of ERK/MAPK and MMP2 signaling and by repression of miR-155 with subsequent increase of FBXW7. Whether protective or detrimental, MALAT1 seems to be an important component of GBM pathogenesis and hence; novels studies are needed in versatile models, including many different primary GBM cultures, orthotopic and xenogreft in vivo models and transgenic mice

Relationship of intraoperative ultrasound characteristics with pathological grades and Ki-67 proliferation index in intracranial gliomas

The purpose of the present study was to investigate the relationship between the intraoperative ultrasonographic appearances and the histopathological characteristics of glial tumors using the pathological grading system and the Ki-67 proliferation index