CDH1 hypermethylation: a potential molecular pathway for invasiveness in glioblastoma.

Glioblastoma is the most aggressive central nervous system primary tumor. Prognosis is poor, mainly due to the malignant characteristics of the tumor, such as high cell proliferation and invasiveness. CDH1 hypermethylation is linked to the invasive potential in various cancer types, but its importance is still unknown in glioblastoma. In this context, the methylation status of CDH1 was analyzed using MSP-PCR (Methylation-specific Polymerase Chain Reaction) in glioblastoma (n = 34) and normal glial tissue samples (n = 11). CDH1 hypermethylation was found in 39.4% (13/34) of the tumor samples and none of the normal glial tissue, suggesting a relation between CDH1 hypermethylation and glioblastoma ( P = 0.0195). Finally, this study showed unprecedented information that could contribute to clarifying the molecular pathways involved in the invasiveness and aggressiveness of this type of cancer.

Metabolomics Approach Reveals Important Glioblastoma Plasma Biomarkers for Tumor Biology.

Glioblastoma (GB) is the most aggressive and frequent primary malignant tumor of the central nervous system and is associated with poor overall survival even after treatment. To better understand tumor biochemical alterations and broaden the potential targets of GB, this study aimed to evaluate differential plasma biomarkers between GB patients and healthy individuals using metabolomics analysis. Plasma samples from both groups were analyzed via untargeted metabolomics using direct injection with an electrospray ionization source and an LTQ mass spectrometer. GB biomarkers were selected via Partial Least Squares Discriminant and Fold-Change analyses and were identified using tandem mass spectrometry with in silico fragmentation, consultation of metabolomics databases, and a literature search. Seven GB biomarkers were identified, some of which were unprecedented biomarkers for GB, including arginylproline (m/z 294), 5-hydroxymethyluracil (m/z 143), and N-acylphosphatidylethanolamine (m/z 982). Notably, four other metabolites were identified. The roles of all seven metabolites in epigenetic modulation, energy metabolism, protein catabolism or folding processes, and signaling pathways that activate cell proliferation and invasion were elucidated. Overall, the findings of this study highlight new molecular targets to guide future investigations on GB. These molecular targets can also be further evaluated to derive their potential as biomedical analytical tools for peripheral blood samples.

Differential Plasma Metabolites between High- and Low-Grade Meningioma Cases.

Meningiomas (MGMs) are currently classified into grades I, II, and III. High-grade tumors are correlated with decreased survival rates and increased recurrence rates. The current grading classification is based on histological criteria and determined only after surgical tumor sampling. This study aimed to identify plasma metabolic alterations in meningiomas of different grades, which would aid surgeons in predefining the ideal surgical strategy. Plasma samples were collected from 51 patients with meningioma and classified into low-grade (LG) (grade I; n = 43), and high-grade (HG) samples (grade II, n = 5; grade III, n = 3). An untargeted metabolomic approach was used to analyze plasma metabolites. Statistical analyses were performed to select differential biomarkers among HG and LG groups. Metabolites were identified using tandem mass spectrometry along with database verification. Five and four differential biomarkers were identified for HG and LG meningiomas, respectively. To evaluate the potential of HG MGM metabolites to differentiate between HG and LG tumors, a receiving operating characteristic curve was constructed, which revealed an area under the curve of 95.7%. This indicates that the five HG MGM metabolites represent metabolic alterations that can differentiate between LG and HG meningiomas. These metabolites may indicate tumor grade even before the appearance of histological features.

Conservative management of pituitary tumor apoplexy.

Pituitary tumor apoplexy is a rare neuroendocrine syndrome resulting, in most cases, from hemorrhage or infarctation of a pre-existing pituitary adenoma. Treatment recommendations vary; some authors advocate urgent surgical decompression of the tumor, whereas others suggest that conservative management can lead to recovery of neuro-ophthalmologic function. We describe two patients with pituitary tumor apoplexy who had clinically non-functioning macroadenomas and hypopituitarism, including hypogonadism. They were treated conservatively without surgery, and achieved tumor remission.

Intrasellar chondroid chordoma: a case report.

Chordomas are tumors derived from cells that are remnants of the notochord, particularly from its proximal and distal extremes, they are mainly midline and represent approximately 1% of all malignant bone tumors and 0.1 to 0.2% of intracranial neoplasms. Chordomas involving the sellar region are rare. Herein, we describe a 57-year-old male patient presenting with a history of retro-orbital headache, progressive loss of vision, and clinical features of hypopituitarism, for over 2 months. During evaluation, the CT scan revealed a large contrast-enhancing intrasellar tumor with a 3.6-cm largest diameter. The patient underwent transsphenoidal partial resection of the tumor, and histological examination was consistent with the diagnosis of chondroid chordoma. Although chordomas are rare, they may be considered to constitute a differential diagnostic of pituitary adenomas, especially if a calcified intrasellar tumor with bone erosion is diagnosed.

Giant fusiform aneurysm arising from fenestrated posterior cerebral artery and basilar tip variation: case report.

OBJECTIVE: A giant fusiform aneurysm in the posterior cerebral artery (PCA) is rare, as is fenestration of the PCA and basilar apex variation. We describe the angiographic and surgical findings of a giant fusiform aneurysm in the P1-P2 PCA segment associated with PCA bilateral fenestration and superior cerebellar artery double origin. CLINICAL PRESENTATION: A 26-year-old woman presented with a 2-month history of visual blurring. Digital subtraction angiography showed a giant (2.5 cm) fusiform PCA aneurysm in the right P1-P2 segment. The 3-dimensional view showed a caudal fusion pattern from the upper portion of the basilar artery associated with a bilateral long fenestration of the P1 and P2 segments and superior cerebellar artery double origin. INTERVENTION: Surgical trapping of the right P1-P2 segment, including the posterior communicating artery, was performed by a pretemporal approach. Angiograms performed 3 and 13 months after surgery showed complete aneurysm exclusion, and the PCA was permeated and filled the PCA territory. Clinical follow-up at 14 months showed the patient with no deficits and a return to normal life. CONCLUSION: To our knowledge, this is the first report of a giant fusiform aneurysm of the PCA associated with P1-P2 segment fenestration and other variations of the basilar apex (bilateral superior cerebellar artery duplication and caudal fusion). Comprehension of the embryology and anatomy of the PCA and its related vessels and branches is fundamental to the decision-making process for a PCA aneurysm, especially when parent vessel occlusion is planned.

A form of dysplasia or a fortuitous association? A cerebral aneurysm inside an arachnoid cyst: case report.

OBJECTIVE: Although arachnoid cysts and intracranial aneurysms are very common lesions, their association in the same patient is rare. We present a case of a middle cerebral artery aneurysm ruptured into an arachnoid cyst. We found only six cases with intracystic hemorrhage reported in the literature. The presence of an arachnoid cyst can mislead clinical presentation. The patient presented a paradoxically small temporal fossa and thickening of the temporal and sphenoid bone. The authors suggest that this uncommon association (arachnoid cyst, atypical cranial vault, and "mirror-like" cerebral aneurysm) could represent a form of dysplasia. CLINICAL PRESENTATION: A 46-year-old patient presented with a 3-week history of slight headaches, which had worsened in the last 3 days before presentation. Computed tomographic scans showed a cystic lesion located in the middle cranial fossa and sylvian fissure with suspected aneurysm dilation inside. Magnetic resonance imaging scans showed an intracystic hemorrhage but not subarachnoid hemorrhage. Paradoxically, changes in the cranial vault around the cyst were noted. Digital subtraction angiography showed bilateral "mirror" middle cerebral artery aneurysms. INTERVENTION: A large right pterional craniotomy was performed with full microsurgical removal of the arachnoid cyst walls and aneurysm clipping. The aneurysm was in the medial wall of the arachnoid cyst with its dome inside the cyst. The contralateral aneurysm was clipped 2 weeks later. The follow-up period was uneventful, and the patient returned to normal life. CONCLUSION: Rupture of a cerebral aneurysm into an arachnoid cyst is rare. Clinical presentation may be unusual because the cyst can prevent subarachnoid hemorrhage. A middle fossa cranial arachnoid cyst in the presence of temporal bone depression, small middle fossa, and thickness of squamous temporal bone and the lesser wing of sphenoid is rare and suggests that congenital factors may play an important role in their development. The exceptional association between "mirror" aneurysms and arachnoid cyst with bone changes suggests a possible congenital form of dysplasia.

A resposta metabólica ao trauma cranioencefálico é autolimitada?: análise das proteínas de fase aguda e glicemia / Is the metabolic response self-limited in head trauma?: analysis of acute phase proteins and glycemia

Nos últimos anos tem havido referências à limitaçao da resposta metabólica nas duas primeiras semanas após trauma cranioencefálico (TCE). Foi feita proposta de estudo a partir de experimento clínico em pacientes com trauma encefálico grave, que foram avaliados por volta de 7 dias após a lesao (MI). A segunda avaliaçao ocorreu 4 dias após (M2), e a terceira 3 a 4 dias após (M3). Em um período de 2 anos, foram selecionados 28 pacientes do sexo masculino, com trauma encefálico grave, escala de gravidade de Glasgow entre 4 e 6. Dentre os 28 pacientes, 6 completaram o estudo proposto. Os pacientes foram acompanhados clinicamente durante toda a fase do experimento. Em cada um dos momentos de análise, foram feitas análises da excreçao nitrogenada e proteínas de fase aguda. Da mesma forma foram feitas determinaçoes da glicemia plasmática. N-amínico e triglicerídeos. Os resultados do estudo demonstraram nao haver modificaçoes no balanço nitrogenado, normalizaçao da proteína-C-reativa e reduçao relativa da glicemia ao final do experimento. Os autores tecem consideraçoes sobre os possíveis mecanismos envolvidos na modulaçao da resposta metabólica e concluem que o hipermetabolismo, a basear-se na análise de glicemia e das proteínas de fase aguda, nao persiste além do 13º dia do período de recuperaçao pós-trauma. Sao feitas sugestoes de estudos futuros que possam elucidar os mecanismos envolvidos na normalizaçao do hipercatabolismo e hipermetabolismo observados nas duas primeiras semanas após TCE.

Oligodendroglioma cístico e positividade das reaçöes para cisticercose: relato de caso / Cystic oligodendroglioma and positivity of reactions for cysticercosis: report of a case

Säo poucos os estudos sobre gliomas <>. Os oligodendrogliomas representam de 1,3 a 10% dos tumores intracerebrais. A neurocisticercose é uma das mais graves parasitoses do SNC, com evidente polimorfismo clínico e laboratorial. O objetivo deste estudo é relatar o caso de um doente com cefaléia, perda progressiva da visäo, alteraçäo do comportamento e provas imunológicas positivas para cisticercose no liquido cístico e cefalorraqueano. Após tentativas para tratamento da neurocisticercose, sem muito sucesso, foi submetido a craniotomia frontal para exérese de tumor cístico, que revelou tratar-se de oligodendroglioma. Discutem-se aspectos relacionados aos possíveis mecanismos para associaçäo de neurocisticercose e oligodendroglioma