“
“We present two cases of atypical meningioma WHO grade II with a history of multiple local recurrences and late pulmonary metastases. Comparative cytogenetic analyses on 1p and 22q confirmed clonal origin of the primary intracranial meningiomas and the pulmonary metastases in both cases. These cases illustrate the importance of close neuroradiological follow-up to detect tumor recurrence in patients with

atypical meningiomas WHO grade II even with clinically stable disease Pritelivir datasheet and should sensitize clinicians to late extracranial metastases of these tumors, especially to the lung. In an effort to elucidate common clinical features of metastatic meningiomas, especially to the lung, the literature

was PD98059 cost reviewed from 1995 to 2014, identifying a total of 45 published cases. “
“M. Thangarajh and D. H. Gutmann (2012) Neuropathology and Applied Neurobiology38, 241–253 Low-grade gliomas as neurodevelopmental disorders: insights from mouse models of neurofibromatosis-1 Over the past few years, the traditional view of brain tumorigenesis has been revolutionized by advances in genomic medicine, molecular biology, stem cell biology and genetically engineered small-animal modelling. We now appreciate that paediatric brain tumours arise following specific genetic mutations in specialized groups of progenitor cells in concert with permissive changes in the local tumour microenvironment. This interplay between preneoplastic/neoplastic cells and non-neoplastic stromal cells is nicely illustrated by the neurofibromatosis type 1-inherited cancer syndrome, in which affected children develop

low-grade astrocytic gliomas. In this review, we will use neurofibromatosis type 1 as a model system to highlight the critical role of growth control pathways, non-neoplastic cellular elements and brain region-specific properties in the development of childhood gliomas. The insights derived from examining each of these contributing factors will be instructive in the design of new therapies for gliomas in the paediatric population. “
“There is a great deal of evidence suggesting an important role for systemic inflammation Orotidine 5′-phosphate decarboxylase in the pathogenesis of Alzheimer’s disease. The role of systemic inflammation, and indeed inflammation in general, is still largely considered to be as a contributor to the disease process rather than of aetiological importance although there is emerging evidence to suggest that its role may predate the deposition of amyloid. Therapies aimed at reducing inflammation in individuals with mild cognitive impairment and Alzheimer’s disease have been disappointing and have largely focused on the need to ameliorate central inflammation with little attention to the importance of dampening down systemic inflammation.