1,888 results match your criteria Brain Pathology[Journal]


Severe White Matter Astrocytopathy in CADASIL.

Brain Pathol 2018 May 14. Epub 2018 May 14.

Neurovascular Research Group, Institute of Neuroscience.

Objectives Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is characterised by strategic white matter (WM) hyperintensities on MRI. Pathological features include WM degeneration, arteriolosclerosis, lacunar infarcts and the deposition of granular osmiophilic material. Based on the hypothesis that the gliovascular unit is compromised, we assessed the nature of astrocyte damage in the deep WM of CADASIL subjects. Read More

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May 2018
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68-Year Old Woman with Multiple Sclerosis, Cutaneous T-Cell Lymphoma and Seizures.

Brain Pathol 2018 May;28(3):439-440

Department of Pathology, Saint Louis University, Saint Louis, MO, USA.

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Astrocytes, an active player in Aicardi-Goutières syndrome.

Brain Pathol 2018 May;28(3):399-407

Division of Neurology, Children's Hospital of Philadelphia, Philadelphia, PA.

Aicardi-Goutières syndrome (AGS) is an early-onset, autoimmune and genetically heterogeneous disorder with severe neurologic injury. Molecular studies have established that autosomal recessive mutations in one of the following genes are causative: TREX1, RNASEH2A, RNASEH2B, RNASEH2C, SAMHD1, ADAR1 and IFIH1/MDA5. The phenotypic presentation and pathophysiology of AGS is associated with over-production of the cytokine Interferon-alpha (IFN-α) and its downstream signaling, characterized as type I interferonopathy. Read More

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A 25-Year-Old Male with a Subgaleal Mass.

Brain Pathol 2018 May;28(3):435-436

Department of Neuropathology, Northwestern University, Chicago, IL.

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A 37-Year-Old Woman with Progressive Right Side Ptosis for One Month.

Brain Pathol 2018 May;28(3):441-442

Department of Neurosurgery, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan.

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Alexander disease: an astrocytopathy that produces a leukodystrophy.

Brain Pathol 2018 May;28(3):388-398

Departments of Pathology and Cell Biology, Columbia University, New York, NY.

Alexander Disease (AxD) is a degenerative disorder caused by mutations in the GFAP gene, which encodes the major intermediate filament of astrocytes. As other cells in the CNS do not express GFAP, AxD is a primary astrocyte disease. Astrocytes acquire a large number of pathological features, including changes in morphology, the loss or diminution of a number of critical astrocyte functions and the activation of cell stress and inflammatory pathways. Read More

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Corrigendum.

Authors:

Brain Pathol 2018 May;28(3):446

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Vanishing white matter: a leukodystrophy due to astrocytic dysfunction.

Brain Pathol 2018 May;28(3):408-421

Departments of Pathology, Child Neurology, and Functional Genomics, VU University Medical Center, Amsterdam Neuroscience, Amsterdam, The Netherlands.

VWM is one of the most prevalent leukodystrophies with unique clinical, pathological and molecular features. It mostly affects children, but may develop at all ages, from birth to senescence. It is dominated by cerebellar ataxia and susceptible to stresses that act as factors provoking disease onset or episodes of rapid neurological deterioration possibly leading to death. Read More

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Genetic defects disrupting glial ion and water homeostasis in the brain.

Brain Pathol 2018 May;28(3):372-387

Department of Child Neurology, Amsterdam Neuroscience, VU University Medical Center, Amsterdam, The Netherlands.

Electrical activity of neurons in the brain, caused by the movement of ions between intracellular and extracellular compartments, is the basis of all our thoughts and actions. Maintaining the correct ionic concentration gradients is therefore crucial for brain functioning. Ion fluxes are accompanied by the displacement of osmotically obliged water. Read More

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Leukodystrophies due to astroyctic dysfunction.

Brain Pathol 2018 May;28(3):369-371

Department of Child Neurology, VU University Medical Centre, Amsterdam Neuroscience, Amsterdam, The Netherlands.

Leukodystrophies are genetically determined disorders due to defects in any structural components of the brain white matter. This mini-symposium presents a selection of leukodystrophies due to astrocytic dysfunction, the astrocytopathies. Examples are provided of astrocytopathies due to defects in astrocyte-specific proteins and in which astrocytes play a major role in the pathophysiology. Read More

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Four-repeat tau dominant pathology in a congenital myotonic dystrophy type 1 patient with mental retardation.

Brain Pathol 2018 May;28(3):431-433

Department of Neuropathology, Graduate School of Medical Sciences, Kyushu University, Fukuoka Prefecture, Japan.

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Corrigendum.

Authors:

Brain Pathol 2018 May;28(3):447

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PATHOGENIC VARIANTS IN THE ABCC6 GENE ARE ASSOCIATED WITH AN INCREASED RISK FOR ISCHEMIC STROKE.

Brain Pathol 2018 May 3. Epub 2018 May 3.

Center for Medical Genetics Ghent, Ghent University Hospital, Ghent, Belgium.

Ischemic stroke causes a high mortality and morbidity worldwide. It results from a complex interplay of incompletely known environmental and genetic risk factors. We investigated the ABCC6 gene as a candidate risk factor for ischemic stroke because of the increased ischemic stroke incidence in the autosomal recessive disorder pseudoxanthoma elasticum, caused by biallelic pathogenic ABCC6 variants, the higher cardiovascular risk in heterozygous carriers and the established role of ABCC6 dysfunction in myocardial ischemia. Read More

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EWSR1-PATZ1 gene fusion may define a new glioneuronal tumor entity.

Brain Pathol 2018 Apr 21. Epub 2018 Apr 21.

Department of Pathology, Toulouse University Hospital, Toulouse, France.

We investigated the challenging diagnostic case of a ventricular cystic glioneuronal tumor with papillary features, by RNA sequencing using the Illumina TruSight RNA Fusion panel. We did not retrieve the SLC44A1-PRKCA fusion gene specific for papillary glioneuronal tumor, but an EWSR1-PATZ1 fusion transcript. RT-PCR followed by Sanger sequencing confirmed the EWSR1-PATZ1 fusion. Read More

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April 2018
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A unique telomere DNA expansion phenotype in human retinal rod photoreceptors associated with aging and disease.

Brain Pathol 2018 Apr 18. Epub 2018 Apr 18.

Departments of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD.

We have identified a discrete, focal telomere DNA expansion phenotype in the photoreceptor cell layer of normal, non-neoplastic human retinas. This phenotype is similar to that observed in a subset of human cancers, including a large fraction of tumors of the central nervous system, which maintain their telomeres via the non-telomerase-mediated alternative lengthening of telomeres (ALT) mechanism. We observed that these large, ultra-bright telomere DNA foci are restricted to the rod photoreceptors and are not observed in other cell types. Read More

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April 2018
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A role for astrocyte-derived amyloid β peptides in the degeneration of neurons in an animal model of Temporal Lobe Epilepsy.

Brain Pathol 2018 Apr 17. Epub 2018 Apr 17.

Departments of Psychiatry, University of Alberta, Edmonton, Alberta, Canada T6G 2M8.

Kainic acid, an analogue of the excitatory neurotransmitter glutamate, can trigger seizures and neurotoxicity in the hippocampus and other limbic structures in a manner that mirrors the neuropathology of human temporal lobe epilepsy (TLE). However, the underlying mechanisms associated with the neurotoxicity remain unclear. Since amyloid-β (Aβ) peptides, which are critical in the development of Alzheimer's disease, can mediate toxicity by activating glutamatergic NMDA receptors, it is likely that the enhanced glutamatergic transmission that renders hippocampal neurons vulnerable to kainic acid treatment may involve Aβ peptides. Read More

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April 2018
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Grading of meningeal solitary fibrous tumors/hemangiopericytomas: analysis of the prognostic value of the Marseille Grading System in a cohort of 132 patients.

Brain Pathol 2018 Mar 30. Epub 2018 Mar 30.

Department of Pathology and Neuropathology, Timone Hospital, Marseille, France.

The finding that meningeal solitary fibrous tumors (SFTs) and meningeal hemangiopericytomas (HPCs) are both characterized by NAB2-STAT6 gene fusion has pushed their inclusion in the WHO 2016 Classification of tumors of the central nervous system (CNS) as different manifestations of the same entity. Given that the clinical behavior of the CNS SFT/HPC spectrum ranges from benign to malignant, it is presently unclear whether the grading criteria are still adequate. Here, we present the results of a study that analyzed the prognostic value of an updated version of the Marseille Grading System (MGS) in a retrospectively assembled cohort of 132 primary meningeal SFTs/HPCs with nuclear overexpression of STAT6. Read More

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March 2018
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A 39-Year-Old Gentleman with Headache, Visual Blurring and a Renal Mass.

Brain Pathol 2018 03;28(2):301-302

Department of Neurosurgery, Postgraduate Institute of Medical Education and Research, Chandigarh, India.

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March 2018
1 Read

A 27-Year-Old Female with Multiple Intracranial Lesions.

Brain Pathol 2018 03;28(2):303-305

Department of Neurosurgery, Ibn Alhaytham Hospital, Amman, Jordan.

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March 2018
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Screening for gene mutations in central nervous system metastases of non-small-cell lung cancer.

Brain Pathol 2018 03;28(2):295-297

Departments of Pneumonology, Oncology and Allergology, Medical University of Lublin, 20-954, Lublin, Poland.

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March 2018
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A 40-Year-Old Female with Dural-Based Lesions.

Brain Pathol 2018 03;28(2):299-300

Department of Neurosurgery, Hirslanden Hospital, Hirslanden, Switzerland.

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March 2018
1 Read

A 55-Year-Old Male with Intermittent Headache.

Brain Pathol 2018 03;28(2):307-308

Department of Neurosurgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.

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March 2018
1 Read

Creutzfeldt astrocytes may be seen in IDH-wildtype glioblastoma and retain expression of DNA repair and chromatin binding proteins.

Brain Pathol 2018 Mar 6. Epub 2018 Mar 6.

Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, TX.

Astrocytes with multiple micronuclei ("Creutzfeldt cells") in a brain biopsy are classically associated with demyelinating disease. However, glioblastoma may also have prominent Creutzfeldt astrocytes, along with granular mitoses. Therefore, Creutzfeldt cells may raise the diagnostic dilemma of high-grade glioma vs tumefactive demyelination. Read More

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March 2018
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ABNORMAL DEVELOPMENT OF THE INFERIOR TEMPORAL REGION IN FETUSES WITH DOWN SYNDROME.

Brain Pathol 2018 Mar 6. Epub 2018 Mar 6.

Department of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy.

Down syndrome (DS) is a genetic condition associated with impairment in several cognitive domains. Previous evidence showed a notable neurogenesis reduction in the hippocampal region of DS fetuses, which may account for the impairment of declarative memory that characterizes DS starting from early life stages. The fusiform gyrus (FG) and the inferior temporal gyrus (ITG) play a key role in visual recognition memory, a function that is impaired in children and adults with DS. Read More

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March 2018
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Generation of novel neuroinvasive prions following intravenous challenge.

Brain Pathol 2018 Mar 5. Epub 2018 Mar 5.

Departments of Pathology and Medicine, UC San Diego, La Jolla, CA 92093, USA.

Prion aggregates typically spread into the central nervous system (CNS), likely via peripheral nerves. Yet prion conformers differ in their capacity to penetrate the CNS; certain fibrillar prions replicate persistently in lymphoid tissues with no CNS entry, leading to chronic silent carriers. Subclinical carriers of variant Creutzfeldt-Jakob (vCJD) prions in the United Kingdom have been estimated at 1:2000, and vCJD prions have been transmitted through blood transfusion, however the circulating prion conformers that neuroinvade remain unclear. Read More

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March 2018
3 Reads

Higher levels of kallikrein-8 in female brain may increase the risk for Alzheimer's disease.

Brain Pathol 2018 Mar 5. Epub 2018 Mar 5.

Institute of Neuropathology, University of Duisburg-Essen, Hufelandstr. 55, 45122 Essen, Germany.

Women seem to have a higher vulnerability to Alzheimer's disease (AD), but the underlying mechanisms of this sex dichotomy are not well understood. Here, we first determined the influence of sex on various aspects of Alzheimer's pathology in transgenic CRND8 mice. We demonstrate that beta-amyloid (Aβ) plaque burden starts to be more severe around P180 (moderate disease stage) in female transgenics when compared to males and that aging aggravates this sex-specific difference. Read More

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March 2018
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Brain alpha-amylase: a novel energy regulator important in Alzheimer disease?

Brain Pathol 2018 Feb 27. Epub 2018 Feb 27.

Clinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden.

Reduced glucose metabolism and formation of polyglucosan bodies (PGB) are, beside amyloid beta plaques and neurofibrillary tangles, well-known pathological findings associated with Alzheimer's disease (AD). Since both glucose availability and PGB are regulated by enzymatic degradation of glycogen, we hypothesize that dysfunctional glycogen degradation is a critical event in AD progression. We therefore investigated whether alpha (α)-amylase, an enzyme known to efficiently degrade polysaccharides in the gastrointestinal tract, is expressed in the hippocampal CA1/subiculum and if the expression is altered in AD patients. Read More

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February 2018
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New clinicopathological associations and histoprognostic markers in ILAE types of hippocampal sclerosis.

Brain Pathol 2018 Feb 24. Epub 2018 Feb 24.

Department of Neuropathology, AP-HP, Hôpitaux Universitaires Pitié-Salpêtrière Charles Foix, Paris, France.

Mesial temporal lobe epilepsy with hippocampal sclerosis (MTLE-HS) is a heterogeneous syndrome. Surgery results in seizure freedom for most pharmacoresistant patients, but the epileptic and cognitive prognosis remains variable. The 2013 International League Against Epilepsy (ILAE) histopathological classification of hippocampal sclerosis (HS) has fostered research to understand MTLE-HS heterogeneity. Read More

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February 2018
2 Reads

Epigenomic signature of adrenoleukodystrophy predicts compromised oligodendrocyte differentiation.

Brain Pathol 2018 Feb 24. Epub 2018 Feb 24.

Neurometabolic Diseases Laboratory, Bellvitge Biomedical Research Institute (IDIBELL), 08908 L'Hospitalet de Llobregat, Barcelona, Spain.

Epigenomic changes may either cause disease or modulate its expressivity, adding a layer of complexity to mendelian diseases. X-linked adrenoleukodystrophy (X-ALD) is a rare neurometabolic condition exhibiting discordant phenotypes, ranging from a childhood cerebral inflammatory demyelination (cALD) to an adult-onset mild axonopathy in spinal cords (AMN). The AMN form may occur with superimposed inflammatory brain demyelination (cAMN). Read More

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February 2018
1 Read

Early movement restriction leads to enduring disorders in muscle and locomotion.

Brain Pathol 2018 Feb 13. Epub 2018 Feb 13.

Neurosciences Intégratives et Adaptatives, UMR 7260, CNRS, Aix-Marseille Université, Marseille, France.

Motor control and body representation in the central nervous system (CNS) as well as musculoskeletal architecture and physiology are shaped during development by sensorimotor experience and feedback, but the emergence of locomotor disorders during maturation and their persistence over time remain a matter of debate in the absence of brain damage. By using transient immobilization of the hind limbs, we investigated the enduring impact of postnatal sensorimotor restriction (SMR) on gait and posture on treadmill, age-related changes in locomotion, musculoskeletal histopathology and Hoffmann reflex in adult rats without brain damage. SMR degrades most gait parameters and induces overextended knees and ankles, leading to digitigrade locomotion that resembles equinus. Read More

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February 2018
3 Reads

Aging-related tau astrogliopathy (ARTAG): not only tau phosphorylation in astrocytes.

Brain Pathol 2018 Feb 3. Epub 2018 Feb 3.

Ministry of Economy and Competitiveness, CIBERNED (Network Centre of Biomedical Research of Neurodegenerative Diseases), Institute of Health Carlos III, Barcelona, Spain.

Aging-related tau astrogliopathy (ARTAG) is defined by the presence of two types of tau-bearing astrocytes: thorn-shaped astrocytes (TSAs) and granular/fuzzy astrocytes in the brain of old-aged individuals. The present study is focused on TSAs in rare forms of ARTAG with no neuronal tau pathology or restricted to entorhinal and transentorhinal cortices, to avoid bias from associated tauopathies. TSAs show 4Rtau phosphorylation at several specific sites and abnormal tau conformation, but they lack ubiquitin and they are not immunostained with tau-C3 antibodies which recognize truncated tau at Asp421. Read More

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February 2018
3 Reads

Purine-related metabolites and their converting enzymes are altered in frontal, parietal and temporal cortex at early stages of Alzheimer's disease pathology.

Brain Pathol 2018 Jan 24. Epub 2018 Jan 24.

Facultad de Ciencias y Tecnologías Químicas/Facultad de Medicina de Ciudad Real, Departamento de Química Inorgánica, Orgánica y Bioquímica, Centro Regional de Investigaciones Biomédicas, Universidad de Castilla-La Mancha, Ciudad Real, Spain.

Adenosine, hypoxanthine, xanthine, guanosine and inosine levels were assessed by HPLC, and the activity of related enzymes 5'-nucleotidase (5'-NT), adenosine deaminase (ADA) and purine nucleoside phosphorylase (PNP) measured in frontal (FC), parietal (PC) and temporal (TC) cortices at different stages of disease progression in Alzheimer's disease (AD) and in age-matched controls. Significantly decreased levels of adenosine, guanosine, hypoxanthine and xanthine, and apparently less inosine, are found in FC from the early stages of AD; PC and TC show an opposing pattern, as adenosine, guanosine and inosine are significantly increased at least at determinate stages of AD whereas hypoxanthine and xanthine levels remain unaltered. 5'-NT is reduced in membranes and cytosol in FC mainly at early stages but not in PC, and only at advanced stages in cytosol in TC. Read More

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January 2018
5 Reads

Autonomous Purkinje cell axonal dystrophy causes ataxia in peroxisomal multifunctional protein-2 deficiency.

Brain Pathol 2018 Jan 17. Epub 2018 Jan 17.

Department of Pharmaceutical and Pharmacological Sciences, Cell Metabolism, KU Leuven - University of Leuven, Leuven, Belgium.

Peroxisomes play a crucial role in normal neurodevelopment and in the maintenance of the adult brain. This depends largely on intact peroxisomal β-oxidation given the similarities in pathologies between peroxisome biogenesis disorders and deficiency of multifunctional protein-2 (MFP2), the central enzyme of this pathway. Recently, adult patients diagnosed with cerebellar ataxia were shown to have mild mutations in the MFP2 gene, hydroxy-steroid dehydrogenase (17 beta) type 4 (HSD17B4). Read More

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January 2018
9 Reads

Synapsin III is a key component of α-synuclein fibrils in Lewy bodies of PD brains.

Brain Pathol 2018 Jan 13. Epub 2018 Jan 13.

Department of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.

Lewy bodies (LB) and Lewy neurites (LN), which are primarily composed of α-synuclein (α-syn), are neuropathological hallmarks of Parkinson's disease (PD) and dementia with Lewy bodies (DLB). We recently found that the neuronal phosphoprotein synapsin III (syn III) controls dopamine release via cooperation with α-syn and modulates α-syn aggregation. Here, we observed that LB and LN, in the substantia nigra of PD patients and hippocampus of one subject with DLB, displayed a marked immunopositivity for syn III. Read More

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January 2018
4 Reads

A 68-Year-Old Woman with A Left Orbital and Temporal Mass.

Brain Pathol 2018 01;28(1):133-134

Division of Pathology, Department of Medical Sciences, University of Turin, Turin, Italy.

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January 2018
4 Reads

A 72-Year-Old Male with A Slow Growing Pineal Region Tumor.

Brain Pathol 2018 01;28(1):129-130

Department of Neurosurgery, McMaster University, Hamilton, ON, Canada.

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January 2018
4 Reads

A 62-Year-Old Woman with A History of Muscle Pain and Skin Rash for 1 Month.

Brain Pathol 2018 01;28(1):121-122

Department of Genome Medicine Development, Medical Genome Center, National Center of Neurology and Psychiatry (NCNP), Tokyo, Japan.

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January 2018
4 Reads

A 44-Year-Old Female with Familial Mediterranean Fever, Cardiomyopathy and End Stage Renal Disease.

Brain Pathol 2018 01;28(1):135-136

Section of Neuropathology, Brain Research Institute, Ronald Reagan University of California, Los Angeles, CA.

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January 2018
4 Reads

A 60-Year-Old Woman with Multifocal Subcortical Infarcts.

Brain Pathol 2018 01;28(1):131-132

Department of Pathology and Immunology, Division of Neuropathology, Washington University School of Medicine, St. Louis, MO.

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January 2018
6 Reads

A 31-Year-Old Man with Slowly Progressive Limb Muscle Weakness and Respiratory Insufficiency.

Brain Pathol 2018 01;28(1):123-124

Department of Genome Medicine Development, Medical Genome Center, Tokyo, Japan.

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January 2018
4 Reads

An 8-Year-Old Girl with A Supratentorial Mass.

Brain Pathol 2018 01;28(1):125-126

Department of Pathology and Immunology, Mallinckrodt Institute of Radiology, St. Louis, MO.

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January 2018
4 Reads

A 39-Year-Old Woman with Progressive Vision Impairment.

Brain Pathol 2018 01;28(1):127-128

Department of Neurosurgery, Military Institute of Medicine, Warsaw, Poland.

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January 2018
4 Reads

CNS high-grade neuroepithelial tumor with BCOR internal tandem duplication: a comparison with its counterparts in the kidney and soft tissue.

Brain Pathol 2017 Dec 11. Epub 2017 Dec 11.

Department of Human Pathology, Gunma University Graduate School of Medicine, Maebashi, Japan.

Central nervous system high-grade neuroepithelial tumors with BCOR alteration (CNS HGNET-BCOR) are a recently reported rare entity, identified as a small fraction of tumors previously institutionally diagnosed as so-called CNS primitive neuroectodermal tumors. Their genetic characteristic is a somatic internal tandem duplication in the 3' end of BCOR (BCOR ITD), which has also been found in clear cell sarcomas of the kidney (CCSK) and soft tissue undifferentiated round cell sarcomas/primitive myxoid mesenchymal tumors of infancy (URCS/PMMTI), and these BCOR ITD-positive tumors have been reported to share similar pathological features. In this study, we performed a clinicopathological and molecular analysis of six cases of CNS HGNET-BCOR, and compared them with their counterparts in the kidney and soft tissue. Read More

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December 2017
13 Reads

Dominant role of microglial and macrophage innate immune responses in human ischemic infarcts.

Brain Pathol 2017 Dec 8. Epub 2017 Dec 8.

Center for Brain Research, Medical University of Vienna, Austria.

Inflammatory mechanisms, involving granulocytes, T-cells, B-cells, macrophages and activated microglia, have been suggested to play a pathogenic role in experimental models of stroke and may be targets for therapeutic intervention. However, knowledge on the inflammatory response in human stroke lesions is limited. Here, we performed a quantitative study on the inflammatory reaction in human ischemic infarct lesions. Read More

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December 2017
4 Reads

RELN signaling modulates glioblastoma growth and substrate-dependent migration.

Brain Pathol 2017 Dec 8. Epub 2017 Dec 8.

Department of Neuropathology, Regensburg University Hospital, Regensburg, Germany.

Glioblastoma (GBM) represents the most common and most malignant type of primary brain tumor and significantly contributes to cancer morbidity and mortality. Invasion into the healthy brain parenchyma is a major feature of glioblastoma aggressiveness. Reelin (RELN) is a large secreted extracellular matrix glycoprotein that regulates neuronal migration and positioning in the developing brain and sustains functionality in the adult brain. Read More

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December 2017
4 Reads

BRAF V600E, TERT promoter mutations and CDKN2A/B homozygous deletions are frequent in epithelioid glioblastomas: a histological and molecular analysis focusing on intratumoral heterogeneity.

Brain Pathol 2017 Nov 4. Epub 2017 Nov 4.

Department of Human Pathology, Gunma University Graduate School of Medicine, Maebashi, Japan.

Epithelioid glioblastoma (E-GBM) is a rare aggressive variant of IDH-wildtype glioblastoma newly recognized in the 2016 World Health Organization classification, composed predominantly of monotonous, patternless sheets of round cells with laterally positioned nuclei and plump eosinophilic cytoplasm. Approximately 50% of E-GBM harbor BRAF V600E, which is much less frequently found in other types of glioblastomas. Most E-GBM are recognized as primary/de novo lesions; however, several E-GBM with co- or pre-existing lower-grade lesions have been reported. Read More

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November 2017
6 Reads