Choroid Plexus Neoplasms ; pathology ; Female ; Humans ; Infant ; Lateral Ventricles ; pathology

Angiomatosis ; complications ; pathology ; Brain ; blood supply ; Brain Diseases ; complications ; pathology ; Brain Neoplasms ; complications ; pathology ; Epilepsy ; etiology ; pathology ; surgery ; Ganglioglioma ; complications ; pathology ; Humans ; Malformations of Cortical Development ; classification ; complications ; pathology ; Meninges ; blood supply

Astrocytoma ; genetics ; metabolism ; pathology ; Brain Neoplasms ; classification ; genetics ; metabolism ; pathology ; Child ; Child, Preschool ; Chromosomal Proteins, Non-Histone ; genetics ; metabolism ; Chromosome Deletion ; Cyclin-Dependent Kinase Inhibitor p16 ; genetics ; metabolism ; DNA-Binding Proteins ; genetics ; metabolism ; Ependymoma ; genetics ; metabolism ; pathology ; Hedgehog Proteins ; genetics ; metabolism ; Humans ; Medulloblastoma ; classification ; genetics ; metabolism ; pathology ; Proto-Oncogene Proteins B-raf ; genetics ; metabolism ; Rhabdoid Tumor ; genetics ; metabolism ; pathology ; SMARCB1 Protein ; Signal Transduction ; Transcription Factors ; genetics ; metabolism ; Wnt Proteins ; metabolism ; beta Catenin ; genetics ; metabolism

Adenocarcinoma ; genetics ; metabolism ; Angiomyolipoma ; etiology ; Antibiotics, Antineoplastic ; therapeutic use ; Astrocytoma ; etiology ; Brain Neoplasms ; etiology ; Breast Neoplasms ; genetics ; metabolism ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; Humans ; Kidney Neoplasms ; etiology ; Lung Neoplasms ; genetics ; metabolism ; Mutation ; Sirolimus ; therapeutic use ; TOR Serine-Threonine Kinases ; antagonists & inhibitors ; metabolism ; Tuberous Sclerosis ; complications ; drug therapy ; genetics ; metabolism ; Tumor Suppressor Proteins ; genetics ; metabolism

Objective To quantify the neurons in the temporal lobe white matter and find their distribution in the neurologically normal individuals.Methods The temporal lobe at the level of exterior geniculata body from brain autopsy samples of 14 neurologically normal individuals were made into large slice followed by quantitative analysis of neuron density,cell density,ratio and diameter of the neuronal nuclear and the distribution of white matter neurons using two-dimensional cell counting methods.Results With the depth of the white matter of the temporal lobe increasing,the neuron density decreased from 29.26 neurons/ mm~2 to 7.32 neurons/mm~2 and 0.00 neurons/mm~2,respectively;the cell density,neuron ratio and diameter of the neuronal nuclei all decreased.Conclusion There are neurons in the temporal lobe white matter of neurologically normal individuals,whose distribution of neurons is related to the depth of white matter.

OBJECTIVETo investigate the diagnostic significance of D2-40 and annexin-1 in the ependymal tumors.

METHODSTo analyses the expression of D2-40, annexin-1, EMA and Ki-67 by immunohistochemistry in 52 cases of ependymal tumors (48 cases of ependymomas, 4 cases of choroid plexus papilloma) from Xuanwu Hospital from 2005 to 2009. Ten cases of corresponding normal brain tissue were also obtained as control.

RESULTSThirty-two of forty-eight (66.7%) cases of ependymomas were positive for D2-40. "Dot-like" and "ring-like" structures were commonly observed in ependymomas (55.3%, 21 of 38 cases) and anaplastic ependymomas (5 of 6 cases) with D2-40 staining. There was no difference in the expression between D2-40 and Ki-67 (r(s) = -0.013, P = 0.931). For annexin-1, 87.5% (42 of 48 cases) of the ependymomas were positive. The specific "granular structures" and cilium were observed in ependymomas (1 of 4 cases of myxopapillary ependymomas and 11 of 38 cases of ependymomas respectively) for annexin-1. The difference in expression between annexin-1 and Ki-67 was statistically significant (r(s) = -0.405, P = 0.005). D2-40 in combination of EMA and annexin-1 increased the positive rate to 100% in ependymomas. Choroid plexus papillomas were all positive for D2-40 and annexin-1. The control tissue was negative for D2-40 but positive for annexin-1 in the capillaries.

CONCLUSIONSThe specific structures are valuable in diagnosing of ependymal-genetic tumors, and are highlighted by D2-40 and annexin-1. D2-40 in combination of EMA and annexin-1 is a useful diagnostic marker for ependymal tumors.

Adolescent ; Adult ; Annexin A1 ; metabolism ; Biomarkers, Tumor ; metabolism ; Brain Neoplasms ; diagnosis ; metabolism ; pathology ; Child ; Child, Preschool ; Ependymoma ; diagnosis ; metabolism ; pathology ; Female ; Humans ; Immunohistochemistry ; Ki-67 Antigen ; metabolism ; Male ; Membrane Glycoproteins ; metabolism ; Middle Aged ; Mucin-1 ; metabolism ; Papilloma, Choroid Plexus ; diagnosis ; metabolism ; pathology ; Young Adult

OBJECTIVETo study the clinicopathologic features of brain tumors occurring in patients with medically intractable epilepsy.

METHODSThe clinical, radiologic and pathologic features of brain tumors occurring in 35 patients with intractable epilepsy encountered during the period from January, 2005 to April, 2008 in Xuanwu Hospital were retrospectively reviewed.

RESULTSThe mean age of seizure onset and duration of disease were 14.3-year-old and 8.6 years, respectively. Abnormal signals were observed in 94.3% of cases (33/35) by magnetic resonance imaging. The histologic types of brain tumors included ganglioglioma (13/35, WHO grade I and 6/35, WHO grade II), dysembryoplastic neuroepithelial tumor (3/35, WHO grade I), pleomorphic xanthoastrocytoma (3/35, WHO grade II), diffuse astrocytoma (1/35, WHO grade II), oligoastrocytoma (1/35, WHO grade II), angiocentric glioma (1/35, WHO grade I) and meningioangiomatosis (1/35). The 6 remaining cases showed features seen in between glioneuronal hamartoma and mixed neuronal-glial tumor. Most of these tumors were located in the temporal lobe (27/35) and associated with focal cortical dysplasia. Immunohistochemical study showed a remarkable expression of CD34 in gangliogliomas.

CONCLUSIONSBrain tumors in patients with medically intractable epilepsy are almost always benign and located in the temporal lobe. Most of them represent mixed neuronal-glial tumors and some show transitional features in-between glioneuronal hamartoma and mixed neuronal-glial neoplasm. The similar morphologic pattern and biological behavior of glioneuronal hamartoma and mixed neuronal-glial tumor may suggest a common pathogenetic mechanism.

Adolescent ; Adult ; Antigens, CD34 ; metabolism ; Astrocytoma ; complications ; metabolism ; pathology ; Brain Diseases ; complications ; metabolism ; pathology ; Brain Neoplasms ; complications ; metabolism ; pathology ; Child ; Child, Preschool ; Epilepsy ; etiology ; metabolism ; Female ; Ganglioglioma ; complications ; metabolism ; pathology ; Glioma ; complications ; metabolism ; pathology ; Hamartoma ; complications ; metabolism ; pathology ; Humans ; Infant ; Magnetic Resonance Imaging ; Male ; Oligodendroglioma ; complications ; metabolism ; pathology ; Retrospective Studies ; Temporal Lobe ; pathology ; Young Adult

OBJECTIVETo investigate the expression of TSC1, TSC2, p-mTOR, p-4E-BP1, p-p70S6K and p-S6 in refractory epilepsy associated malformation of cortical development (MCD) tissues.

METHODSA total of 43 cases of refractory epilepsy were involved in the study, and all the patients were treated in Xuanwu Hospital during 2005 - 2008, including focal cortical dysplasia type IIa (11 cases) and type IIb (11 cases), tuberous sclerosis complex (10 cases) and ganalioglioma (11 cases), and other 12 cases were used as control. These cases were divided into 7 study groups and immunohistochemical EnVision method was used. To detect the location and intensity of TSC1, TSC2, p-mTOR, p-4E-BP1, p-p70S6K and p-S6 expression in every group. Then the Image-Pro Plus 6.0 image processing and analysis software were used to measure the number, area, integrating absorbance (IA) of positive cells in every samples. The statistical software SPSS 16.0 was used to analyze the data.

RESULTSThe immunolocalization of TSC1 and TSC2 was similar. It could be observed the expression of various levels in the cytoplasm of dysmorphic neurons, balloon cells, giant cells, ganglioglioma cells and normal neurons. TSC1 staining in normal neurons was more notably than others but TSC2 staining in giant cells was weaker than other samples. p-mTOR mainly presented in giant cells, which could also be observed in astrocyte. P-4E-BP1 presented in the cytoplasm and nuclear membrane of balloon cells, giant cells and ganglioglioma cells, the staining of giant cells was stronger than balloon cells, but their staining were weaker than ganglioglioma cells. P-p70S6K mainly expressed in giant cells and less commonly presented in balloon cells. P-S6 typically presented in all abnormal glioneuronal cells and it nearly did not present in the normal neurons of N-CTX group.

CONCLUSIONSPI3K pathway, at least in part, involves in the occurrence of MCD, and may play an important role in the pathogenesis.

Adaptor Proteins, Signal Transducing ; metabolism ; Adolescent ; Adult ; Child ; Epilepsy ; metabolism ; pathology ; Female ; Ganglioglioma ; metabolism ; pathology ; Humans ; Male ; Malformations of Cortical Development ; metabolism ; pathology ; Phosphatidylinositol 3-Kinases ; metabolism ; Phosphoproteins ; metabolism ; Ribosomal Protein S6 Kinases ; metabolism ; Ribosomal Protein S6 Kinases, 70-kDa ; metabolism ; Signal Transduction ; TOR Serine-Threonine Kinases ; metabolism ; Tuberous Sclerosis ; metabolism ; pathology ; Tumor Suppressor Proteins ; metabolism ; Young Adult

OBJECTIVETo investigate the clinicopathologic features of focal cortical dysplasia (FCD) in patients with refractory epilepsy.

METHODSThe clinical, radiologic and pathologic features of 38 cases of FCD receiving surgical treatment in 2005 were reviewed retrospectively.

RESULTSThe mean age of disease onset was 9.2 years. The disease lasted for 11.9 years on average and often presented as complex partial seizure. Radiologic examination revealed hippocampal sclerosis, or abnormal signals in the grey matter in 21 cases. According to Palmini's classification system, the following pathologic subgroups were identified: FCD type IA (3/38), FCD type IB (20/38), FCD type IIA (5/38) and FCD type IIB (5/38). The remaining 5 cases were classified as mild cortical dysplasia. Topographically, FCD type II was often seen in the extratemporal region (8/10), predominantly in the frontal lobe (5/8). Dual pathology was identified only in cases with FCD type IB. Immunohistochemical study showed that the giant neurons, immature neurons and dysmorphic neurons were strongly positive for NeuN. A small number of balloon cells expressed nestin.

CONCLUSIONSFCD is a common cause of refractory epilepsy. FCD type IB is the predominant pathologic subtype. Associated hippocampal sclerosis is sometimes seen. Clinicopathologic differences between FCD type I and FCD type II are observed.

Adolescent ; Adult ; Antigens, Nuclear ; metabolism ; Cerebral Cortex ; pathology ; ultrastructure ; Child ; Child, Preschool ; Epilepsy ; etiology ; Female ; Humans ; Infant ; Male ; Malformations of Cortical Development ; classification ; complications ; metabolism ; pathology ; Microtubule-Associated Proteins ; metabolism ; Nerve Tissue Proteins ; metabolism ; Neurons ; metabolism ; Retrospective Studies ; Young Adult

OBJECTIVETo study the loss of heterozygosity (LOH) at chromosomes 1p or 19q in oligodendroglial tumors.

METHODSTwenty-eight cases of oligodendroglial tumors were enrolled into the study. Real-time quantitative polymerase chain reaction-based microsatellite analysis was performed on paraffin-embedded tumor tissues in order to study the status of chromosomes 1p and 19q.

RESULTSAmong the 28 cases of oligodendroglial tumors, 24 cases (85.7%) showed 1p LOH, while 18 cases (64.3%) showed 19q LOH and 17 cases (60.7%) showed LOH of both 1p and 19q. LOH at 1p or 19q was present in 25 (89.3%) of the 28 cases.

CONCLUSIONSReal-time quantitative polymerase chain reaction-based microsatellite analysis is a rapid and specific way in detecting LOH in paraffin-embedded tumor tissues. LOH at 1p or 19q is present in majority of the oligodendroglial tumors studied.

Adult ; Brain Neoplasms ; genetics ; Chromosomes, Human, Pair 1 ; Chromosomes, Human, Pair 19 ; Female ; Humans ; Loss of Heterozygosity ; Male ; Microsatellite Repeats ; Middle Aged ; Oligodendroglioma ; genetics ; Polymerase Chain Reaction ; methods