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1.
Vet Pathol ; 61(1): 46-57, 2024 01.
Artigo em Inglês | MEDLINE | ID: mdl-37358305

RESUMO

Neural stem cell (NSC) lineage cells have not been fully identified in feline brains, and the NSC-like nature of feline glial tumors has not been determined. In this study, 6 normal cat brains (3 newborn and 3 older cats) and 13 feline glial tumors were analyzed using immunohistochemical NSC lineage markers. The feline glial tumors were subjected to immunohistochemical scoring followed by hierarchical cluster analysis. In newborn brains, glial acidic fibrillary protein (GFAP)/nestin/sex-determining region Y-box transcription factor 2 (SOX2)-immunopositive NSCs, SOX2-immunopositive intermediate progenitor cells, oligodendrocyte transcription factor 2 (OLIG2)/platelet-derived growth factor receptor-α (PDGFR-α)-immunopositive oligodendrocyte precursor cells (OPCs), OLIG2/GFAP-immunopositive immature astrocytes, and neuronal nuclear (NeuN)/ß-3 tubulin-immunopositive mature neuronal cells were observed. The apical membrane of NSCs was also immunopositive for Na+/H+ exchanger regulatory factor 1 (NHERF1). In mature brains, the NSC lineage cells were similar to those of the newborn brains. A total of 13 glial tumors consisted of 2 oligodendrogliomas, 4 astrocytomas, 3 subependymomas, and 4 ependymomas. Astrocytomas, subependymomas, and ependymomas were immunopositive for GFAP, nestin, and SOX2. Subependymomas and ependymomas showed dot-like or apical membrane immunolabeling for NHERF1, respectively. Astrocytomas were immunopositive for OLIG2. Oligodendrogliomas and subependymomas were immunopositive for OLIG2 and PDGFR-α. Feline glial tumors also showed variable immunolabeling for ß-3 tubulin, NeuN, and synaptophysin. Based on these results, feline astrocytomas, subependymomas, and ependymomas appear to have an NSC-like immunophenotype. In addition, astrocytomas, subependymomas, and ependymomas have the characteristics of glial, oligodendrocyte precursor, and ependymal cells, respectively. Feline oligodendrogliomas likely have an OPC-like immunophenotype. In addition, feline glial tumors may have multipotential stemness for differentiation into neuronal cells. These preliminary results should be validated by gene expression analyses in future studies with larger case numbers.


Assuntos
Astrocitoma , Doenças do Gato , Ependimoma , Glioma Subependimal , Glioma , Células-Tronco Neurais , Oligodendroglioma , Gatos , Animais , Oligodendroglioma/patologia , Oligodendroglioma/veterinária , Nestina , Glioma Subependimal/metabolismo , Glioma Subependimal/patologia , Glioma Subependimal/veterinária , Tubulina (Proteína)/metabolismo , Glioma/patologia , Glioma/veterinária , Encéfalo/patologia , Astrocitoma/patologia , Astrocitoma/veterinária , Ependimoma/veterinária , Células-Tronco Neurais/metabolismo , Células-Tronco Neurais/patologia , Proteína Glial Fibrilar Ácida/metabolismo
2.
PLoS One ; 10(6): e0131367, 2015.
Artigo em Inglês | MEDLINE | ID: mdl-26115524

RESUMO

BACKGROUND: We analyzed aquaporin 4 and -1 expression in subependymomas, benign and slow growing brain tumors WHO grade I. Ten subependymoma cases were investigated, five of the fossa inferior and five of the fossa superior. METHODS AND RESULTS: Using immunohistochemistry, we observed different aquaporin expression patterns depending on localization: aquaporin 4 and -1 were detected in infratentorial subependymomas in the entire tumor tissue. In contrast, supratentorial subependymomas revealed aquaporin 4 and -1 expression only in border areas of the tumor. PCR analyses however showed no difference in aquaporin 4 expression between all subependymomas independent of localization but at higher levels than in normal brain. In contrast, aquaporin 1 RNA levels were found to be higher only in infratentorial samples compared to supratentorial and normal brain samples. The reason for the different distribution pattern of aquaporin 4 in subependymomas still remains unclear. On the cellular level, aquaporin 4 was redistributed on the surface of the tumor cells, and in freeze fracture replicas no orthogonal arrays of particles were found. This was similar to our previous findings in malignant glioblastomas. From these studies, we know that extracellular matrix molecules within the tumor like agrin and its receptor alpha-dystroglycan are involved in forming orthogonal arrays of particles. In subependymomas neither agrin nor alpha-dystroglycan were detected around blood vessels. CONCLUSIONS: Taken together, we show in this study that in the benign subependymomas aquaporins 1 and 4 are dramatically redistributed and upregulated. We speculate that extracellular environments of infra- and supratentorial subependymomas are different and lead to different distribution patterns of aquaporin 4 and -1.


Assuntos
Aquaporina 1/biossíntese , Aquaporina 4/biossíntese , Neoplasias Encefálicas/metabolismo , Regulação Neoplásica da Expressão Gênica , Glioma Subependimal/metabolismo , Proteínas de Neoplasias/biossíntese , Adulto , Idoso , Neoplasias Encefálicas/patologia , Feminino , Glioma Subependimal/patologia , Humanos , Masculino , Pessoa de Meia-Idade
3.
J Neuroimmunol ; 277(1-2): 168-75, 2014 Dec 15.
Artigo em Inglês | MEDLINE | ID: mdl-25465288

RESUMO

Subependymomas are usually treated with surgical resection; however, no standard, defined alternative medical therapy is recommended for patients who are not surgical candidates, owing to a paucity of molecular, immunological, and genetic characterization. To address this, an ex vivo functional analysis of the immune microenvironment in subependymoma was conducted, a subependymoma cytokine/chemokine microarray was constructed for the evaluation of operational immune and molecular pathways, and a subependymoma cell line was derived and used to test a variety of cytotoxic agents that target operational pathways identified in subependymoma. We found that immune effectors are detectable within the microenvironment of subependymoma; however, marked immune suppression is not observed. The subependymoma tissue microarrays demonstrated tumor expression of p53, MDM2, HIF-1α, topoisomerase II-ß, p-STAT3, and nucleolin, but not EGFRvIII, EphA2, IL-13RA2, CMV, CTLA-4, FoxP3, PD-1, PD-L1, EGFR, PDGF-α, PDGF-ß, PDGFR-α, PDGFR-ß, PTEN, IGFBP2, PI3K, MDM4, IDH1, mTOR, or Jak2. A topoisomerase inhibitor (WP744, IC50=0.83 µM) and a p-STAT3/HIF-1α inhibitor (WP1066, IC50=3.15 µM) demonstrated a growth inhibition of the subependymoma cell proliferation. Cumulatively, these data suggest that those agents that interfere with oncogenes operational in subependymoma may have clinical impact.


Assuntos
Neoplasias Encefálicas/patologia , Ensaios de Seleção de Medicamentos Antitumorais , Glioma Subependimal/patologia , Proteínas de Neoplasias/metabolismo , Antineoplásicos/química , Antineoplásicos/farmacologia , Antineoplásicos/uso terapêutico , Neoplasias Encefálicas/embriologia , Neoplasias Encefálicas/metabolismo , Linhagem Celular Tumoral/efeitos dos fármacos , Proliferação de Células/efeitos dos fármacos , Ensaio de Unidades Formadoras de Colônias , Citocinas/genética , Citocinas/metabolismo , Testes Imunológicos de Citotoxicidade , Relação Dose-Resposta a Droga , Citometria de Fluxo , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , Glioma Subependimal/imunologia , Glioma Subependimal/metabolismo , Humanos , Proteínas de Neoplasias/genética , Células-Tronco Neoplásicas/efeitos dos fármacos , Células-Tronco Neoplásicas/imunologia , Células-Tronco Neoplásicas/metabolismo , Piridinas/química , Piridinas/farmacologia , Transdução de Sinais/efeitos dos fármacos , Transdução de Sinais/fisiologia , Linfócitos T/efeitos dos fármacos , Linfócitos T/imunologia , Análise Serial de Tecidos , Tirfostinas/química , Tirfostinas/farmacologia
4.
J Neurosurg ; 119(6): 1424-31, 2013 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-24116725

RESUMO

OBJECT: Ependymal tumors are highly variable in clinical and molecular behavior and affect both children and adults. Regarding the paucity of appropriate experimental models, the underlying molecular mechanisms of their behavioral variability are poorly understood. Considering the increasing evidence of epigenetic changes in various tumors, in addition to the preclinical success of epigenetic-based therapeutics in tumors of the CNS, epigenetic study of ependymal tumors is warranted. METHODS: Using immunohistochemistry, the authors investigated the patterns of global acetylation of lysine position 9 of histone 3 (H3K9Ac), an epigenetic marker of active gene transcription, in 85 ependymal tumors with various WHO grades and clinicopathological characteristics. RESULTS: Most of the nuclei in all ependymal tumors were H3K9Ac negative (mean ± SD 65.9% ± 26.5 vs 34.1% ± 26.5% positive, p < 0.0001). Subependymomas had more H3K9Ac-positive nuclei (67.2% ± 10.2%) than myxopapillary ependymomas, ependymomas, and anaplastic ependymomas (p < 0.05). Additionally, intracranial parenchymal tumors had significantly fewer H3K9Ac-positive nuclei (13.1% ± 21.9%) than tumors of other CNS localizations (p < 0.001), and supratentorial ventricular tumors had the highest number of H3K9Ac-positive nuclei (66.4% ± 11.8%) among CNS ependymal tumors (p < 0.0001). The H3K9Ac pattern in ependymal tumors also revealed prognostic significance such that tumors with less than 20% acetylated nuclei had a higher probability of recurrence than tumors with 20% or more acetylated nuclei (p = 0.0327), and recurrent tumors had significantly fewer H3K9Ac-positive nuclei than primary ones (16% ± 22.5% vs. 38% ± 25.8%; p < 0.0001). However, the effect of tumor location on survival of patients was nonsignificant in a multivariate survival analysis, and H3K9 acetylation levels of tumors contributed independently to the survival of patients. In addition, ependymal tumors with more than or equal to 20% H3K9 acetylated cells had lower MIB-1 expression than those with less than 20% H3K9 acetylated cells (p < 0.01). CONCLUSIONS: Global H3K9Ac contributes independently to the prognosis of patients with ependymal tumors such that tumors with lower H3K9Ac values have a higher probability of recurrence and are more proliferative. Additionally, subependymomas have a higher H3K9Ac profile than other ependymal tumor subclasses, underlining their benign clinical behavior.


Assuntos
Ependimoma/metabolismo , Histonas/metabolismo , Lisina/metabolismo , Bancos de Tecidos , Acetilação , Biomarcadores/metabolismo , Ependimoma/classificação , Ependimoma/patologia , Glioma Subependimal/metabolismo , Glioma Subependimal/patologia , Humanos , Gradação de Tumores , Recidiva Local de Neoplasia , Estadiamento de Neoplasias , Prognóstico , Análise de Sobrevida , Ubiquitina-Proteína Ligases/metabolismo
7.
Neurol India ; 57(2): 191-3, 2009.
Artigo em Inglês | MEDLINE | ID: mdl-19439853

RESUMO

Subependymomas of the lateral ventricles are rare tumors. We present two patients with subependymomas of the lateral ventricle, who underwent gross total resection of the tumor via transcallosal approach. The patient, with increased Ki-67 labeling index had recurrence of tumor two years after the initial operation. We emphasize at the risk of recurrence which is probably correlated with Ki-67 labeling index.


Assuntos
Neoplasias do Ventrículo Cerebral/metabolismo , Glioma Subependimal/metabolismo , Antígeno Ki-67/metabolismo , Ventrículos Laterais/patologia , Recidiva Local de Neoplasia/metabolismo , Adulto , Neoplasias do Ventrículo Cerebral/patologia , Feminino , Glioma Subependimal/patologia , Humanos , Imageamento por Ressonância Magnética/métodos , Estatística como Assunto
8.
Neuroscience ; 156(1): 203-15, 2008 Sep 22.
Artigo em Inglês | MEDLINE | ID: mdl-18706978

RESUMO

Tuberous sclerosis complex (TSC) is an autosomal dominant disorder associated with cortical malformations (cortical tubers) and the development of glial tumors (subependymal giant-cell tumors, SGCTs). Expression of metabotropic glutamate receptor (mGluR) subtypes is developmentally regulated and several studies suggest an involvement of mGluR-mediated glutamate signaling in the regulation of proliferation and survival of neural stem-progenitor cells, as well as in the control of tumor growth. In the present study, we have investigated the expression and cell-specific distribution of group I (mGluR1, mGluR5), group II (mGluR2/3) and group III (mGluR4 and mGluR8) mGluR subtypes in human TSC specimens of both cortical tubers and SGCTs, using immunocytochemistry. Strong group I mGluR immunoreactivity (IR) was observed in the large majority of TSC specimens in dysplastic neurons and in giant cells within cortical tubers, as well as in tumor cells within SGCTs. In particular mGluR5 appeared to be most frequently expressed, whereas mGluR1alpha was detected in a subpopulation of neurons and giant cells. Cells expressing mGluR1alpha and mGluR5, demonstrate IR for phospho-S6 ribosomal protein (PS6), which is a marker of the mammalian target of rapamycin (mTOR) pathway activation. Group II and particularly group III mGluR IR was less frequently observed than group I mGluRs in dysplastic neurons and giant cells of tubers and tumor cells of SGCTs. Reactive astrocytes were mainly stained with mGluR5 and mGluR2/3. These findings expand our knowledge concerning the cellular phenotype in cortical tubers and in SGCTs and highlight the role of group I mGluRs as important mediators of glutamate signaling in TSC brain lesions. Individual mGluR subtypes may represent potential pharmacological targets for the treatment of the neurological manifestations associated with TSC brain lesions.


Assuntos
Neoplasias Encefálicas/metabolismo , Córtex Cerebral/metabolismo , Células Gigantes/metabolismo , Glioma Subependimal/metabolismo , Receptores de Glutamato Metabotrópico/metabolismo , Esclerose Tuberosa/metabolismo , Adolescente , Adulto , Astrócitos/metabolismo , Astrócitos/patologia , Biomarcadores Tumorais/análise , Biomarcadores Tumorais/metabolismo , Neoplasias Encefálicas/patologia , Córtex Cerebral/patologia , Criança , Pré-Escolar , Feminino , Células Gigantes/patologia , Glioma Subependimal/patologia , Ácido Glutâmico/metabolismo , Humanos , Imuno-Histoquímica , Lactente , Masculino , Neurônios/metabolismo , Neurônios/patologia , Proteínas Quinases/metabolismo , Receptor de Glutamato Metabotrópico 5 , Serina-Treonina Quinases TOR , Esclerose Tuberosa/patologia , Adulto Jovem
9.
Brain Pathol ; 18(4): 469-73, 2008 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-18397339

RESUMO

Subependymomas (SE) are slow-growing brain tumors that tend to occur within the ventricles of middle-aged and elderly adults. The World Health Organization classifies these tumors within the ependymoma group. Previous limited analysis of this tumor type had not revealed significant underlying cytogenetic abnormalities. We have used microarray comparative genomic hybridization to study a series of SE (n = 12). A whole-genome array at 0.97-Mb resolution showed copy number abnormalities in five of 12 cases (42%). Two cases (17%) showed regions of loss on chromosome 6. More detailed analysis of all cases using a chromosome 6 tile-path array confirmed the presence of overlapping regions of loss in only these two cases. One of these cases also showed trisomy chromosome 7. Monosomy of chromosome 8 was seen in a further two cases (17%), and a partial loss on chromosome 14 was observed in one additional case. This is the first array-based, genome-wide study of SE. The observation that five of 12 cases examined (42%) at 0.97-Mb resolution showed chromosomal copy number abnormalities is a novel finding in this tumor type.


Assuntos
Neoplasias do Ventrículo Cerebral/genética , Cromossomos Humanos/genética , Dosagem de Genes/genética , Predisposição Genética para Doença/genética , Glioma Subependimal/genética , Monossomia , Trissomia , Adulto , Idoso , Neoplasias do Ventrículo Cerebral/metabolismo , Neoplasias do Ventrículo Cerebral/patologia , Cromossomos Humanos Par 14/genética , Cromossomos Humanos Par 6/genética , Cromossomos Humanos Par 7/genética , Cromossomos Humanos Par 8/genética , Análise Mutacional de DNA , Feminino , Perfilação da Expressão Gênica , Biblioteca Genômica , Genótipo , Glioma Subependimal/metabolismo , Glioma Subependimal/patologia , Humanos , Masculino , Pessoa de Meia-Idade , Mutação/genética , Análise de Sequência com Séries de Oligonucleotídeos , Deleção de Sequência
10.
J Neurooncol ; 74(1): 1-8, 2005 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-16078101

RESUMO

For investigation of histogenesis of central neurocytomas (CNs), subependymoma (SEs), subependymal giant cell astrocytomas (SEGAs), we studied expression of various neuronal and glial biomarkers by immunohistochemical (IHC) study and reverse transcriptase-polymerase chain reaction (RT-PCR). The materials for IHC were paraffin section of seven CNs, three SEs, and eight SEGAs and those for RT-PCR were frozen tissues of seven CNs, three SEs, and five SEGAs. Control group was five ependymomas (EPs) and four pilocytic astrocytomas (PAs). The neuronal biomarkers included nestin, chromogranin A (chrA), synaptophysin (SNP), neuronal cell adhesion molecule (NCAM), neuron specific enolase (NSE), neuronal nuclear antigen (NeuN), neurofilament (NF) and the glial marker was GFAP. CNs expressed all neuronal markers except NF (0%), SNP (100%), NCAM (100%), NSE (100%), NeuN (100%), nestin (29%) and chrA (43%), but GFAP expression was found only in one case (14%). SEGA coexpressed several neuronal markers and a glial marker; NeuN (100%), NSE (88%), NCAM (63%), nestin (100%), SNP (weakly and focally, 100%), and GFAP (100%), however, other neuronal markers including chrA, SNP and NF were all negative. SE expressed nonspecific neuronal markers (NCAM (100%) and NSE (100%)) which showed weak intensity and a GFAP (100%), but not nestin. Among control cases of EPs and PAs, no one case expressed neuronal markers except nonspecific neuronal marker of NCAM, but robustly expressed GFAP. RT-PCR product of nestin was expressed in 29% of CNs (2/7cases), 60% of SEGAs (3/5 cases), 100% of SEs (3/3 cases), 80% of EPs (4/5 cases), and 25% of PAs (1/4 cases). Conclusively, coexpression of neuronal and glial markers and expression of nestin in CNs, SEGAs and SEs suggested the origin of these tumor cells might be the stem cells being able to differentiate into both neuronal and glial phenotypes. But CNs might be originated from rather neuronally committed stem cells and SEs from rather glially committed stem cells.


Assuntos
Astrocitoma/metabolismo , Biomarcadores Tumorais/análise , Neoplasias Encefálicas/metabolismo , Glioma Subependimal/metabolismo , Neurocitoma/metabolismo , Astrocitoma/patologia , Neoplasias Encefálicas/patologia , Glioma Subependimal/patologia , Humanos , Imuno-Histoquímica , Proteínas de Filamentos Intermediários/biossíntese , Proteínas do Tecido Nervoso/biossíntese , Nestina , Neurocitoma/patologia , Neuroglia/metabolismo , Neurônios/metabolismo , Reação em Cadeia da Polimerase Via Transcriptase Reversa
11.
Cancer ; 103(12): 2598-605, 2005 Jun 15.
Artigo em Inglês | MEDLINE | ID: mdl-15861411

RESUMO

BACKGROUND: Published research on the clinicopathologic features of extraventricular ependymal neoplasms of the cerebral hemispheres has been scant. METHODS: Thirty-two archival cases were studied to investigate the prognostic impact of clinicopathologic parameters including flow cytometry, the proliferation (Ki-67) labeling index, and p53 expression. RESULTS: Among these 32 cases were 2 subependymomas, 19 ependymomas, and 11 anaplastic ependymomas. No significant gender predilection was observed, and 45% of patients were in their second or third decade of life. The left cerebral hemisphere was 1.5 times more commonly involved. On available imaging studies, lesions were often cystic, with or without a mural nodule. Tumors expressed glial fibrillary acidic protein (87%), S-100 protein (77%), cytokeratin (43%), and epithelial membrane antigen (17%). Ki-67 proliferation index paralleled tumor grade. Immunoreactivity for p53 protein was observed in the 2 cases of subependymoma, in 10 of 11 anaplastic ependymomas, and in 6 of 17 ependymomas. Flow cytometry performed in 27 tumors revealed diploidy in 20 cases and aneuploidy in 4 cases (3 anaplastic and 1 classic ependymomas), with S-phase fraction ranging from 0.2-9.7. Eleven subjects were additionally treated with radiotherapy, and 3 with chemotherapy. Follow up was available in 25 (78%) patients. CONCLUSIONS: The results of the current study suggest that there is no significant relation between histopathology, Ki-67 proliferation index, p53 immunolabeling, tumor ploidy, and biologic behavior.


Assuntos
Neoplasias Encefálicas/patologia , Neoplasias do Ventrículo Cerebral/patologia , Ependimoma/patologia , Glioma Subependimal/patologia , Neoplasias Supratentoriais/patologia , Adolescente , Adulto , Idoso , Neoplasias Encefálicas/metabolismo , Neoplasias Encefálicas/terapia , Proliferação de Células , Neoplasias do Ventrículo Cerebral/metabolismo , Neoplasias do Ventrículo Cerebral/terapia , Criança , Pré-Escolar , Ependimoma/metabolismo , Ependimoma/terapia , Feminino , Citometria de Fluxo , Glioma Subependimal/metabolismo , Glioma Subependimal/terapia , Humanos , Lactente , Antígeno Ki-67/metabolismo , Masculino , Pessoa de Meia-Idade , Ploidias , Prognóstico , Fase S , Neoplasias Supratentoriais/metabolismo , Neoplasias Supratentoriais/terapia , Proteína Supressora de Tumor p53
12.
Pathology ; 36(2): 139-44, 2004 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-15203749

RESUMO

AIMS: To gain a better insight into the biological behaviour of subependymal giant cell astrocytoma (SEGA), tumour suppressor gene protein expression and various proliferative indices were studied in these tumours and correlated with histological features and clinical outcome. METHODS: We studied 23 cases of SEGA, 19 from our own Institute and four from the National Institute of Mental Health and Neurological Sciences (NIMHANS), Bangalore, India. Immunohistochemical staining for various glial and neuronal markers, proliferative markers (MIB-1, Topoisomerase II alpha PCNA) and tumour suppressor gene protein expression of p53 and retinoblastoma (Rb) were performed. RESULTS: Nineteen cases of SEGA were collected over a period of 23 years (January 1978-December 2001), which accounted for 0.16% of all intracranial tumours and 0.51% of all gliomas reported at this centre. Ages ranged from 4 to 37 years (mean 13.2 years) with a male preponderance. Nine of the 23 cases were associated with tuberous sclerosis (TS), six at the time of diagnosis, while three developed TS during the follow-up period. Treatment consisted of surgical resection (total in nine cases and subtotal in 14 cases) followed by radiotherapy in seven cases. Except for two patients who died in the immediate post-operative period of surgical complications, the remaining patients were all alive in the follow-up period (mean 37.1 months). One patient experienced recurrence 22 years after the first surgery and a second patient after 2 years. Necrosis and/or mitoses were observed in five cases. Immunohistochemically, tumours were positive for both glial and neuronal markers. Interspersed inflammatory cells were a mixture of mast cells and lymphocytes of T immunophenotype. The MIB-1 labelling index (LI) ranged from 0 to 8% (mean 3.0%), topoisomerase II alpha (topo II alpha) LI from 0 to 9.5% (mean 2.9%) and PCNA LI from 10 to 59% (mean 32.5%). The difference in the labelling indices of tumours with and without mitoses and/or necrosis was not statistically significant. None of the tumours revealed loss of Rb gene protein expression. p53 immunopositivity was seen in 14 cases (labelling indices ranged from 1 to 7.3% with a mean of 2.4%). The correlation between the MIB-1 LI and topo II alpha LI, and topo II alpha LI and PCNA LI was significant (P<0.05) but not so with other parameters like p53 protein expression, duration of survival and morphological features such as mitoses and necrosis. CONCLUSIONS: SEGAs are rare intraventricular tumours associated with TS and express both neuronal and glial markers. They have a low proliferative potential. Mitoses and necrosis are not associated with a worse prognosis. In view of the low proliferative indices and long survival of these patients without recurrence, the role of post-operative radiotherapy is questionable. These patients should be followed up closely as many of them develop stigmata of tuberous sclerosis at a later stage.


Assuntos
Biomarcadores Tumorais/metabolismo , Neoplasias do Ventrículo Cerebral/patologia , Glioma Subependimal/patologia , Proteína do Retinoblastoma/metabolismo , Proteína Supressora de Tumor p53/metabolismo , Adolescente , Adulto , Antígenos de Neoplasias , Neoplasias do Ventrículo Cerebral/metabolismo , Neoplasias do Ventrículo Cerebral/cirurgia , Ventriculografia Cerebral , Criança , Pré-Escolar , DNA Topoisomerases Tipo II/análise , Proteínas de Ligação a DNA , Feminino , Células Gigantes/metabolismo , Células Gigantes/patologia , Glioma Subependimal/metabolismo , Glioma Subependimal/cirurgia , Humanos , Antígeno Ki-67/análise , Masculino , Mitose , Antígeno Nuclear de Célula em Proliferação/análise , Proteína do Retinoblastoma/genética , Tomografia Computadorizada por Raios X , Resultado do Tratamento , Proteína Supressora de Tumor p53/genética
13.
Neurosurg Clin N Am ; 14(4): 469-82, 2003 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-15024796

RESUMO

Tumors that primarily or exclusively involve the ventricular system constitute a rare and heterogeneous group. Certain histologic tumor types predominantly occur in children, whereas others are more common in adults. Tumor location provides additional clues to correct diagnosis. When used in conjunction with clinical and radiologic data, histopathologic features can distinguish among this wide range of possibilities to provide the correct diagnosis for optimal patient management.


Assuntos
Neoplasias do Ventrículo Cerebral/epidemiologia , Neoplasias do Ventrículo Cerebral/patologia , Biomarcadores , Carcinoma/metabolismo , Carcinoma/patologia , Neoplasias do Ventrículo Cerebral/imunologia , Neoplasias do Plexo Corióideo/metabolismo , Neoplasias do Plexo Corióideo/patologia , Diagnóstico Diferencial , Ependimoma/epidemiologia , Ependimoma/metabolismo , Ependimoma/patologia , Glioma Subependimal/epidemiologia , Glioma Subependimal/metabolismo , Glioma Subependimal/patologia , Humanos , Imuno-Histoquímica , Papiloma/metabolismo , Papiloma/patologia
14.
J Neuropathol Exp Neurol ; 60(10): 984-93, 2001 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-11589429

RESUMO

Microtubule-associated protein 2 (MAP2), a protein linked to the neuronal cytoskeleton in the mature central nervous system (CNS), has recently been identified in glial precursors indicating a potential role during glial development. In the present study, we systematically analyzed the expression of MAP2 in a series of 237 human neuroepithelial tumors including paraffin-embedded specimens and tumor tissue microarrays from oligodendrogliomas, mixed gliomas, astrocytomas, glioblastomas, ependymomas, as well as dysembryoplastic neuroepithelial tumors (DNT), and central neurocytomas. In addition, MAP2-immunoreactive precursor cells were studied in the developing human brain. Three monoclonal antibodies generated against MAP2A-B or MAP2A-D isoforms were used. Variable immunoreactivity for MAP2 could be observed in all gliomas with the exception of ependymomas. Oligodendrogliomas exhibited a consistently strong and distinct pattern of expression characterized by perinuclear cytoplasmic staining without significant process labeling. Tumor cells with immunoreactive bi- or multi-polar processes were mostly encountered in astroglial neoplasms, whereas the small cell component in neurocytomas and DNT was not labeled. These features render MAP2 immunoreactivity a helpful diagnostic tool for the distinction of oligodendrogliomas and other neuroepithelial neoplasms. RT-PCR, Western blot analysis, and in situ hybridization confirmed the expression of MAP2A-C (including the novel MAP2+ 13 transcript) in both oligodendrogliomas and astrocytomas. Double fluorescent laser scanning microscopy showed that GFAP and MAP2 labeled different tumor cell populations. In embryonic human brains, MAP2-immunoreactive glial precursor cells were identified within the subventricular or intermediate zones. These precursors exhibit morphology closely resembling the immunolabeled neoplastic cells observed in glial tumors. Our findings demonstrate MAP2 expression in astrocytic and oligodendroglial neoplasms. The distinct pattern of immunoreactivity in oligodendrogliomas may be useful as a diagnostic tool. Since MAP2 expression occurs transiently in migrating immature glial cells, our findings are in line with an assumed origin of diffuse gliomas from glial precursors.


Assuntos
Biomarcadores Tumorais/biossíntese , Proteínas Associadas aos Microtúbulos/biossíntese , Neoplasias Neuroepiteliomatosas/metabolismo , Neuroglia/metabolismo , Oligodendroglioma/metabolismo , Células-Tronco/metabolismo , Adulto , Idoso , Especificidade de Anticorpos , Reações Antígeno-Anticorpo , Biomarcadores Tumorais/imunologia , Diagnóstico Diferencial , Feto , Glioma/diagnóstico , Glioma/metabolismo , Glioma/patologia , Glioma Subependimal/diagnóstico , Glioma Subependimal/metabolismo , Glioma Subependimal/patologia , Humanos , Lactente , Recém-Nascido , Proteínas Associadas aos Microtúbulos/imunologia , Pessoa de Meia-Idade , Neoplasias Neuroepiteliomatosas/diagnóstico , Neoplasias Neuroepiteliomatosas/patologia , Neuroglia/citologia , Oligodendroglioma/diagnóstico , Oligodendroglioma/patologia , Isoformas de Proteínas/biossíntese
15.
Oncol Rep ; 5(5): 1199-203, 1998.
Artigo em Inglês | MEDLINE | ID: mdl-9683835

RESUMO

In this study we report an in vitro 1H magnetic resonance spectroscopy (MRS) characterization of water soluble metabolites obtained from 17 low grade extra and intracerebral human tumors (8 meningiomas, 5 oligodendrogliomas, 2 subependimomas and 2 ependimomas). In addition, the in vivo localized 1H MRS results for 4 of the meningiomas are reported. The main metabolic features characterizing low grade tumors were investigated. Meningiomas are characterized by high Cho/Cr and Ala/Cr ratios; in many cases both in the in vitro and the in vivo spectra these ratios cannot be evaluated, due to the absence of the Cr metabolite. Low grade oligodendrogliomas are characterized by low Cho/Cr ratios. High amounts of myo-inositol are found in the spectra of ependimomas and subependimomas which are distinguished by different Cho/Cr ratio values and by a different Ala content.


Assuntos
Neoplasias Encefálicas/metabolismo , Glioma/metabolismo , Neoplasias Encefálicas/patologia , Neoplasias Encefálicas/cirurgia , Glioma/patologia , Glioma/cirurgia , Glioma Subependimal/metabolismo , Glioma Subependimal/patologia , Glioma Subependimal/cirurgia , Humanos , Hidrogênio , Espectroscopia de Ressonância Magnética/métodos , Neoplasias Meníngeas/metabolismo , Neoplasias Meníngeas/patologia , Neoplasias Meníngeas/cirurgia , Meningioma/metabolismo , Meningioma/patologia , Meningioma/cirurgia , Oligodendroglioma/metabolismo , Oligodendroglioma/patologia , Oligodendroglioma/cirurgia
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