1/10. Deletion of the NF2 region in both meningioma and juxtaposed meningioangiomatosis: case report supporting a neoplastic relationship.We report a case of juxtaposed atypical meningioma and meningioangiomatosis (MA) in an 8-year-old boy with no clinical stigmata or family history of neurofibromatosis. We studied the proliferative activity and genetic changes in the two lesions in an attempt to define their biologic and pathogenetic relationships. The MIB-1 index was 11% in the meningioma and <1% in the MA, indicating increased proliferative activity in the meningioma. fluorescence in situ hybridization was done for two chromosomal regions commonly deleted in meningiomas. There was loss of the neurofibromatosis 2 locus (22q12) in both the meningioma and MA. Conversely, the region of 1p32 was not deleted. Our results indicate that both the meningioma and MA arose from the same clonal process, with the meningioma probably undergoing additional, but undefined, genetic alterations that confer upon it a more proliferative potential. This loss of 22q12 in the MA raises doubt about the presumed hamartomatous nature of MA.- - - - - - - - - - ranking = 1keywords = hybridization (Clic here for more details about this article) |
2/10. Biphasic malignant meningioma: a comparative genomic hybridization study.To ascertain if a carcinoma-like component within a fibroblastic meningioma represented a metastatic carcinoma to a meningioma or malignant progression, we employed traditional immunohistochemical methods as well as comparative genomic hybridization (CGH) which compares chromosomal alterations. vimentin and epithelial membrane antigen were strongly immunoreactive in both the fibroblastic and carcinoma-like components. The CGH profile in both components had similar chromosomal alterations, including losses of 1p, 14, 16p13-->p10 and 22. However, the CGH profiles from the fibroblastic component showed losses of 4p, 10q23-->q24 and 18, along with gains of 1q, 6q25-->qter and 13q32-->qter. The profile of the carcinoma-like component showed losses of chromosome 4, in addition to gains of 3p12-->q13.11, 5q14.3-->q23.2, 6pter-->p23, and 13q14.2-->qter. CGH analysis of a biphasic malignant meningioma confirmed that the disparate histologic components were genetically related and likely derivative from a common precursor, demonstrating genetic instability and clonal expansion. Furthermore, CGH showed that the histologically appearing low-grade fibroblastic component had not solely the characteristic alterations of a benign meningioma but had already progressed to an atypical meningioma.- - - - - - - - - - ranking = 5keywords = hybridization (Clic here for more details about this article) |
3/10. Malignant rhabdoid meningioma arising in the setting of preexisting ganglioglioma: a diagnosis supported by fluorescence in situ hybridization. Case report.A highly malignant brain neoplasm with rhabdoid morphological features emerged in the bed of a subtotally resected ganglioglioma in a 54-year-old retired nuclear submarine officer. A combined application of neuroimaging, immunohistochemical studies, electron microscopy, and fluorescence in situ hybridization (FISH) was used to establish the morphological identity of the tumor. The rhabdoid appearance of the tumor cells indicated either an especially malignant variant of rhabdoid meningioma or an atypical teratoid/rhabdoid tumor with an unusually late onset. Whereas immunohistochemical studies and electron microscopy could only be used to narrow down the differential diagnosis, FISH revealed loss of one copy of NF2 with preservation of the INI1 region on 22q, thus establishing the identity of the tumor.- - - - - - - - - - ranking = 5keywords = hybridization (Clic here for more details about this article) |
4/10. Histologically benign metastatic meningioma: morphological and cytogenetic study. Case report.The authors report on a 75-year-old man with histologically benign fibroblastic meningioma metastasizing to the lung, liver, spleen, and kidney. The original tumor exhibited a complex karyotype involving different structural and numerical anomalies associated with monosomy of chromosome 22. The implication of chromosome 1p36 was confirmed by fluorescence in situ hybridization in most interphase nuclei. Metastases occurred 4 months after incomplete resection with prior therapeutic embolization. The recurrent tumor in turn displayed anaplastic features and an increased Ki-67 labeling index. Genetic alterations in such morphologically benign meningiomas have been implicated in the malignant development and progression of these tumors.- - - - - - - - - - ranking = 1keywords = hybridization (Clic here for more details about this article) |
5/10. Primitive neuroectodermal tumor in the cerebellopontine angle with isochromosome 17q presenting as meningioma in a woman 26 years of age.An unusual posterior fossa neoplasm in a 26-year-old woman with short history of the cerebellar symptoms is presented. CT and MR images showed the tumor within the cerebellopontine angle, suspected as meningioma. At surgery, the tumor was dura-attached and did not infiltrate the arachnoid. Histologically, the neoplasm was a small blue cell tumor with solid and microcystic pattern, consistent with primitive neuroectodermal tumor (PNET). Immunohistochemically the cells were strongly positive for NCAM and GFAP. fluorescence in situ hybridization (FISH) was performed with the cosmids G9 and F7 (flanking EWSR1/22q12 region) dna probes and dual-color spectrum-orange LSI HER-2/neu (17q11.2)/spectrum green CEP17 (17p11.1-q11.1) DNA probe. The presence of isochromosome 17q within neoplastic cells was found. The tumor was classified as a medulloblastoma. We demonstrate the utility of a multidisciplinary approach to nervous system tumor diagnosis. The clinical features together with histological, immunohistochemical, and characteristic molecular alteration allowed classification of the presented case.- - - - - - - - - - ranking = 1keywords = hybridization (Clic here for more details about this article) |
6/10. Melanocytic colonization of a meningothelial meningioma: histopathological and ultrastructural findings with immunohistochemical and genetic correlation: case report.OBJECTIVE AND IMPORTANCE: Melanocytic colonization of nonpigmented extracranial tumors has been reported in adenocarcinomas, squamous cell carcinomas, skin appendage tumors, and dermatofibrosarcoma protuberans. To our knowledge, melanocytic colonization of a meningioma has not previously been described. CLINICAL PRESENTATION: We report an unusual case of a 70-year-old African-American woman who presented with a large frontoparietal meningioma that extended through the calvarium. INTERVENTION: craniotomy with gross total resection of the tumor was performed. Histochemistry, immunocytochemistry, ultrastructural analysis, and molecular genetic study via fluorescence in situ hybridization confirmed melanocytic colonization of a meningothelial meningioma. CONCLUSION: With the inclusion of meningothelial meningioma, the spectrum of tumors affected by melanocytic colonization continues to expand.- - - - - - - - - - ranking = 1keywords = hybridization (Clic here for more details about this article) |
7/10. Abnormalities of chromosome 22 in meningiomas and confirmation of the origin of a dicentric 22 by in situ hybridization.We report three cases of meningioma. Case 1 had a dicentric chromosome number 22 resulting in partial monosomy for a portion of the q-arm, i.e., 46,XX,idic(22)(pter-->q11.2::q11.2-->pter) and 46,XX,psu dic(22)(pter-->q11.2::q11.2-->pter), which was the sole clonal abnormality. The origin of the dicentric chromosome from 22 was confirmed by in situ hybridization studies, using biotin-labeled alpha centromeric dna probes for the acrocentric chromosomes. Case 2 had two distinct clonal abnormalities: deletion of 22q and monosomy of 22. Case 3 also had a deleted 22q.- - - - - - - - - - ranking = 5keywords = hybridization (Clic here for more details about this article) |
8/10. Cytogenetic and in situ DNA-hybridization studies in intracranial tumors of a patient with central neurofibromatosis.We have studied a meningioma and an acoustic neurinoma of a patient with central neurofibromatosis. In the meningioma cells, one chromosome 22 was replaced by an almost metacentric, bisatellited marker chromosome that appeared monocentric after CBG-staining. in situ hybridization with a chromosome 22 centromere specific DNA probe (p22hom48.4) revealed specific signals in the pericentromeric region of the marker chromosome, indicating the presence of at least the short arm and the centromere of chromosome 22. The pericentromeric localization of the hybridization signals suggest the marker consists of an isoformation of the short arm of chromosome 22, resulting in a monosomy for the long arm of chromosome 22. In contrast to these findings in meningioma cells, no chromosomal abnormality could be detected in acoustic neurinoma cells. Our findings provide further evidence that loss of genetic material on the long arm of chromosome 22 is associated with the development of central neurofibromatosis.- - - - - - - - - - ranking = 6keywords = hybridization (Clic here for more details about this article) |
9/10. Germline deletion in a neurofibromatosis type 2 kindred inactivates the NF2 gene and a candidate meningioma locus.Neurofibromatosis type 2 (NF2) is an autosomal dominant disease which predisposes to the development of schwannomas, meningiomas, ependymomas, and juvenile cataracts. The NF2 gene (NF2) has recently been isolated and maps to chromosome 22q12 between the loci D22S212 and D22S32. Deletion studies in sporadic and NF2 associated schwannomas and meningiomas, and the presence of inactivating mutations in NF2 in patients suggest that it acts as a tumor suppressor gene. A candidate meningioma gene (MEN) has also been isolated from the same interval. A new highly polymorphic (CA)n marker, D22S268, which maps very near to NF2, has allowed us to identify a kindred with three living affected individuals, where the disease is presumably caused by a large germline deletion. fluorescence in situ hybridization and pulsed field gel electrophoresis confirm the presence of a 700kb deletion which includes the neurofilament heavy chain subunit gene locus (NEFH), D22S268, NF2 and the putative MEN gene. The absence of meningiomas in this pedigree raises doubts as to the existence of a separate MEN locus in this region. These results support the hypothesis that NF2 results from the inactivation of a tumor suppressor gene on chromosome 22q.- - - - - - - - - - ranking = 1keywords = hybridization (Clic here for more details about this article) |
10/10. erythropoietin synthesis by tumor cells in a case of meningioma associated with erythrocytosis.While secondary erythrocytosis is often associated with tumors arising from the kidney, other tumors have been described to originate in the liver, uterus, ovary, adrenal gland, and central nervous system, among which cerebellar hemangioblastomas are involved in most instances. Two cases of meningioma associated with erythrocytosis have already been reported. We observed a 59-year-old female patient who had developed a frontal meningioma associated with erythrocytosis. Before surgery, she had a significantly elevated total red blood cell volume with a normal plasma volume. serum erythropoietin (Epo) dosage assessed by radioimmunoassay was within the normal range. The tumor was removed and the pathologic study found a meningotheliomatous meningioma. Total rna from the tumor was hybridized to a monkey cDNA Epo probe. A strong 1.6-kb messenger rna (mRNA) signal was observed, which is the expected size of human Epo mRNA. In situ hybridization with the 35S-labeled Epo probe was performed on frozen tumor tissue sections. A significant hybridization was observed in all the tumor cells, whereas the stroma was negative. Therefore, in this meningioma associated with erythrocytosis, Epo was produced by the tumor cells themselves.- - - - - - - - - - ranking = 2keywords = hybridization (Clic here for more details about this article) |
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