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Otmar D Wiestler - One of the best experts on this subject based on the ideXlab platform.
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low frequency of sv40 jc and bk polyomavirus sequences in human medulloblastomas meningiomas and ependymomas
Brain Pathology, 2006Co-Authors: Sascha Weggen, Otmar D Wiestler, Guido Reifenberger, Andreas Von Deimling, Thomas A Bayer, Dietrich Von Schweinitz, Torsten PietschAbstract:Several reports have suggested a role for polyomaviruses in the pathogenesis of human brain tumors. This potential involvement is not conclusively resolved. For the present study, a highly sensitive PCR-assay with fluorescence-labelled primers was developed to search for polyomavirus sequences in human brain tumor and control DNA samples. The assay was shown to detect approximately one viral large T-antigen (TAg) gene per 250 cells. We identified simian virus 40 (SV40)-like sequences in 2/116 medulloblastomas, in 1/131 meningiomas, in 1/25 ependymomas and in 1/2 Subependymomas. A single case of ependymoma contained SV40 VP-1 late gene sequences. Moreover, one of the meningioma samples showed JC virus sequences. In contrast, 60 hepatoblastoma samples and 31 brain samples from schizophrenic patients were consistently negative. BK virus sequences were not detectable in any of our samples. Immunohistochemical analysis of two SV40 positive tumor biopsies failed to detect large TAg in the tumor cells. In the JC positive meningioma, immunoreactivity for the viral late gene product (VP-1) was not observed. Our data do not entirely rule out SV40 and JC virus as an initiative agent with a hit-and-run mechanism. However the low frequency of virus sequences and the absence of TAg protein expression argue against a major role of these viruses in the pathogenesis of human medulloblastomas, meningiomas and ependymomas.
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molecular genetic analysis of ependymal tumors nf2 mutations and chromosome 22q loss occur preferentially in intramedullary spinal ependymomas
American Journal of Pathology, 1999Co-Authors: Christian Ebert, Birgit Meyerputtlitz, Torsten Pietsch, Markus Von Haken, Otmar D Wiestler, Guido Reifenberger, Andreas Von DeimlingAbstract:Ependymal tumors are heterogeneous with regard to morphology, localization, age at first clinical manifestation, and prognosis. Several molecular alterations have been reported in these tumors, including allelic losses on chromosomes 10, 17, and 22 and mutations in the NF2 gene. However, in contrast to astrocytic gliomas, no consistent molecular alterations have been associated with distinct types of ependymal tumors. To evaluate whether morphological subsets of ependymomas are characterized by specific genetic lesions, we analyzed a series of 62 ependymal tumors, including myxopapillary ependymomas, Subependymomas, ependymomas, and anaplastic ependymomas, for allelic losses on chromosome arms 10q and 22q and mutations in the PTEN and NF2 genes. Allelic losses on 10q and 22q were detected in 5 of 56 and 12 of 54 tumors, respectively. Six ependymomas carried somatic NF2 mutations, whereas no mutations were detected in the PTEN gene. All six of the NF2 mutations occurred in ependymomas of WHO grade II and were exclusively observed in tumors with a spinal localization (P = 0.0063). These findings suggest that a considerable fraction of spinal ependymomas are associated with molecular events involving chromosome 22 and that mutations in the NF2 gene may be of primary importance for their genesis. Furthermore, our data suggest that the more favorable clinical course of spinal ependymomas may relate to a distinct pattern of genetic alterations different from that of intracerebral ependymomas.
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association of epidermal growth factor receptor gene amplification with loss of chromosome 10 in human glioblastoma multiforme
Journal of Neurosurgery, 1992Co-Authors: Andreas Von Deimling, David N Louis, Klaus Von Ammon, Iver Petersen, Tomas Hoell, Richard Y Chung, Robert L Martuza, David A Schoenfeld, Gazi M Yasargil, Otmar D WiestlerAbstract:Although the loss of tumor suppressor genes and the activation of oncogenes have been established as two of the fundamental mechanisms of tumorigenesis in human cancer, little is known about the possible interactions between these two mechanisms. Loss of genetic material on chromosome 10 and amplification of the epidermal growth factor receptor (EGFR) gene are the most frequently reported genetic abnormalities in glioblastoma multiforme. In order to examine a possible correlation between these two genetic aberrations, the authors studied 106 gliomas (58 glioblastomas, 14 anaplastic astrocytomas, five astrocytomas, nine pilocytic astrocytomas, seven mixed gliomas, six oligodendrogliomas, two ependymomas, one Subependymoma, one subependymal giant-cell astrocytoma, and three gangliogliomas) with Southern blot analysis for loss of heterozygosity on both arms of chromosome 10 and for amplification of the EGFR gene. Both the loss of genetic material on chromosome 10 and EGFR gene amplification were restricted to the glioblastomas. Of the 58 glioblastoma patients, 72% showed loss of chromosome 10 and 38% showed EGFR gene amplification. The remaining 28% had neither loss of chromosome 10 nor EGFR gene amplification. Without exception, the glioblastomas that exhibited EGFR gene amplification had also lost genetic material on chromosome 10 (p less than 0.001). This invariable association suggests a relationship between the two genetic events. Moreover, the presence of 15 cases of glioblastoma with loss of chromosome 10 but without EGFR gene amplification may further imply that the loss of a tumor suppressor gene (or genes) on chromosome 10 precedes EGFR gene amplification in glioblastoma tumorigenesis.
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association of epidermal growth factor receptor gene amplification with loss of chromosome 10 in human glioblastoma multiforme
Journal of Neurosurgery, 1992Co-Authors: Andreas Von Deimling, David N Louis, Iver Petersen, Tomas Hoell, Richard Y Chung, Robert L Martuza, David A Schoenfeld, Gazi M Yasargil, Klaus Von Ammon, Otmar D WiestlerAbstract:✓ Although the loss of tumor suppressor genes and the activation of oncogenes have been established as two of the fundamental mechanisms of tumorigenesis in human cancer, little is known about the possible interactions between these two mechanisms. Loss of genetic material on chromosome 10 and amplification of the epidermal growth factor receptor (EGFR) gene are the most frequently reported genetic abnormalities in glioblastoma multiforme. In order to examine a possible correlation between these two genetic aberrations, the authors studied 106 gliomas (58 glioblastomas, 14 anaplastic astrocytomas, five astrocytomas, nine pilocytic astrocytomas, seven mixed gliomas, six oligodendrogliomas, two ependymomas, one Subependymoma, one subependymal giant-cell astrocytoma, and three gangliogliomas) with Southern blot analysis for loss of heterozygosity on both arms of chromosome 10 and for amplification of the EGFR gene. Both the loss of genetic material on chromosome 10 and EGFR gene amplification were restricted...
Andreas Von Deimling - One of the best experts on this subject based on the ideXlab platform.
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molecular genetic analysis of ependymal tumors nf2 mutations and chromosome 22q loss occur preferentially in intramedullary spinal ependymomas
American Journal of Pathology, 1999Co-Authors: Christian Ebert, Birgit Meyerputtlitz, Torsten Pietsch, Markus Von Haken, Otmar D Wiestler, Guido Reifenberger, Andreas Von DeimlingAbstract:Ependymal tumors are heterogeneous with regard to morphology, localization, age at first clinical manifestation, and prognosis. Several molecular alterations have been reported in these tumors, including allelic losses on chromosomes 10, 17, and 22 and mutations in the NF2 gene. However, in contrast to astrocytic gliomas, no consistent molecular alterations have been associated with distinct types of ependymal tumors. To evaluate whether morphological subsets of ependymomas are characterized by specific genetic lesions, we analyzed a series of 62 ependymal tumors, including myxopapillary ependymomas, Subependymomas, ependymomas, and anaplastic ependymomas, for allelic losses on chromosome arms 10q and 22q and mutations in the PTEN and NF2 genes. Allelic losses on 10q and 22q were detected in 5 of 56 and 12 of 54 tumors, respectively. Six ependymomas carried somatic NF2 mutations, whereas no mutations were detected in the PTEN gene. All six of the NF2 mutations occurred in ependymomas of WHO grade II and were exclusively observed in tumors with a spinal localization (P = 0.0063). These findings suggest that a considerable fraction of spinal ependymomas are associated with molecular events involving chromosome 22 and that mutations in the NF2 gene may be of primary importance for their genesis. Furthermore, our data suggest that the more favorable clinical course of spinal ependymomas may relate to a distinct pattern of genetic alterations different from that of intracerebral ependymomas.
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association of epidermal growth factor receptor gene amplification with loss of chromosome 10 in human glioblastoma multiforme
Journal of Neurosurgery, 1992Co-Authors: Andreas Von Deimling, David N Louis, Iver Petersen, Tomas Hoell, Richard Y Chung, Robert L Martuza, David A Schoenfeld, Gazi M Yasargil, Klaus Von Ammon, Otmar D WiestlerAbstract:✓ Although the loss of tumor suppressor genes and the activation of oncogenes have been established as two of the fundamental mechanisms of tumorigenesis in human cancer, little is known about the possible interactions between these two mechanisms. Loss of genetic material on chromosome 10 and amplification of the epidermal growth factor receptor (EGFR) gene are the most frequently reported genetic abnormalities in glioblastoma multiforme. In order to examine a possible correlation between these two genetic aberrations, the authors studied 106 gliomas (58 glioblastomas, 14 anaplastic astrocytomas, five astrocytomas, nine pilocytic astrocytomas, seven mixed gliomas, six oligodendrogliomas, two ependymomas, one Subependymoma, one subependymal giant-cell astrocytoma, and three gangliogliomas) with Southern blot analysis for loss of heterozygosity on both arms of chromosome 10 and for amplification of the EGFR gene. Both the loss of genetic material on chromosome 10 and EGFR gene amplification were restricted...
Khalid H Kurtom - One of the best experts on this subject based on the ideXlab platform.
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minimizing cortical disturbance to access ventricular Subependymoma a novel approach utilizing spinal minimally invasive tubular retractor system
Surgical Neurology International, 2019Co-Authors: Eric Klotz, Wendy S Towers, Khalid H KurtomAbstract:Background Subependymomas are rare benign tumors found primarily in the lateral and fourth ventricles. Patients become symptomatic when the tumor obstructs cerebrospinal fluid pathways. We present a novel minimally invasive technique for lateral ventricular Subependymoma resection. Case Description A 57-year-old male presented after a period of progressive ataxia, right upper extremity tremor, and syncopal events. Emergent non-contrast computed tomography of the brain demonstrated a lobulated mass in the left lateral ventricle causing moderate-to-severe obstructive hydrocephalus. Emergent ventriculostomy was placed as a temporizing measure. Subsequent magnetic resonance imaging (MRI) illustrated a large benign appearing mass causing obstruction of the left foramen of Monroe. A small craniotomy was performed utilizing previous ventriculostomy twist hole. The left lateral ventricle was accessed through sequential dilation of ventriculostomy tract using a minimally invasive spine surgery tubular system. Tumor was resected en bloc under microscopic assistance. The patient had an excellent outcome with return to baseline mental status and was discharged from the hospital postoperative day 1. Follow-up MRI demonstrated gross total resection of the mass and decreasing lateral ventricle hydrocephalus with minimal cortical disturbance. Conclusion A minimally invasive tubular system approach to ventricular tumors can be utilized to minimize cortical resection and brain retraction. Minimally invasive surgery also has the potential to decrease the length of stay and enhance postoperative recovery.
Andreas Von Deimling - One of the best experts on this subject based on the ideXlab platform.
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low frequency of sv40 jc and bk polyomavirus sequences in human medulloblastomas meningiomas and ependymomas
Brain Pathology, 2006Co-Authors: Sascha Weggen, Otmar D Wiestler, Guido Reifenberger, Andreas Von Deimling, Thomas A Bayer, Dietrich Von Schweinitz, Torsten PietschAbstract:Several reports have suggested a role for polyomaviruses in the pathogenesis of human brain tumors. This potential involvement is not conclusively resolved. For the present study, a highly sensitive PCR-assay with fluorescence-labelled primers was developed to search for polyomavirus sequences in human brain tumor and control DNA samples. The assay was shown to detect approximately one viral large T-antigen (TAg) gene per 250 cells. We identified simian virus 40 (SV40)-like sequences in 2/116 medulloblastomas, in 1/131 meningiomas, in 1/25 ependymomas and in 1/2 Subependymomas. A single case of ependymoma contained SV40 VP-1 late gene sequences. Moreover, one of the meningioma samples showed JC virus sequences. In contrast, 60 hepatoblastoma samples and 31 brain samples from schizophrenic patients were consistently negative. BK virus sequences were not detectable in any of our samples. Immunohistochemical analysis of two SV40 positive tumor biopsies failed to detect large TAg in the tumor cells. In the JC positive meningioma, immunoreactivity for the viral late gene product (VP-1) was not observed. Our data do not entirely rule out SV40 and JC virus as an initiative agent with a hit-and-run mechanism. However the low frequency of virus sequences and the absence of TAg protein expression argue against a major role of these viruses in the pathogenesis of human medulloblastomas, meningiomas and ependymomas.
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association of epidermal growth factor receptor gene amplification with loss of chromosome 10 in human glioblastoma multiforme
Journal of Neurosurgery, 1992Co-Authors: Andreas Von Deimling, David N Louis, Klaus Von Ammon, Iver Petersen, Tomas Hoell, Richard Y Chung, Robert L Martuza, David A Schoenfeld, Gazi M Yasargil, Otmar D WiestlerAbstract:Although the loss of tumor suppressor genes and the activation of oncogenes have been established as two of the fundamental mechanisms of tumorigenesis in human cancer, little is known about the possible interactions between these two mechanisms. Loss of genetic material on chromosome 10 and amplification of the epidermal growth factor receptor (EGFR) gene are the most frequently reported genetic abnormalities in glioblastoma multiforme. In order to examine a possible correlation between these two genetic aberrations, the authors studied 106 gliomas (58 glioblastomas, 14 anaplastic astrocytomas, five astrocytomas, nine pilocytic astrocytomas, seven mixed gliomas, six oligodendrogliomas, two ependymomas, one Subependymoma, one subependymal giant-cell astrocytoma, and three gangliogliomas) with Southern blot analysis for loss of heterozygosity on both arms of chromosome 10 and for amplification of the EGFR gene. Both the loss of genetic material on chromosome 10 and EGFR gene amplification were restricted to the glioblastomas. Of the 58 glioblastoma patients, 72% showed loss of chromosome 10 and 38% showed EGFR gene amplification. The remaining 28% had neither loss of chromosome 10 nor EGFR gene amplification. Without exception, the glioblastomas that exhibited EGFR gene amplification had also lost genetic material on chromosome 10 (p less than 0.001). This invariable association suggests a relationship between the two genetic events. Moreover, the presence of 15 cases of glioblastoma with loss of chromosome 10 but without EGFR gene amplification may further imply that the loss of a tumor suppressor gene (or genes) on chromosome 10 precedes EGFR gene amplification in glioblastoma tumorigenesis.
Iver Petersen - One of the best experts on this subject based on the ideXlab platform.
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association of epidermal growth factor receptor gene amplification with loss of chromosome 10 in human glioblastoma multiforme
Journal of Neurosurgery, 1992Co-Authors: Andreas Von Deimling, David N Louis, Klaus Von Ammon, Iver Petersen, Tomas Hoell, Richard Y Chung, Robert L Martuza, David A Schoenfeld, Gazi M Yasargil, Otmar D WiestlerAbstract:Although the loss of tumor suppressor genes and the activation of oncogenes have been established as two of the fundamental mechanisms of tumorigenesis in human cancer, little is known about the possible interactions between these two mechanisms. Loss of genetic material on chromosome 10 and amplification of the epidermal growth factor receptor (EGFR) gene are the most frequently reported genetic abnormalities in glioblastoma multiforme. In order to examine a possible correlation between these two genetic aberrations, the authors studied 106 gliomas (58 glioblastomas, 14 anaplastic astrocytomas, five astrocytomas, nine pilocytic astrocytomas, seven mixed gliomas, six oligodendrogliomas, two ependymomas, one Subependymoma, one subependymal giant-cell astrocytoma, and three gangliogliomas) with Southern blot analysis for loss of heterozygosity on both arms of chromosome 10 and for amplification of the EGFR gene. Both the loss of genetic material on chromosome 10 and EGFR gene amplification were restricted to the glioblastomas. Of the 58 glioblastoma patients, 72% showed loss of chromosome 10 and 38% showed EGFR gene amplification. The remaining 28% had neither loss of chromosome 10 nor EGFR gene amplification. Without exception, the glioblastomas that exhibited EGFR gene amplification had also lost genetic material on chromosome 10 (p less than 0.001). This invariable association suggests a relationship between the two genetic events. Moreover, the presence of 15 cases of glioblastoma with loss of chromosome 10 but without EGFR gene amplification may further imply that the loss of a tumor suppressor gene (or genes) on chromosome 10 precedes EGFR gene amplification in glioblastoma tumorigenesis.
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association of epidermal growth factor receptor gene amplification with loss of chromosome 10 in human glioblastoma multiforme
Journal of Neurosurgery, 1992Co-Authors: Andreas Von Deimling, David N Louis, Iver Petersen, Tomas Hoell, Richard Y Chung, Robert L Martuza, David A Schoenfeld, Gazi M Yasargil, Klaus Von Ammon, Otmar D WiestlerAbstract:✓ Although the loss of tumor suppressor genes and the activation of oncogenes have been established as two of the fundamental mechanisms of tumorigenesis in human cancer, little is known about the possible interactions between these two mechanisms. Loss of genetic material on chromosome 10 and amplification of the epidermal growth factor receptor (EGFR) gene are the most frequently reported genetic abnormalities in glioblastoma multiforme. In order to examine a possible correlation between these two genetic aberrations, the authors studied 106 gliomas (58 glioblastomas, 14 anaplastic astrocytomas, five astrocytomas, nine pilocytic astrocytomas, seven mixed gliomas, six oligodendrogliomas, two ependymomas, one Subependymoma, one subependymal giant-cell astrocytoma, and three gangliogliomas) with Southern blot analysis for loss of heterozygosity on both arms of chromosome 10 and for amplification of the EGFR gene. Both the loss of genetic material on chromosome 10 and EGFR gene amplification were restricted...
