Molecular genetic alterations on chromosomes 11 and 22 in ependymomas

Lamszus, Katrin; Lachenmayer, L.; Heinemann, Uta; Kluwe, Lan; Finckh, Ulrich; Höppner, Wolfgang; Stavrou, D.; Fillbrandt, Regina; Westphal, Manfred

doi:10.1002/1097-0215(200002)9999:9999<::aid-ijc1134>3.0.co;2-p

Cited by 99 publications

(50 citation statements)

References 39 publications

(32 reference statements)

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“…[5][6][7][8][9][10][11][12]14,15 No previous genetic studies have focused specifically on the clear cell variant of ependymoma. Like NF2, DAL-1 (18p11.3) is a member of the protein 4.1 superfamily, a group of functionally related proteins with homologous transmembrane proteinbinding domains.…”

Section: Radiologic Featuresmentioning

confidence: 99%

“…Clearly distinct from astrocytomas and oligodendrogliomas at the molecular level, the most frequently reported abnormality is deletion of chromosome 22. [5][6][7][8][9][10][11][12][13][14][15] Gains of chromosome 1q (16 -18) and losses involving chromosomes 22q (16), 6q (19), and 17p (11) appear to be particularly prevalent in pediatric examples. In a recent study by Singh et al, NF2 and DAL-1, two members of the protein 4.1 superfamily, were implicated in the pathogenesis of ependymomas.…”

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confidence: 99%

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Clear cell ependymoma: A clinicopathologic and radiographic analysis of 10 patients

Fouladi

Helton

Dalton

et al. 2003

Cancer

125

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Changes in conductivity with repeated fabric extension were investigated to improve the properties of conductive electrode pad material used for electrotherapy when it is subjected to various movement of human body. Highly stretchable and conductive fabrics were prepared by in situ chemical polymerization of polypyrrole on nylon–spandex stretch fabric in aqueous solutions with 0.5 M pyrrole, 1.165 M FeCl3, and 0.165 M benzenesulfonic acid at 5°C for 1 h. Performance of prepared stretchable conductive fabric was evaluated in terms of conductivity changes as a function of tensile strain, repeated extension, and current application time. As the degree of extension increased, the conductivity increased and leveled off when the fabric was subjected to 60% extension. The number of fiber contacts in nylon–spandex fabric with electrode increased as the applied extension increased. However, the conductivity of the composite decreased under excessive extension over 60% since the intrinsic elasticity of fabric became gradually reduced. Generally, the fabric conductivity decreased as the number of extension cycles increased. However, the fabric conductivity was well maintained after repeated extension over 30 cycles at 40% extension. In addition, it was found that the effect of charging during the electrotherapy treatment on a current flow through prepared electrode pad was negligible. © 2003 Wiley Periodicals, Inc. J Appl Polym Sci 88: 1225–1229, 2003

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Section: Radiologic Featuresmentioning

confidence: 99%

mentioning

confidence: 99%

Clear cell ependymoma: A clinicopathologic and radiographic analysis of 10 patients

Fouladi

Helton

Dalton

et al. 2003

Cancer

125

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“…As a hereditary form, neurofibromatosis type 2 is associated with spinal ependymomas, indicating a functional role of the NF2 tumor suppressor gene in these tumors. 9,10 In contrast to adults in which spinal tumors predominate, ϳ90% of all pediatric ependymomas are of intraSupported by the Bundesministerium fü r Bildung und Forschung (FKZ 01 KW 9937 and NGFN 01 GR 0101). K. N. is a scholar of the Deutsche José Carreras Leukä mie-Stiftung e.V…”

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confidence: 99%

“…As a hereditary form, neurofibromatosis type 2 is associated with spinal ependymomas, indicating a functional role of the NF2 tumor suppressor gene in these tumors. 9,10 In contrast to adults in which spinal tumors predominate, ϳ90% of all pediatric ependymomas are of intra-cranial origin with most tumors arising infratentorially. 2 In addition, pediatric ependymoma patients tend to have a poorer outcome than adults.…”

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confidence: 99%

Gene Expression Patterns in Ependymomas Correlate with Tumor Location, Grade, and Patient Age

Korshunov¹,

Neben²,

Wrobel³

et al. 2003

The American Journal of Pathology

147

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To elucidate the molecular events responsible for tumorigenesis and progression of ependymomas, we analyzed molecular alterations on the gene expression level in a series of newly diagnosed ependymal neoplasms (n ‫؍‬ 39). To this aim, tumor RNA was hybridized to microarrays comprising 2600 different genes with relevance to mitosis, cell-cycle control, oncogenesis, or apoptosis. For CLU, IGF-2, and RAF-1, which are apparent candidate genes because they had been previously described to be involved in tumorigenesis of other human malignancies, we found a high expression on the mRNA as well as the protein level. We identified gene expression signatures for the differentiation of tumors with respect to location, grade, and patient age. Spinal ependymomas were characterized by high-expression levels of HOXB5, PLA2G, and CDKN2A and tumors in young patients (<16 years of age) by high-expression levels of LDHB and STAM. Notably, we were able to classify supratentorial grade II and III tumors with 100% accuracy, whereas this did not apply for infratentorial Ependymal tumors arise from the ependymal lining of the cerebral ventricles and from the remnants of the central canal of the spinal cord. This neoplasm constitutes ϳ3 to 5% of all intracranial malignancies and is the third most common brain tumor in children and young adults. 1,2 In ependymomas, the morphological features and biological behavior vary considerably. Patients with spinal tumor location have usually a favorable prognosis after gross total resection, whereas local tumor progression is the predominant reason for death in patients with intracranial ependymomas, resulting in a 5-year overall survival of ϳ60%. [3][4][5] Because ependymomas are characterized by tremendous variability in clinical behavior, the understanding of the complex changes taking place at the genomic level might lead to more precise understanding of the tumor biology. Cytogenetic studies revealed numerous chromosomal aberrations in ependymomas. In particular, a 30 to 50% incidence of aberrations involving chromosome 22, including monosomy 22 as well as deletions of 22q, prevailed the most frequent finding. 6 -8 Recently, Hirose and co-workers 7 reported on different patterns of chromosomal abnormalities with respect to tumor location detected by comparative genomic hybridization. In intracranial tumors, gain of 1q and losses on 6q, 9, and 13 were frequent, whereas gains on chromosome 7 were recognized almost exclusively in spinal cord tumors and were associated with various other chromosomal aberrations including frequent loss of 22q, suggesting that intracranial and spinal cord ependymomas progress along substantially different pathways. As a hereditary form, neurofibromatosis type 2 is associated with spinal ependymomas, indicating a functional role of the NF2 tumor suppressor gene in these tumors. 9,10 In contrast to adults in which spinal tumors predominate, ϳ90% of all pediatric ependymomas are of intraSupported by the Bundesministerium fü r Bildung und Forschung (FKZ 01 KW 9937 and...

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“…14 The most common is chromosome 22 deletion, with inactivation of the NF2 gene on 22q12 and loss of its protein product, merlin being specifically implicated in the spinal ependymomas. [15][16][17][18] Data suggest that other 22q-associated genes and other chromosomal regions are likely involved in the intracranial counterparts. Amplification and/or overexpression of mdm2 may also be involved in ependymal tumorigenesis and response of tumor to chemotherapy, 19 although additional studies are needed to confirm this finding.…”

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confidence: 99%

9p21 and 13q14 dosages in ependymomas. A clinicopathologic study of 101 cases

et al. 2004

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Ependymomas are glial neoplasms whose clinical behavior is difficult to predict based on histology alone. Recently, a comparative genomic hybridization study identified frequent chromosome 9p and 13q losses in anaplastic ependymomas, suggesting that p16 and RB alterations may be involved in tumor progression. In order to test this hypothesis further, 101 myxopapillary, conventional, and anaplastic ependymomas (51 spinal and 50 intracranial tumors) were tested for RB and p16 deletions using fluorescence in situ hybridization. Clinical follow-up, ranging from 2 to 198 months (median 46 months), was obtained in 90 cases (91%). RB and p16 deletions were seen in 22 of 92 (24%) and 22 of 89 (25%) informative cases, respectively. Polysomies were more frequent in the grade I and II spinal tumors, consistent with prior reports of increased aneuploidy in such cases. No significant genetic associations were seen with tumor grade, recurrence, or death, suggesting that 9p and 13q deletions do not play a prominent role in the malignant progression of ependymomas, as has been implicated in other glioma subtypes.

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Molecular genetic alterations on chromosomes 11 and 22 in ependymomas

Cited by 99 publications

References 39 publications

Clear cell ependymoma: A clinicopathologic and radiographic analysis of 10 patients

Clear cell ependymoma: A clinicopathologic and radiographic analysis of 10 patients

Gene Expression Patterns in Ependymomas Correlate with Tumor Location, Grade, and Patient Age

9p21 and 13q14 dosages in ependymomas. A clinicopathologic study of 101 cases

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