Involvement of chromosome 22 in ependymomas

Wernicke, Catrin; Thiel, Gundula; Lozanova, T; Vogel, Siegfried; Kintzel, Dieter; Jänisch, W; Lehmann, Karin; Witkowski, Regine

doi:10.1016/0165-4608(94)00148-5

Cited by 36 publications

(30 citation statements)

References 23 publications

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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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“…The present study has shown a loss of chromosomal region in 22q in a non-NF2 family with ependymoma, supporting a recently proposed perspective for a pathogenesis of rare familial ependymomas (Bijlsma et al, 1995;Ransom et al, 1992;Weremowicz et al, 1992;Wernicke et al, 1995). Although we could not define the exact locus of the responsible gene in this study, our results suggest that 22q deletions could play an important role in the pathogenesis of ependymomas.…”

Section: Discussionmentioning

confidence: 34%

“…Because type-2 neurofibromatosis is caused by a single NF2 gene mutation, and their associated ependymoma usually represent a loss of heterozygosity in the NF2 gene locus on chromosome 22, significant contribution of this gene for the pathogenesis of ependymoma has been proposed. Those studies have reported several cytogenetic alterations in ependymomas, among which deletions or translocations involving chromosome 22q have been the most frequent changes (Bijlsma et al, 1995;Ransom et al, 1992;Weremowicz et al, 1992;Wernicke et al, 1995). However, there is considerable variability in the frequency of allelic losses involving chromosome 22q in various studies.…”

Section: Discussionmentioning

confidence: 99%

A family with spinal anaplastic ependymoma: evidence of loss of chromosome 22q in tumor

et al. 2003

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Familial ependymal tumors are a very rare disease, the pathogenesis of which is unknown. Previous studies indicate an involvement of tumor suppressor genes localized within chromosomal region 22q, whereas details are still unclear. Here we report a non-neurofibromatosis type-2 (non-NF2) Japanese family in which two of the four members are affected with cervical spinal cord ependymoma, and one of the four is affected with schwannoma. Loss of heterozygosity (LOH) studies were carried out searching for common allelic loss at chromosomal region 22q11.2-qtel in two of the affected patients. Our findings support a prediction for existence of a tumor suppressor gene on chromosome 22 especially related to the tumorigenesis of familial ependymal tumors.

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“…Whereas ependymomas occur in both children and adults, subependymomas and myxopapillary ependymomas are more common in adults. 267 The CGAP website identifies 106 ependymoma karyotypes 1,22,50,62,64,83,92,117,161,175,207,209,225,227,257,270,278,281,293,294 (also reviewed by Mazewski,et al 161 ). The karyotypes described are predominantly normal, and when abnormal are near-diploid, and are characterized by gains and losses of entire chromosomes.…”

Section: Neurosurg Focus / Volume 19 / November 2005mentioning

confidence: 99%

Molecular cytogenetic analysis in the study of brain tumors: findings and applications

Bayani¹,

Pandita²,

Squire³

2005

FOC

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Classic cytogenetics has evolved from black and white to technicolor images of chromosomes as a result of advances in fluorescence in situ hybridization (FISH) techniques, and is now called molecular cytogenetics. Improvements in the quality and diversity of probes suitable for FISH, coupled with advances in computerized image analysis, now permit the genome or tissue of interest to be analyzed in detail on a glass slide. It is evident that the growing list of options for cytogenetic analysis has improved the understanding of chromosomal changes in disease initiation, progression, and response to treatment. The contributions of classic and molecular cytogenetics to the study of brain tumors have provided scientists and clinicians alike with new avenues for investigation. In this review the authors summarize the contributions of molecular cytogenetics to the study of brain tumors, encompassing the findings of classic cytogenetics, interphase- and metaphase-based FISH studies, spectral karyotyping, and metaphase- and array-based comparative genomic hybridization. In addition, this review also details the role of molecular cytogenetic techniques in other aspects of understanding the pathogenesis of brain tumors, including xenograft, cancer stem cell, and telomere length studies.

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Involvement of chromosome 22 in ependymomas

Cited by 36 publications

References 23 publications

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

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

A family with spinal anaplastic ependymoma: evidence of loss of chromosome 22q in tumor

Molecular cytogenetic analysis in the study of brain tumors: findings and applications

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