Chromosome arm 6q loss is the most common recurrent autosomal alteration detected in primary pediatric ependymoma

Reardon, David A.; Entrekin, Ruth E.; Sublett, Jack; Ragsdale, Susan T.; Li, Hao; Boyett, James M.; Kepner, James L.; Look, A. Thomas

doi:10.1002/(sici)1098-2264(199903)24:3<230::aid-gcc8>3.0.co;2-c

Cited by 94 publications

(53 citation statements)

References 51 publications

(64 reference statements)

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“…This is reinforced by the CGH finding that a balanced genomic profile, without chromosomal gain or loss, can be seen in 36% to 58% of pediatric ependymomas and is significantly associated with children under 3 years of age. By contrast, a balanced genome is found in less than 10% of adult cases (58,59,62,69,71).…”

Section: Molecular Distinctions Between Pediatric and Adult Ependymomasmentioning

confidence: 97%

“…4A) frequently show whole chromosomal imbalances such as gain of chromosomes 7, 9, 11, 18, and 20 or loss of chromosomes 1, 2, and 10, whereas intracranial ependymomas are characterized by gain of chromosome 1q and often show loss of chromosomes 22, 3, 9p, and 13q (58)(59)(60)(61)(62)(63)(64)(66)(67)(68)(69)(70)(71). This again reinforces a possible association between intermediate ploidy and improved patient outcome, which is often seen with cases of intramedullary ependymomas detected by CGH analysis.…”

Section: Ependymoma Heterogeneity and Tumor Locationmentioning

confidence: 99%

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Pediatric Ependymoma: Biological Perspectives

Kilday

Rahman

Dyer

et al. 2009

Molecular Cancer Research

167

204

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Pediatric ependymomas are enigmatic tumors that continue to present a clinical management challenge despite advances in neurosurgery, neuroimaging techniques, and radiation therapy. Difficulty in predicting tumor behavior from clinical and histological factors has shifted the focus to the molecular and cellular biology of ependymoma in order to identify new correlates of disease outcome and novel therapeutic targets. This article reviews our current understanding of pediatric ependymoma biology and includes a meta-analysis of all comparative genomic hybridization (CGH) studies done on primary ependymomas to date, examining more than 300 tumors. From this meta-analysis and a review of the literature, we show that ependymomas in children exhibit a different genomic profile to those in adults and reinforce the evidence that ependymomas from different locations within the central nervous system (CNS) are distinguishable at a genomic level. Potential biological markers of prognosis in pediatric ependymoma are assessed and the ependymoma cancer stem cell hypothesis is highlighted with respect to tumor resistance and recurrence. We also discuss the shifting paradigm for treatment modalities in ependymoma that target molecular alterations in tumor-initiating cell populations. (Mol Cancer Res 2009;7(6):765-86)

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Section: Molecular Distinctions Between Pediatric and Adult Ependymomasmentioning

confidence: 97%

Section: Ependymoma Heterogeneity and Tumor Locationmentioning

confidence: 99%

Pediatric Ependymoma: Biological Perspectives

Kilday

Rahman

Dyer

et al. 2009

Molecular Cancer Research

167

204

View full text Add to dashboard Cite

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“…The TP53 gene was found to be infrequently mutated in medulloblastoma, indicating that TP53 is not the target on 17p (Saylors et al, 1991). Using comparative genomic hybridization technique, several groups have demonstrated the involvement of multiple chromosomes in medulloblastoma (Avet-Loiseau et al, 1999;Gilhuis et al, 2000;Nicholson et al, 1999;Reardon et al, 1997). Of those chromosomes that show deletions, losses of chromosomes 10q and 8p are recurrent genetic alterations, with about 30% of tumors showing such abnormalities.…”

Section: Introductionmentioning

confidence: 99%

Identification of a region of homozygous deletion on 8p22–23.1 in medulloblastoma

Yin

Pang

2002

Oncogene

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To identify critical tumor suppressor loci that are associated with the development of medulloblastoma, we performed a comprehensive genome-wide allelotype analysis in a series of 12 medulloblastomas. Non-random allelic imbalances were identi®ed on chromosomes 7q (58.3%), 8p (66.7%), 16q (58.3%), 17p (58.3%) and 17q (66.7%). Comparative genomic hybridization analysis con®rmed that allelic imbalances on 8p, 16q and 17p were due to loss of genetic materials. Finer deletion mapping in an expanded series of 23 medulloblastomas localized the common deletion region on 8p to an interval of 18.14 cM on 8p22 ± 23.2. We then searched within the region of loss on 8p for loci that might contain homozygous deletion using comparative duplex PCR. An overlapping homozygous deletion region was identi®ed in a 1.8 cM interval on 8p22 ± 23.1, between markers D8S520 and D8S1130, in two medulloblastomas. This region of homozygous deletion also encompasses the 1.4 cM minimal deletion region detected on 8p in ductal carcinoma in situ of breast. In conclusion, we reported for the ®rst time a detailed deletion mapping on 8p in medulloblastoma and have identi®ed a region of homozygous deletion on 8p22 ± 23.1 that is likely to contain a critical tumor suppressor gene involved in the development of medulloblastoma.

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“…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.…”

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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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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Chromosome arm 6q loss is the most common recurrent autosomal alteration detected in primary pediatric ependymoma

Cited by 94 publications

References 51 publications

Pediatric Ependymoma: Biological Perspectives

Pediatric Ependymoma: Biological Perspectives

Identification of a region of homozygous deletion on 8p22–23.1 in medulloblastoma

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

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