Identification of Tumor-Specific Molecular Signatures in Intracranial Ependymoma and Association With Clinical Characteristics

Modena, Piergiorgio; Lualdi, Elena; Facchinetti, Federica; Veltman, Joris A.; Reid, James F.; Minardi, Simone; Janssen, Irene M.; Giangaspero, Felice; Forni, Marco; Finocchiaro, Gaetano; Genitori, Lorenzo; Giordano, Flavio; Riccardi, Riccardo; Schoenmakers, Eric; Massimino, Maura; Sozzi, Gabriella

doi:10.1200/jco.2006.06.3701

Cited by 192 publications

(187 citation statements)

References 33 publications

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“…Despite this, similar findings were shown by one aCGH study of 24 intracranial ependymomas that revealed that tumors from younger patients had significantly smaller, partial regions of genomic imbalances than older patients (76).…”

Section: Molecular Distinctions Between Pediatric and Adult Ependymomasmentioning

confidence: 69%

“…The region 22q13.3 has also been highlighted as a frequent region of genomic loss in ependymoma (76,156,157). Gene expression analysis within this locus has revealed downregulation of SULT4A, a gene widely expressed in several compartments of the human brain (76,77,148).…”

Section: Immunohistochemical and Genomic Markersmentioning

confidence: 99%

“…Mixed age, adult and pediatric (<16 y). 32,35,36,58,59,76,78,86,. However, only a few of these candidates have been analyzed in sufficient numbers of childhood ependymoma to allow consideration as prognostic markers in this age group.…”

Section: Immunohistochemical and Genomic Markersmentioning

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: 69%

Section: Immunohistochemical and Genomic Markersmentioning

confidence: 99%

See 1 more Smart Citation

Pediatric Ependymoma: Biological Perspectives

Kilday

Rahman

Dyer

et al. 2009

Molecular Cancer Research

167

204

View full text Add to dashboard Cite

show abstract

“…On the contrary, elevated expression of TLX has been reported in various types of human glioma [68][69][70][71][72][73] and glioma cell lines [74], and TLX overexpression seems to be associated with a poor prognosis for patients with glioma [74]. A recent study further reported that TLX promotes the progression of neuroblastoma and is correlated with poor survival [56].…”

Section: Tlx and Human Diseasesmentioning

confidence: 99%

The Orphan Nuclear Receptor TLX/NR2E1 in Neural Stem Cells and Diseases

Wang

Xiong

2016

Neurosci. Bull.

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The human TLX gene encodes an orphan nuclear receptor predominantly expressed in the central nervous system. Tailess and Tlx, the TLX homologues in Drosophila and mouse, play essential roles in body-pattern formation and neurogenesis during early embryogenesis and perform crucial functions in maintaining stemness and controlling the differentiation of adult neural stem cells in the central nervous system, especially the visual system. Multiple target genes and signaling pathways are regulated by TLX and its homologues in specific tissues during various developmental stages. This review aims to summarize previous studies including many recent updates from different aspects concerning TLX and its homologues in Drosophila and mouse.

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“…60,[62][63][64][65][66][67][68][69][70][71] Beside its genomic amplification, YAP protein levels and nuclear localization have been shown to be elevated in multiple types of cancer. 31,60,[72][73][74][75] Overexpression of YAP in mammary epithelial cells is sufficient to promote epithelial-mesenchymal transition (EMT), induce a proliferative advantage, inhibit apoptosis and induce anchorage-independent growth, characteristics associated with transforming oncogenes. 76 YAP oncogenic activity was also demonstrated in a mouse model of hepatocellular carcinoma, where YAP amplification contributes to tumor development.…”

Section: Sav1 (Ww45)mentioning

confidence: 99%