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Angela thankyou for the wonderful support you give our group.

Our prayers and thoughts with you - that Nicky's scan is all clear. Its always a tough time - I still try the mindful mediation and visualise a positive outcome. That being said its still tough. Love to you all - and thanks again for the info, moderator support you provide our group.

Liz Rutter (Australia)
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Pediatric Ependymoma: Biological Perspectives

John-Paul Kilday1,
Ruman Rahman1,
Sara Dyer3,
Lee Ridley1,
James Lowe2,
Beth Coyle1 and
Richard Grundy1

+ Author Affiliations

1The Children's Brain Tumour Research Centre, and 2School of Molecular Medical Sciences, Faculty of Medicine and Health Sciences, University of Nottingham, Nottingham, and 3West Midlands Regional Genetics Laboratory, Women's Hospital Birmingham, Birmingham, United Kingdom

Requests for reprints:
Richard Grundy, The Children's Brain Tumour Research Centre, University of Nottingham, The Medical School, Queen's Medical Centre, Nottingham NG7 2UH, United Kingdom. Phone: 44-0115-823-0696; Fax: 44-0115-823-0696. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it.

Note: J.P. Kilday and R. Rahman contributed equally to this work.




Abstract

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)
Footnotes

Grant support: The Joseph Foote Foundation funds ependymoma research at The Children's Brain Tumour Research Centre (CBTRC), and J.P. Kilday receives funding from The James Tudor Foundation as a Clinical Research Fellow within the CBTRC.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received December 23, 2008.
Revision received March 19, 2009.
Accepted March 19, 2009.
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A clinically relevant orthotopic xenograft model of ependymoma that maintains the genomic signature of the primary tumor and preserves cancer stem cells in vivo

Blanca Suarez-Merino,
Mike Hubank,
Tamas Revesz,
William Harkness,
Richard Hayward,
Dominic Thompson,
John L. Darling,
David G.T. Thomas and
Tracy J. Warr3

- Author Affiliations

Department of Molecular Neuroscience (B.S.-M., T.R., T.J.W.) and Division of Neurosurgery (D.G.T.T.), Institute of Neurology, National Hospital for Neurology and Neurosurgery, and Department of Molecular Haematology, Institute of Child Health (M.H.), University College London, London; Department of Neurosurgery, Great Ormond Street Hospital for Sick Children NHS Trust, London (W.H., R.H., D.T.); Research Institute in Healthcare Science, University of Wolverhampton, Wolverhampton (J.L.D.); UK

3 Address correspondence to Tracy J. Warr, Department of Molecular Neuroscience, Neuro-Oncology Group, Institute of Neurology, Queen Square, London WC1N 3BG, UK ( This e-mail address is being protected from spambots. You need JavaScript enabled to view it. ).

Received June 14, 2004.
Accepted September 2, 2004.




Abstract

Ependymomas are glial cell-derived tumors characterized by varying degrees of chromosomal abnormalities and variability in clinical behavior. Cytogenetic analy-sis of pediatric ependymoma has failed to identify consistent patterns of abnormalities, with the exception of monosomy of 22 or structural abnormalities of 22q. In this study, a total of 19 pediatric ependymoma samples were used in a series of expression profiling, quantitative real-time PCR (Q-PCR), and loss of heterozygosity experiments to identify candidate genes involved in the development of this type of pediatric malignancy. Of the 12,627 genes analyzed, a subset of 112 genes emerged as being abnormally expressed when compared to three normal brain controls. Genes with increased expression included the oncogene WNT5A; the p53 homologue p63; and several cell cycle, cell adhesion, and proliferation genes. Underexpressed genes comprised the NF2 interact-ing gene SCHIP-1 and the adenomatous polyposis coli (APC)-associated gene EB1 among others. We validated the abnormal expression of six of these genes by Q-PCR. The subset of differentially expressed genes also included four underexpressed transcripts mapping to 22q12.3-13.3. By Q-PCR we show that one of these genes, CBX7 (22q13.1), was deleted in 55% of cases. Other genes mapping to cytogenetic hot spots included two overexpressed and three underexpressed genes mapping to 1q31-41 and 6q21-q24.3, respectively. These genes represent candidate genes involved in ependymoma tumorigenesis. To the authors' knowledge, this is the first time microarray analysis and Q-PCR have been linked to identify heterozygous/homozygous deletions.
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We fly into Jude on May 29, and then the MRI the next day then the following day an ABR .... I will post results ...

prayers please !
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Davids MRI is May 31..... prayers for my peace of mind and for Gods grace! (Please dear god let us have a clean scan)
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Very true Tony but according to David angiogram he had done and I saw the blood vessels on the right half were collapsed when the Dr opened up his scull the right was very discolored from the other I would think if it were a hemorage it would have shown on the scan? Dr Greene stated that they r finding that patients who have done protons are starting to develop moyamoya from it. I would like to say that David is doing wonderfully since surgery and his vocabulary has boomed since his left side of the brain doesn't have to work as hard. I guess it goes to say all these treatments are dangerous in themselves I mean look how many children get necrosis?
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yes this was FDA approved to give a possible 3-6 months extra for glioblastoma patients. The Goliath of tumors so a tough one. Yes it proved to be better than chemos that made patients ill - however this product is like a helmet that needs to be worn 20 hours out of a 24 hour day. It's obviously enticing for the patients with glioblastoma but I can't see the benefit for an ependymoma - the cell lines are totally different and no test had been done to conclude this treatment to be an option for ependymoma. I am in so many groups that I study all tumor types now and glioblastoma is a blue cell round cell tumor type and ependymoma is ependymal cells that are oval shaped and sticky that they believe originate from stem cells.

I wish they would do the test on different tumor types to know if this is even worth looking at for the kids.

Thanks for posting the video I hope people will watch it and form their own opinion and research about it too.

ANG
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I read about this today. Is anyone familiar with this? It seems to be something for GBMs (gliobastoma multiforme) but does anyone know if it could be beneficial for Ependymomas.

www.virtualtrials.com/novocure/news.cfm
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Ok, back to the virus story; www.ncbi.nlm.nih.gov/pubmed/21075780

"A single intravenous injection of oncolytic picornavirus SVV-001 eliminates medulloblastomas in primary tumor-based orthotopic xenograft mouse models."

I saw a few clinical trial on viruses and a lot more publications about the connection, we are trying to get NDV (Newcastle disease virus) which is Ironic as I was born in Newcastle, some people have had a CR using this.
Hard to get at the moment.
I am now 100% convinced that a virus is the smoking gun.
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