ArticleBrain pathology (Zurich, Switzerland)2007
Genome wide copy number abnormalities in pediatric medulloblastomas as assessed by array comparative genome hybridization.
Article in Brain pathology (Zurich, Switzerland), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 37 citations in OpenAlex.
- Initial testing (stage 1) of the curaxin CBL0137 by the pediatric preclinical testing program.Pediatric blood & cancer · 2017Article
- An interferon response gene expression signature is activated in a subset of medulloblastomas.Translational oncology · 2012Article
- Genetic alterations in microRNAs in medulloblastomas.Brain pathology (Zurich, Switzerland) · 2012Article
- Novel amplifications in pediatric medulloblastoma identified by genome-wide copy number profiling.Journal of neuro-oncology · 2012Article
- Genome-wide molecular characterization of central nervous system primitive neuroectodermal tumor and pineoblastoma.Neuro-oncology · 2011Article
- Integrative genomic analysis of medulloblastoma identifies a molecular subgroup that drives poor clinical outcome.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2011Article
- Pediatric primary intramedullary spinal cord glioblastoma.Rare tumors · 2010Article
- Central nervous system primitive neuroectodermal tumors: a clinicopathologic and genetic study of 33 cases.Brain pathology (Zurich, Switzerland) · 2010Article
- Article
- Recurrent genomic alterations characterize medulloblastoma arising from DNA double-strand break repair deficiency.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Treatment of pediatric brain tumors.Journal of cellular physiology · 2008Review
- Biological background of pediatric medulloblastoma and ependymoma: a review from a translational research perspective.Neuro-oncology · 2008Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Array-based comparative genomic hybridization was used to characterize 22 medulloblastomas in order to precisely define genetic alterations in these malignant childhood brain tumors. The 17p(-)/17q(+) copy number abnormality (CNA), consistent with the formation of isochromosome 17q, was the most common event (8/22). Amplifications in this series included MYCL, MYCN and MYC previously implicated in medulloblastoma pathogenesis, as well as novel amplicons on chromosomes 2, 4, 11 and 12. Losses involving chromosomes 1, 2, 8, 10, 11, 16 and 19 and gains of chromosomes 4, 7, 8, 9 and 18 were seen in greater than 20% of tumors in this series. A homozygous deletion in 11p15 defines the minimal region of loss on this chromosome arm. In order to map the minimal regions involved in losses, gains and amplifications, we combined aCGH data from this series with that of two others obtained using the same RPCI BAC arrays. As a result of this combined analysis of 72 samples, we have defined specific regions on chromosomes 1, 8p, 10q, 11p and 16q which are frequently involved in CNAs in medulloblastomas. Using high density oligonucleotide expression arrays, candidate genes were identified within these consistently involved regions in a subset of the tumors.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.