ArticleOncogene2005
Stepwise occurrence of a complex unbalanced translocation in neuroblastoma leading to insertion of a telomere sequence and late chromosome 17q gain.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01728155 (European Low and Intermediate Risk Neuroblastoma Protocol), which is not on this map. Cited by 17 papers.
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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.
European Low and Intermediate Risk Neuroblastoma Protocol
Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- A functional landscape for chromosome 17q in neuroblastoma: balancing replication stress and genomic stability.British journal of cancer · 2026Review
- Global, regional, and national epidemiology of childhood neuroblastoma (1990-2021): a statistical analysis of incidence, mortality, and DALYs.EClinicalMedicine · 2025Article
- Review
- Partners in crime: Tbf1 and Vid22 promote expansions of long human telomeric repeats at an interstitial chromosome position in yeast.PNAS nexus · 2022Article
- Article
- Novel therapeutic strategies targeting telomere maintenance mechanisms in high-risk neuroblastoma.Journal of experimental & clinical cancer research : CR · 2020Review
- Article
- Review
- Expansion of Interstitial Telomeric Sequences in Yeast.Cell reports · 2015Article
- Breakpoint features of genomic rearrangements in neuroblastoma with unbalanced translocations and chromothripsis.PloS one · 2013Article
- Molecular pathogenesis of peripheral neuroblastic tumors.Oncogene · 2010Review
- Distribution and neuronal expression of phosphatidylinositol phosphate kinase IIgamma in the mouse brain.The Journal of comparative neurology · 2009Article
- A constitutional translocation t(1;17)(p36.2;q11.2) in a neuroblastoma patient disrupts the human NBPF1 and ACCN1 genes.PloS one · 2008Article
- Article
- Molecular biology of neuroblastoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2007Review
- Chromosomal CGH identifies patients with a higher risk of relapse in neuroblastoma without MYCN amplification.British journal of cancer · 2007Article
- Defining ploidy-specific thresholds in array comparative genomic hybridization to improve the sensitivity of detection of single copy alterations in cell lines.The Journal of molecular diagnostics : JMD · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In neuroblastoma, the most frequent genetic alterations are unbalanced translocations involving chromosome 17. To gain insights into these rearrangements, we have characterized a previously identified der(1)t(1;17) of the CLB-Bar cell line. The 17q breakpoint was mapped by FISH. Subsequently, a rearranged fragment was identified by Southern analysis, cloned in a lambda vector and sequenced. The chromosome rearrangement is more complex than expected due to the presence of an interstitial 4p telomeric sequence between chromosome 1p and 17q. Three different genes, which may play a role in neuroblastoma development, are disrupted by the translocation breakpoints. Indeed, the 3'UTR of the PIP5K2B gene on chromosome 17q is directly fused to the (TTAGGG)n repeat of the chromosome 4p telomere, and the (1;4) fusion disrupts the MACF1 (microtubule-actin crosslinking factor 1) and POLN genes, respectively. Interestingly, the (1;4) fusion was present at diagnosis and at relapse, whereas the (4;17) fusion was detected at relapse only, leading to a secondary 17q gain confirmed by array CGH therefore indicating that 17q gain may not be a primary event in neuroblastoma. Finally, screening of a panel of neuroblastoma cell lines identified interstitial telomeric sequences in three other cases, suggesting that this may be a recurrent mechanism leading to unbalanced translocations in neuroblastoma.
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