ArticleInternational journal of cancer2016
The genetic tumor background is an important determinant for heterogeneous MYCN-amplified neuroblastoma.
Article in International journal of cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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20 citing papers in PubMed, 35 citations in OpenAlex.
- The Role of Precision Medicine in Neuroblastoma: Targeted Therapies and Personalized Approaches-A Narrative Review.Health science reports · 2026Article
- Multicellular model of neuroblastoma proposes unconventional therapy based on multiple roles of p53.PLoS computational biology · 2024Article
- A human neural crest model reveals the developmental impact of neuroblastoma-associated chromosomal aberrations.Nature communications · 2024Article
- Application of the FISH method and high-density SNP arrays to assess genetic changes in neuroblastoma-research by one institute.Acta biochimica Polonica · 2024Article
- Neuroblastoma Interaction with the Tumour Microenvironment and Its Implications for Treatment and Disease Progression.Current oncology (Toronto, Ont.) · 2023Review
- Spatial and temporal intratumour heterogeneity has potential consequences for single biopsy-based neuroblastoma treatment decisions.Nature communications · 2021Article
- Frequency and Prognostic Impact ofJournal of clinical oncology : official journal of the American Society of Clinical Oncology · 2021Article
- Landscape of Bone Marrow Metastasis in Human Neuroblastoma Unraveled by Transcriptomics and Deep Multiplex Imaging.Cancers · 2021Article
- Schwann cell plasticity regulates neuroblastic tumor cell differentiation via epidermal growth factor-like protein 8.Nature communications · 2021Article
- Long-Term Outcome and Role of Biology within Risk-Adapted Treatment Strategies: The Austrian Neuroblastoma Trial A-NB94.Cancers · 2021Article
- Imbalance between genomic gain and loss identifies high-risk neuroblastoma patients with worse outcomes.Neoplasia (New York, N.Y.) · 2021Article
- Implementation of the plasma MYCN/NAGK ratio to detect MYCN amplification in patients with neuroblastoma.Molecular oncology · 2020Article
- Age Dependency of the Prognostic Impact of Tumor Genomics in Localized ResectableJournal of clinical oncology : official journal of the American Society of Clinical Oncology · 2020Article
- Association of heterogeneous MYCN amplification with clinical features, biological characteristics and outcomes in neuroblastoma: A report from the Children's Oncology Group.European journal of cancer (Oxford, England : 1990) · 2020Article
- Heterogeneous MYCN amplification in neuroblastoma: a SIOP Europe Neuroblastoma Study.British journal of cancer · 2018Article
- Article
- Impact of Disseminated Neuroblastoma Cells on the Identification of the Relapse-Seeding Clone.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Article
- 11q deletion in neuroblastoma: a review of biological and clinical implications.Molecular cancer · 2017Review
- Chromosome 1q gain and tenascin-C expression are candidate markers to define different risk groups in pediatric posterior fossa ependymoma.Acta neuropathologica communications · 2016Article
- Article
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Authors and funding
14 authors at 8 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amplification of MYCN is the signature genetic aberration of 20-25% of neuroblastoma and a stratifying marker associated with aggressive tumor behavior. The detection of heterogeneous MYCN amplification (hetMNA) poses a diagnostic dilemma due to the uncertainty of its relevance to tumor behavior. Here, we aimed to shed light on the genomic background which permits hetMNA in neuroblastoma and tied the occurrence to other stratifying markers and disease outcome. We performed SNP analysis using Affymetrix Cytoscan HD arrays on 63 samples including constitutional DNA, tumor, bone marrow and relapse samples of 26 patients with confirmed hetMNA by MYCN-FISH. Tumors of patients ≤18m were mostly aneuploid with numeric chromosomal aberrations (NCAs), presented a prominent MNA subclone and carried none or a few segmental chromosomal aberrations (SCAs). In older patients, tumors were mostly di- or tetraploid, contained a lower number of MNA cells and displayed a multitude of SCAs including concomitant 11q deletions. These patients often suffered disease progression, tumor dissemination and relapse. Restricted to aneuploid tumors, we detected chromosomes with uniparental di- or trisomy (UPD/UPT) in almost every sample. UPD11 was exclusive to tumors of younger patients whereas older patients featured UPD14. In this study, the MNA subclone appears to be constraint by the tumor environment and thus less relevant for tumor behavior in aggressive tumors with a high genomic instability and many segmental aberrations. A more benign tumor background and lower tumor stage may favor an outgrowth of the MNA clone but tumors generally responded better to treatment.
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