Evidence map›Paper›PMID 28459463›Full record

ArticleOncogene2017

MYCN induces neuroblastoma in primary neural crest cells.

R R Olsen, J H Otero, J García-López, K Wallace, D Finkelstein, J E Rehg, Z Yin, Y-D Wang, K W Freeman

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
7.7field-weighted citation impact, top 2% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

61 citing papers in PubMed, 103 citations in OpenAlex.

  1. Review
  2. Epigenetic crosstalk in neuroblastoma development and progression.Frontiers in cell and developmental biology · 2026
    Review
  3. Article
  4. Article
  5. The cell-permeable iron chelator M606 inhibits MYCN-driven neuroblastoma via an E2F3-mediated response.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. AntigeneCancers · 2023
    Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Review
  19. Review
  20. Article

1 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

R R OlsenOncology Department, St. Jude Children's Research Hospital, Memphis, TN, USA.
J H OteroOncology Department, St. Jude Children's Research Hospital, Memphis, TN, USA.
J García-LópezOncology Department, St. Jude Children's Research Hospital, Memphis, TN, USA.
K WallaceOncology Department, St. Jude Children's Research Hospital, Memphis, TN, USA.
D FinkelsteinComputational Biology Department, St. Jude Children's Research Hospital, Memphis, TN, USA.
J E RehgPathology Department, St. Jude Children's Research Hospital, Memphis, TN, USA.
Z YinOncology Department, St. Jude Children's Research Hospital, Memphis, TN, USA.
Y-D WangComputational Biology Department, St. Jude Children's Research Hospital, Memphis, TN, USA.
K W FreemanOncology Department, St. Jude Children's Research Hospital, Memphis, TN, USA.
St. Jude Children's Research Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuroblastoma (NBL) is an embryonal cancer of the sympathetic nervous system (SNS), which causes 15% of pediatric cancer deaths. High-risk NBL is characterized by N-Myc amplification and segmental chromosomal gains and losses. Owing to limited disease models, the etiology of NBL is largely unknown, including both the cell of origin and the majority of oncogenic drivers. We have established a novel system for studying NBL based on the transformation of neural crest cells (NCCs), the progenitor cells of the SNS, isolated from mouse embryonic day 9.5 trunk neural tube explants. Based on pathology and gene expression analysis, we report the first successful transformation of wild-type NCCs into NBL by enforced expression of N-Myc, to generate phenotypically and molecularly accurate tumors that closely model human MYCN-amplified NBL. Using comparative genomic hybridization, we found that NCC-derived NBL tumors acquired copy number gains and losses that are syntenic to those observed in human MYCN-amplified NBL including 17q gain, 2p gain and loss of 1p36. When p53-compromised NCCs were transformed with N-Myc, we generated primitive neuroectodermal tumors with divergent differentiation including osteosarcoma. These subcutaneous tumors were metastatic to regional lymph nodes, liver and lung. Our novel experimental approach accurately models human NBL and establishes a new system with potential to study early stages of NBL oncogenesis, to functionally assess NBL oncogenic drivers and to characterize NBL metastasis.

Indexed as

AnimalsCell Line, TumorCell ProliferationCell Transformation, NeoplasticDisease Models, AnimalFemaleHeterograftsMaleMiceMice, Inbred C57BLMice, NudeNeural CrestNeuroblastomaN-Myc Proto-Oncogene ProteinTumor Suppressor Protein p53MYCN protein, mouseN-Myc Proto-Oncogene ProteinTumor Suppressor Protein p53

Identifiers

PMID28459463
PMCPMC5582212
OpenAlexW2611535275

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

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.