Evidence map›Paper›PMID 30542116›Full record

ArticleOncogene2019

Inhibitors of ribosome biogenesis repress the growth of MYCN-amplified neuroblastoma.

Øyvind H Hald, Lotte Olsen, Gabriel Gallo-Oller, Lotta Helena Maria Elfman, Cecilie Løkke, Per Kogner, Baldur Sveinbjörnsson, Trond Flægstad, John Inge Johnsen, Christer Einvik

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

48 citing papers in PubMed, 70 citations in OpenAlex.

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  6. Molecular regulation and therapeutic targeting ofFrontiers in cell and developmental biology · 2025
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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

10 authors at 4 institutions in 2 countries.

Øyvind H HaldDepartment of Pediatrics, Division of Child and Adolescent Health, UNN - University Hospital of North-Norway, NO-9038, Tromsø, Norway.
Lotte OlsenPediatric Research Group, Department of Clinical Medicine, Faculty of Health Science, The Arctic University of Norway - UiT, NO-9037, Tromsø, Norway.
Gabriel Gallo-OllerChildhood Cancer Research Unit, Department of Women's and Children's Health, Karolinska Institutet, 171 76, Stockholm, Sweden.
Lotta Helena Maria ElfmanChildhood Cancer Research Unit, Department of Women's and Children's Health, Karolinska Institutet, 171 76, Stockholm, Sweden.
Cecilie LøkkePediatric Research Group, Department of Clinical Medicine, Faculty of Health Science, The Arctic University of Norway - UiT, NO-9037, Tromsø, Norway.
Per KognerChildhood Cancer Research Unit, Department of Women's and Children's Health, Karolinska Institutet, 171 76, Stockholm, Sweden.
Baldur SveinbjörnssonChildhood Cancer Research Unit, Department of Women's and Children's Health, Karolinska Institutet, 171 76, Stockholm, Sweden.
Trond FlægstadDepartment of Pediatrics, Division of Child and Adolescent Health, UNN - University Hospital of North-Norway, NO-9038, Tromsø, Norway.
John Inge JohnsenChildhood Cancer Research Unit, Department of Women's and Children's Health, Karolinska Institutet, 171 76, Stockholm, Sweden.ORCID http://orcid.org/0000-0003-1277-812X
Christer EinvikDepartment of Pediatrics, Division of Child and Adolescent Health, UNN - University Hospital of North-Norway, NO-9038, Tromsø, Norway. christer.einvik@uit.no.
Karolinska Institutet · SEUiT The Arctic University of Norway · NOUniversity Hospital of North Norway · NOCenter for Child and Adolescent Mental Health, Eastern and Southern Norway · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Abnormal increases in nucleolar size and number caused by dysregulation of ribosome biogenesis has emerged as a hallmark in the majority of spontaneous cancers. The observed ribosome hyperactivity can be directly induced by the MYC transcription factors controlling the expression of RNA and protein components of the ribosome. Neuroblastoma, a highly malignant childhood tumor of the sympathetic nervous system, is frequently characterized by MYCN gene amplification and high expression of MYCN and c-MYC signature genes. Here, we show a strong correlation between high-risk disease, MYCN expression, poor survival, and ribosome biogenesis in neuroblastoma patients. Treatment of neuroblastoma cells with quarfloxin or CX-5461, two small molecule inhibitors of RNA polymerase I, suppressed MycN expression, induced DNA damage, and activated p53 followed by cell cycle arrest or apoptosis. CX-5461 repressed the growth of established MYCN-amplified neuroblastoma xenograft tumors in nude mice. These findings suggest that inhibition of ribosome biogenesis represent new therapeutic opportunities for children with high-risk neuroblastomas expressing high levels of Myc.

Indexed as

AnimalsApoptosisBenzothiazolesCell Cycle CheckpointsCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMiceMice, NudeNaphthyridinesNeuroblastomaN-Myc Proto-Oncogene ProteinRibosomesRNA Polymerase IBenzothiazolesCX 5461MYCN protein, humanNaphthyridinesN-Myc Proto-Oncogene ProteinRNA Polymerase ITumor Suppressor Protein p53

Identifiers

PMID30542116
PMCPMC6484764
OpenAlexW2905197516

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.