Evidence map›Paper›PMID 32108038›Full record

ArticleCancer genomics & proteomics

Ioannis Panagopoulos, Ludmila Gorunova, Ingvild Lobmaier, Kristin Andersen, Ilyá Kostolomov, Marius Lund-Iversen, Bodil Bjerkehagen, Sverre Heim

Open access · diamondAbstract readCase Reports
In one paragraph

Article in Cancer genomics & proteomics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Proteasomal surveillance of exposed cysteines.bioRxiv : the preprint server for biology · 2026
    Article
  3. Article
  4. Review
  5. RUNX2 and Cancer.International journal of molecular sciences · 2023
    Review
  6. Methylation and copy number profiling: emerging tools to differentiate osteoblastoma from malignant mimics?Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2022
    Article
  7. Review
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

8 authors at 1 institution in 1 country.

Ioannis PanagopoulosSection for Cancer Cytogenetics, Institute for Cancer Genetics and Informatics, The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway ioannis.panagopoulos@rr-research.no.
Ludmila GorunovaSection for Cancer Cytogenetics, Institute for Cancer Genetics and Informatics, The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway.
Ingvild LobmaierDepartment of Pathology, Oslo University Hospital, Oslo, Norway.
Kristin AndersenSection for Cancer Cytogenetics, Institute for Cancer Genetics and Informatics, The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway.
Ilyá KostolomovSection for Applied Informatics, Institute for Cancer Genetics and Informatics, The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway.
Marius Lund-IversenDepartment of Pathology, Oslo University Hospital, Oslo, Norway.
Bodil BjerkehagenDepartment of Pathology, Oslo University Hospital, Oslo, Norway.
Sverre HeimSection for Cancer Cytogenetics, Institute for Cancer Genetics and Informatics, The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway.
Oslo University Hospital · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimOsteoblastoma is a rare benign tumor of the bones in which recurrent rearrangements of FOS have been found. Our aim was to investigate two osteoblastomas for possible genetic aberrations. MATERIALS AND

methodsCytogenetic, RNA sequencing, and molecular analyses were performed.

resultsA FOS-ANKH transcript was found in the first tumor, whereas a FOS-RUNX2 was detected in the second. Exon 4 of FOS fused with sequences either from intron 1 of ANKH or intron 5 of RUNX2. The fusion events introduced a stop codon and removed sequences involved in the regulation of FOS.

conclusionRearrangements and fusions of FOS show similarities with those of HMGA2 (a feature of leiomyomas and lipomas) and CSF1 (tenosynovial giant cell tumors). The replacement of a 3'-untranslated region, controlling the gene's expression, by a new sequence is thus a common pathogenetic theme shared by FOS, HMGA2, and CSF1 in many benign connective tissue tumors.

Indexed as

Base SequenceBone NeoplasmsChildCore Binding Factor Alpha 1 SubunitFemaleGene ExpressionHumansKaryotypeMaleOncogene Proteins, FusionOsteoblastomaPhosphate Transport ProteinsANKH protein, humanCore Binding Factor Alpha 1 SubunitOncogene Proteins, FusionPhosphate Transport ProteinsRUNX2 protein, humancytogeneticsFOSFOS-ANKHFOS-RUNX2fusion geneOsteoblastomaRNA sequencing

Identifiers

PMID32108038
PMCPMC7078835
OpenAlexW3008115049

What OpenQuestion holds

Textmetadata
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.