Evidence map›Paper›PMID 38769442›Full record

ArticleCommunications biology2024

MDM2 amplification in rod-shaped chromosomes provides clues to early stages of circularized gene amplification in liposarcoma.

Saskia Sydow, Paul Piccinelli, Shamik Mitra, Panagiotis Tsagkozis, Asle Hesla, Camila B R De Mattos, Jan Köster, Linda Magnusson, Jenny Nilsson, Adam Ameur and 4 more

Abstract read
In one paragraph

Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Review
  2. TWIST1 bridges p53 and MDM2 and impairs the efficacy of MDM2 inhibitors.Journal of experimental & clinical cancer research : CR · 2026
    Article
  3. Article
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

14 authors.

Saskia SydowDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, 221 84, Lund, Sweden. saskia.sydow@med.lu.se.ORCID 0009-0003-0358-8268
Paul PiccinelliDepartment of Clinical Genetics and Pathology, Office for Medical Services, Region Skåne, 221 85, Lund, Sweden.
Shamik MitraDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, 221 84, Lund, Sweden.ORCID 0000-0001-6995-0600
Panagiotis TsagkozisDepartment of Orthopedics, Karolinska University Hospital, Solna, 17176, Stockholm, Sweden.
Asle HeslaDepartment of Orthopedics, Karolinska University Hospital, Solna, 17176, Stockholm, Sweden.ORCID 0000-0001-6205-0773
Camila B R De MattosDepartment of Orthopedics, Skåne University Hospital, 221 85, Lund, Sweden.ORCID 0000-0002-5698-6281
Jan KösterDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, 221 84, Lund, Sweden.
Linda MagnussonDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, 221 84, Lund, Sweden.
Jenny NilssonDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, 221 84, Lund, Sweden.
Adam AmeurDepartment of Immunology, Genetics and Pathology, Science for Life Laboratory, Uppsala University, Uppsala, Sweden.ORCID 0000-0001-6085-6749
René WardenaarEuropean Research Institute for the Biology of Ageing (ERIBA), University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.ORCID 0000-0001-9891-1897
Floris FoijerEuropean Research Institute for the Biology of Ageing (ERIBA), University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.ORCID 0000-0003-0989-3127
Diana SpieringsEuropean Research Institute for the Biology of Ageing (ERIBA), University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.ORCID 0000-0001-8403-474X
Fredrik MertensDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, 221 84, Lund, Sweden.ORCID 0000-0002-6278-5232

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Well-differentiated liposarcoma (WDLS) displays amplification of genes on chromosome 12 (Chr12) in supernumerary ring or giant marker chromosomes. These structures have been suggested to develop through chromothripsis, followed by circularization and breakage-fusion-bridge (BFB) cycles. To test this hypothesis, we compared WDLSs with Chr12 amplification in rod-shaped chromosomes with WDLSs with rings. Both types of amplicons share the same spectrum of structural variants (SVs), show higher SV frequencies in Chr12 than in co-amplified segments, have SVs that fuse the telomeric ends of co-amplified chromosomes, and lack interspersed deletions. Combined with the finding of cells with transient rod-shaped structures in tumors with ring chromosomes, this suggests a stepwise process starting with the gain of Chr12 material that, after remodeling which does not fit with classical chromothripsis, forms a dicentric structure with other chromosomes. Depending on if and when telomeres from other chromosomes are captured, circularized or linear gain of 12q sequences will predominate.

Indexed as

Gene AmplificationLiposarcomaProto-Oncogene Proteins c-mdm2Chromosomes, Human, Pair 12ChromothripsisHumansRing ChromosomesMDM2 protein, humanProto-Oncogene Proteins c-mdm2

Identifiers

PMID38769442
PMCPMC11106292

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.