Evidence map›Paper›PMID 39605038›Full record

ArticleBreast cancer research : BCR2024

Loss of chromosome cytoband 13q14.2 orchestrates breast cancer pathogenesis and drug response.

Parastoo Shahrouzi, Youness Azimzade, Wioletta Brankiewicz-Kopcinska, Sugandha Bhatia, David Kunke, Derek Richard, Xavier Tekpli, Vessela N Kristensen, Pascal H G Duijf

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Breast cancer research : BCR, 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. Article
  2. Article
  3. 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

9 authors.

Parastoo ShahrouziDepartment of Medical Genetics, Institute of Clinical Medicine, Faculty of Medicine, University of Oslo and Oslo University Hospital, Oslo, Norway. parastoo.shahrouzi@medisin.uio.no.
Youness AzimzadeOslo Center for Biostatistics and Epidemiology, University of Oslo, Oslo, Norway.
Wioletta Brankiewicz-KopcinskaDepartment of Medical Genetics, Institute of Clinical Medicine, Faculty of Medicine, University of Oslo and Oslo University Hospital, Oslo, Norway.
Sugandha BhatiaSchool of Biomedical Sciences, Centre for Genomics and Personalised Health at the Translational Research Institute, Queensland University of Technology (QUT), Woolloongabba, QLD, 4102, Australia.
David KunkeDepartment of Medical Genetics, Institute of Clinical Medicine, Faculty of Medicine, University of Oslo and Oslo University Hospital, Oslo, Norway.
Derek RichardFaculty of Health, School of Biomedical Sciences, Queensland University of Technology (QUT), Woolloongabba,, QLD, 4102, Australia.
Xavier TekpliDepartment of Medical Genetics, Institute of Clinical Medicine, Faculty of Medicine, University of Oslo and Oslo University Hospital, Oslo, Norway.
Vessela N KristensenDepartment of Medical Genetics, Institute of Clinical Medicine, Faculty of Medicine, University of Oslo and Oslo University Hospital, Oslo, Norway. v.n.kristensen@medisin.uio.no.
Pascal H G DuijfDepartment of Medical Genetics, Institute of Clinical Medicine, Faculty of Medicine, University of Oslo and Oslo University Hospital, Oslo, Norway. pascal.duijf@unisa.edu.au.

Funding

Cancer Council NSW RG21-13European Union's Horizon 2020 Research and Innovation program under the Marie Skłodowska- Curie Actions 80113
6 · The paper itself

Abstract

Breast cancer (BCa) is a major global health challenge. The BCa genome often carries extensive somatic copy number alterations (CNAs), including gains/amplifications and losses/deletions. These CNAs significantly affect tumor development, drug response and patient survival. However, how individual CNAs contribute is mostly elusive. We identified loss of chromosome 13q14.2 as a key CNA in BCa, occurring in up to 63% of patients, depending on the subtype, and correlating with poor survival. Through multi-omics and in vitro analyses, we uncover a paradoxical role of 13q14.2 loss, promoting both cell cycle and pro-apoptotic pathways in cancer cells, while also associating with increased NK cell and macrophage populations in the tumor microenvironment. Notably, 13q14.2 loss increases BCa susceptibility to BCL2 inhibitors, both in vitro and in patient-derived xenografts. Thus, 13q14.2 loss could serve as a biomarker for BCa prognosis and treatment, potentially improving outcomes for BCa patients.

Indexed as

Breast NeoplasmsChromosomes, Human, Pair 13DNA Copy Number VariationsAnimalsAntineoplastic AgentsApoptosisBiomarkers, TumorCell Line, TumorChromosome DeletionFemaleGene Expression Regulation, NeoplasticHumansKiller Cells, NaturalMicePrognosisProto-Oncogene Proteins c-bcl-2Antineoplastic AgentsBiomarkers, TumorProto-Oncogene Proteins c-bcl-2BiomarkerBreast cancerChromosome 13q14.2Copy number alterationsDrug sensitivityTumor microenvironment

Identifiers

PMID39605038
PMCPMC11600738

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Registered trials

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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.