Evidence map›Paper›PMID 35994654›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2022

Metastatic triple negative breast cancer adapts its metabolism to destination tissues while retaining key metabolic signatures.

Fariba Roshanzamir, Jonathan L Robinson, Daniel Cook, Mohammad Hossein Karimi-Jafari, Jens Nielsen

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
5.2field-weighted citation impact, top 3% 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

45 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
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  4. Reconstruction of human metabolic models with large language models.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  12. Metabolic adaptations of brain metastasis.Nature reviews. Cancer · 2025
    Review
  13. Resistance to neoadjuvant chemotherapy in breast cancers: a metabolic perspective.Journal of experimental & clinical cancer research : CR · 2025
    Review
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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

5 authors at 4 institutions in 3 countries.

Fariba RoshanzamirDepartment of Bioinformatics, Institute of Biochemistry and Biophysics, University of Tehran, Tehran, 6619-14155, Iran.
Jonathan L RobinsonNational Bioinformatics Infrastructure Sweden, Science for Life Laboratory, Department of Biology and Biological Engineering, Chalmers University of Technology, SE-41258 Gothenburg, Sweden.
Daniel CookSystems and Synthetic Biology, Department of Biology and Biological Engineering, Chalmers University of Technology, SE-412 96, Gothenburg, Sweden.
Mohammad Hossein Karimi-JafariDepartment of Bioinformatics, Institute of Biochemistry and Biophysics, University of Tehran, Tehran, 6619-14155, Iran.
Jens NielsenSystems and Synthetic Biology, Department of Biology and Biological Engineering, Chalmers University of Technology, SE-412 96, Gothenburg, Sweden.ORCID 0000-0002-9955-6003
University of Tehran · IRBioInnovation Institute · DKChalmers University of Technology · SEScience for Life Laboratory · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Triple negative breast cancer (TNBC) metastases are assumed to exhibit similar functions in different organs as in the original primary tumor. However, studies of metastasis are often limited to a comparison of metastatic tumors with primary tumors of their origin, and little is known about the adaptation to the local environment of the metastatic sites. We therefore used transcriptomic data and metabolic network analyses to investigate whether metastatic tumors adapt their metabolism to the metastatic site and found that metastatic tumors adopt a metabolic signature with some similarity to primary tumors of their destinations. The extent of adaptation, however, varies across different organs, and metastatic tumors retain metabolic signatures associated with TNBC. Our findings suggest that a combination of anti-metastatic approaches and metabolic inhibitors selected specifically for different metastatic sites, rather than solely targeting TNBC primary tumors, may constitute a more effective treatment approach.

Indexed as

Metabolic Networks and PathwaysNeoplasm MetastasisOrgan SpecificityTriple Negative Breast NeoplasmsHumansTranscriptomegene expressiongenome-scale metabolic modelsmetastasissystems biologytriple negative breast cancer

Identifiers

PMID35994654
PMCPMC9436376
OpenAlexW4292651737

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.