Evidence map›Paper›PMID 23397111›Full record

ArticleMolecular & cellular proteomics : MCP2013

Proteomics of genetically engineered mouse mammary tumors identifies fatty acid metabolism members as potential predictive markers for cisplatin resistance.

Marc Warmoes, Janneke E Jaspers, Guotai Xu, Bharath K Sampadi, Thang V Pham, Jaco C Knol, Sander R Piersma, Epie Boven, Jos Jonkers, Sven Rottenberg and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular & cellular proteomics : MCP, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

20 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Review
  3. Interplay between altered metabolism and DNA damage and repair in ovarian cancer.BioEssays : news and reviews in molecular, cellular and developmental biology · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. Cisplatin Resistance and Redox-Metabolic Vulnerability: A Second Alteration.International journal of molecular sciences · 2021
    Review
  8. Review
  9. Article
  10. GRP94 Is Involved in the Lipid Phenotype of Brain Metastatic Cells.International journal of molecular sciences · 2019
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
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  20. 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

11 authors at 4 institutions in 2 countries.

Marc WarmoesOncoProteomics Laboratory, Department of Medical Oncology, VU University Medical Center, De Boelelaan 1117, 1081HV Amsterdam, The Netherlands.
Janneke E Jaspers
Guotai Xu
Bharath K Sampadi
Thang V Pham
Jaco C Knol
Sander R Piersma
Epie Boven
Jos Jonkers
Sven Rottenberg
Connie R Jimenez
University Medical Center · USMolecular Oncology (United States) · USAmsterdam UMC Location VUmc · NLThe Netherlands Cancer Institute · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In contrast to various signatures that predict the prognosis of breast cancer patients, markers that predict chemotherapy response are still elusive. To detect such predictive biomarkers, we investigated early changes in protein expression using two mouse models for distinct breast cancer subtypes who have a differential knock-out status for the breast cancer 1, early onset (Brca1) gene. The proteome of cisplatin-sensitive BRCA1-deficient mammary tumors was compared with that of cisplatin-resistant mammary tumors resembling pleomorphic invasive lobular carcinoma. The analyses were performed 24 h after administration of the maximum tolerable dose of cisplatin. At this time point, drug-sensitive BRCA1-deficient tumors showed DNA damage, but cells were largely viable. By applying paired statistics and quantitative filtering, we identified highly discriminatory markers for the sensitive and resistant model. Proteins up-regulated in the sensitive model are involved in centrosome organization, chromosome condensation, homology-directed DNA repair, and nucleotide metabolism. Major discriminatory markers that were up-regulated in the resistant model were predominantly involved in fatty acid metabolism, such as fatty-acid synthase. Specific inhibition of fatty-acid synthase sensitized resistant cells to cisplatin. Our data suggest that exploring the functional link between the DNA damage response and cancer metabolism shortly after the initial treatment may be a useful strategy to predict the efficacy of cisplatin.

Indexed as

Drug Resistance, NeoplasmAnimalsAntineoplastic AgentsBiomarkers, TumorBiosynthetic PathwaysCdh1 ProteinsCisplatinFatty AcidsFatty Acid Synthase, Type IFemaleGene Knockdown TechniquesGenes, BRCA1Genes, p53Mammary Neoplasms, ExperimentalMiceMice, KnockoutAntineoplastic AgentsBiomarkers, TumorCdh1 ProteinsCisplatinFatty AcidsFatty Acid Synthase, Type IFzr1 protein, mouseProteome

Identifiers

PMID23397111
PMCPMC3650342
OpenAlexW2169310855

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.