Evidence map›Paper›PMID 32691367›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2020

Metabolomic profiling of mouse mammary tumor-derived cell lines reveals targeted therapy options for cancer subtypes.

Martin P Ogrodzinski, Shao Thing Teoh, Sophia Y Lunt

Abstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Phosphorescent Metal Halide Nanoclusters for Tunable Photodynamic Therapy.Chemistry (Weinheim an der Bergstrasse, Germany) · 2023
    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

3 authors.

Martin P OgrodzinskiDepartment of Biochemistry and Molecular Biology, Michigan State University, East Lansing, MI, USA.
Shao Thing TeohDepartment of Biochemistry and Molecular Biology, Michigan State University, East Lansing, MI, USA.
Sophia Y LuntDepartment of Biochemistry and Molecular Biology, Michigan State University, East Lansing, MI, USA. sophia@msu.edu.

Funding

Congressionally Directed Medical Research Programs W81XWH-15-1-0453
6 · The paper itself

Abstract

purposeBreast cancer is a heterogeneous disease with several subtypes that currently do not have targeted therapeutic options. Metabolomics has the potential to uncover novel targeted treatment strategies by identifying metabolic pathways required for cancer cells to survive and proliferate.

methodsThe metabolic profiles of two histologically distinct breast cancer subtypes from a MMTV-Myc mouse model, epithelial-mesenchymal-transition (EMT) and papillary, were investigated using mass spectrometry-based metabolomics methods. Based on metabolic profiles, drugs most likely to be effective against each subtype were selected and tested.

resultsWe found that the EMT and papillary subtypes display different metabolic preferences. Compared to the papillary subtype, the EMT subtype exhibited increased glutathione and TCA cycle metabolism, while the papillary subtype exhibited increased nucleotide biosynthesis compared to the EMT subtype. Targeting these distinct metabolic pathways effectively inhibited cancer cell proliferation in a subtype-specific manner.

conclusionsOur results demonstrate the feasibility of metabolic profiling to develop novel personalized therapy strategies for different subtypes of breast cancer. Schematic overview of the experimental design for drug selection based on breast cancer subtype-specific metabolism. The epithelial mesenchymal transition (EMT) and papillary tumors are histologically distinct mouse mammary tumor subtypes from the MMTV-Myc mouse model. Cell lines derived from tumors can be used to determine metabolic pathways that can be used to select drug candidates for each subtype.

Indexed as

MetabolomicsMolecular Targeted TherapyAnimalsAntineoplastic AgentsCarbon IsotopesCell Line, TumorCitric Acid CycleEpithelial-Mesenchymal TransitionFemaleMammary Neoplasms, AnimalMammary Tumor Virus, MouseMetabolomeMiceNucleotidesProto-Oncogene Proteins c-mycAntineoplastic AgentsCarbon-13Carbon IsotopesNucleotidesProto-Oncogene Proteins c-mycBreast cancerCancer subtypesMass spectrometryMetabolic profileMetabolomicsTargeted therapy

Identifiers

PMID32691367
PMCPMC12990690

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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.