ArticlePloS one2013
Fatty acid metabolites in rapidly proliferating breast cancer.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 44 citations in OpenAlex.
- Exploratory metabolomic analysis for identifying systemic signatures ofFrontiers in immunology · 2026Article
- Mechanism of ferroptosis in breast cancer and research progress of natural compounds regulating ferroptosis.Journal of cellular and molecular medicine · 2024Review
- Multi-Omics Approach Points to the Importance of Oxylipins Metabolism in Early-Stage Breast Cancer.Cancers · 2022Article
- Peri-tumoural spatial distribution of lipid composition and tubule formation in breast cancer.BMC cancer · 2022Article
- Integrative analysis of transcriptomics and metabolomics to reveal the melanogenesis pathway of muscle and related meat characters in Wuliangshan black-boned chickens.BMC genomics · 2022Article
- Eicosanoids in the pancreatic tumor microenvironment - a multicellular, multifaceted progression.Gastro hep advances · 2022Article
- 15-Lipoxygenase and its metabolites in the pathogenesis of breast cancer: A double-edged sword.Lipids in health and disease · 2021Review
- The Influence of Supplementation with Zinc in Micro and Nano Forms on the Metabolism of Fatty Acids in Livers of Rats with Breast Cancer.Nutrients · 2021Article
- Validation of plasma metabolites associated with breast cancer risk among Mexican Americans.Cancer epidemiology · 2020Article
- Expression and Function of Eicosanoid-Producing Cytochrome P450 Enzymes in Solid Tumors.Frontiers in pharmacology · 2020Review
- Breast cancer risk in relation to plasma metabolites among Hispanic and African American women.Breast cancer research and treatment · 2019Article
- DHRS2 mediates cell growth inhibition induced by Trichothecin in nasopharyngeal carcinoma.Journal of experimental & clinical cancer research : CR · 2019Article
- Suppression of chemotherapy-induced cytokine/lipid mediator surge and ovarian cancer by a dual COX-2/sEH inhibitor.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Emerging role of 12/15-Lipoxygenase (ALOX15) in human pathologies.Progress in lipid research · 2019Review
- A high-throughput mass spectrometric assay for discovery of human lipoxygenase inhibitors and allosteric effectors.Analytical biochemistry · 2015Article
- Potent and selective inhibitors of human reticulocyte 12/15-lipoxygenase as anti-stroke therapies.Journal of medicinal chemistry · 2014Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
purposeBreast cancers that over-express a lipoxygenase or cyclooxygenase are associated with poor survival possibly because they overproduce metabolites that alter the cancer's malignant behaviors. However, these metabolites and behaviors have not been identified. We here identify which metabolites among those that stimulate breast cancer cell proliferation in vitro are associated with rapidly proliferating breast cancer. EXPERIMENTAL
designWe used selective ion monitoring-mass spectrometry to quantify in the cancer and normal breast tissue of 27 patients metabolites that stimulate (15-, 12-, 5-hydroxy-, and 5-oxo-eicosatetraenoate, 13-hydroxy-octadecaenoate [HODE]) or inhibit (prostaglandin [PG]E2 and D2) breast cancer cell proliferation. We then related their levels to each cancer's proliferation rate as defined by its Mib1 score.
results13-HODE was the only metabolite strongly, significantly, and positively associated with Mib1 scores. It was similarly associated with aggressive grade and a key component of grade, mitosis, and also trended to be associated with lymph node metastasis. PGE2 and PGD2 trended to be negatively associated with these markers. No other metabolite in cancer and no metabolite in normal tissue had this profile of associations.
conclusionsOur data fit a model wherein the overproduction of 13-HODE by 15-lipoxygenase-1 shortens breast cancer survival by stimulating its cells to proliferate and possibly metastasize; no other oxygenase-metabolite pathway, including cyclooxygenase-PGE2/D2 pathways, uses this specific mechanism to shorten survival.
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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.