ReviewJournal of molecular medicine (Berlin, Germany)2014
Metabolic implication of tumor:stroma crosstalk in breast cancer.
Review in Journal of molecular medicine (Berlin, Germany), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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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.
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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.
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Who cites it
12 citing papers in PubMed, 28 citations in OpenAlex.
- Lactate shuttle: from substance exchange to regulatory mechanism.Human cell · 2022Review
- Distinguishing metastatic triple-negative breast cancer from nonmetastatic breast cancer using second harmonic generation imaging and resonance Raman spectroscopy.Journal of biophotonics · 2020Article
- Article
- Eugenol inhibits oxidative phosphorylation and fatty acid oxidation via downregulation of c-Myc/PGC-1β/ERRα signaling pathway in MCF10A-ras cells.Scientific reports · 2017Article
- Ultraconserved long non-coding RNA uc.63 in breast cancer.Oncotarget · 2017Article
- Tumor stroma interaction is mediated by monocarboxylate metabolism.Experimental cell research · 2017Article
- Characterization of the Tumor Microenvironment and Tumor-Stroma Interaction by Non-invasive Preclinical Imaging.Frontiers in oncology · 2017Review
- Hypoxia-Activated Prodrug TH-302 Targets Hypoxic Bone Marrow Niches in Preclinical Leukemia Models.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Article
- Targeting hypoxic response for cancer therapy.Oncotarget · 2016Review
- Targeting stromal-induced pyruvate kinase M2 nuclear translocation impairs oxphos and prostate cancer metastatic spread.Oncotarget · 2015Article
- Modeling cancer metabolism on a genome scale.Molecular systems biology · 2015Review
- Collagen density regulates xenobiotic and hypoxic response of mammary epithelial cells.Environmental toxicology and pharmacology · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The metabolic properties of cancer cells significantly differ from those of normal cells. In particular, cancer cells are largely dependent on aerobic glycolysis, a phenomenon that has been exploited clinically by using labelled glucose for positron emission tomography imaging. Importantly, cancer-associated alterations in metabolism are not merely due to the resulting response to cell proliferation and survival. Indeed, direct metabolic regulation could be driven by tumor oncogenes and/or suppressors, as demonstrated in several solid tumors, including breast cancer. Despite the fact that most breast cancer studies have focused on the intrinsic characteristics of breast tumor cells, it is now widely accepted that tumor microenvironment plays an important role in defining and reprogramming cancer cell metabolism. Tumor:stroma crosstalk, as well as inflammatory cues, concurs to outlining the cancer metabolism, impact on cancer aggressiveness and ultimately on patient survival and therapeutic responses. The aim of this review is to (i) gather the most recent data regarding the metabolic alterations in breast cancer, (ii) describe the role of tumor microenvironment in breast cancer cell metabolic reprogramming, and (iii) contemplate how targeting metabolic pathways aberrantly activated in breast cancer could help current therapeutic regimens.
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Registered trials
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.