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Metabolites
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Cancer Metabolomics 2024
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Cancer Metabolomics 2024

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Cell Metabolism".

Deadline for manuscript submissions: closed (25 February 2025) | Viewed by 4517

Special Issue Editor

Dr. Bénédicte Elena-Herrmann

E-Mail Website
Guest Editor
Institute for Advanced Biosciences, University Grenoble Alpes/CNRS/INSERM, Grenoble, France
Interests: cancer metabolomics; molecular epidemiology; metabolism and epigenetics; advanced NMR methods; chemometrics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We welcome the submission of original research articles or review papers as contributions to this Special Issue of Metabolites dedicated to Cancer Metabolomics.

The aim for this issue is to highlight innovative metabolomic approaches for fundamental and clinical research in cancerology. These include new achievements in metabolomics research in oncology that provide mechanistic information on model systems or involve translational and clinical studies on cancer patients.

We encourage contributions that include cross-disciplinary research, large-scale data collection and analysis, or multi-omics studies for integrative medicine. Investigations of metabolic markers of risk, early markers of disease, and prognostic metabolites markers of the evolution of responses to cancer treatment will be highly relevant contributions to this Special Issue. New approaches based on mass spectrometry or nuclear magnetic resonance (NMR), as well as broader technological and analytical developments leading to future advances in the field of cancer metabolomics, are also very welcome.

We hope with this Special Issue to provide our readers with a timely contribution to metabolomics research and perspectives in the broad area of cancerology.

Dr. Bénédicte Elena-Herrmann
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Metabolites is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • metabolomics approaches and technologies
  • cancer and chronic diseases
  • diagnosis or predictive metabolic biomarkers
  • multi-omics studies
  • tumor metabolism
  • molecular epidemiology of cancer

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Published Papers (3 papers)

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Research

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11 pages, 1529 KiB  
Article
Singlet Oxygen-Induced Mitochondrial Reset in Cancer: A Novel Approach for Ovarian Cancer Therapy
by Jorgelindo da Veiga Moreira, Laurent Schwartz and Mario Jolicoeur
Metabolites 2024, 14(12), 648; https://doi.org/10.3390/metabo14120648 - 21 Nov 2024
Viewed by 973
Abstract
Background/Objectives: This study explores the generation of singlet oxygen (SO) through methylene blue (MB) activation as a metabolic intervention for ovarian cancer. We aimed to examine the role of SO in modulating mitochondrial function, cellular metabolism, and proliferation in ovarian cancer cell [...] Read more.
Background/Objectives: This study explores the generation of singlet oxygen (SO) through methylene blue (MB) activation as a metabolic intervention for ovarian cancer. We aimed to examine the role of SO in modulating mitochondrial function, cellular metabolism, and proliferation in ovarian cancer cell lines compared to control cells. Methods: The study utilized two ovarian cancer cell lines, OV1369-R2 and TOV1369, along with ARPE-19 control cells. Following MB treatment and light activation, mitochondrial function and ATP synthesis were assessed. Metabolomic analyses were performed to evaluate changes in central carbon metabolism, particularly focusing on markers of the Warburg effect. Results: TOV1369 cells exhibited a pronounced sensitivity to MB treatment, resulting in significant inhibition of ATP synthesis and reduced proliferation. Metabolomic analysis indicated that MB-induced SO production partially reversed the Warburg effect, suggesting a shift from glycolysis to oxidative phosphorylation. These effects were less pronounced in OV1369-R2 and ARPE-19 cells, correlating with their lower MB sensitivity. Conclusions: MB-generated SO selectively modulates mitochondrial energetics in ovarian cancer cells, driving a metabolic reorganization that curtails their proliferative capacity. This approach, leveraging the bacterial-like features of cancer metabolism, offers a promising therapeutic avenue to induce apoptosis and enhance treatment outcomes in ovarian cancer. Full article
(This article belongs to the Special Issue Cancer Metabolomics 2024)
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38 pages, 10637 KiB  
Article
A Multiomics, Molecular Atlas of Breast Cancer Survivors
by Brent A. Bauer, Caleb M. Schmidt, Kathryn J. Ruddy, Janet E. Olson, Cem Meydan, Julian C. Schmidt, Sheena Y. Smith, Fergus J. Couch, John C. Earls, Nathan D. Price, Joel T. Dudley, Christopher E. Mason, Bodi Zhang, Stephen M. Phipps and Michael A. Schmidt
Metabolites 2024, 14(7), 396; https://doi.org/10.3390/metabo14070396 - 20 Jul 2024
Viewed by 2122
Abstract
Breast cancer imposes a significant burden globally. While the survival rate is steadily improving, much remains to be elucidated. This observational, single time point, multiomic study utilizing genomics, proteomics, targeted and untargeted metabolomics, and metagenomics in a breast cancer survivor (BCS) and age-matched [...] Read more.
Breast cancer imposes a significant burden globally. While the survival rate is steadily improving, much remains to be elucidated. This observational, single time point, multiomic study utilizing genomics, proteomics, targeted and untargeted metabolomics, and metagenomics in a breast cancer survivor (BCS) and age-matched healthy control cohort (N = 100) provides deep molecular phenotyping of breast cancer survivors. In this study, the BCS cohort had significantly higher polygenic risk scores for breast cancer than the control group. Carnitine and hexanoyl carnitine were significantly different. Several bile acid and fatty acid metabolites were significantly dissimilar, most notably the Omega-3 Index (O3I) (significantly lower in BCS). Proteomic and metagenomic analyses identified group and pathway differences, which warrant further investigation. The database built from this study contributes a wealth of data on breast cancer survivorship where there has been a paucity, affording the ability to identify patterns and novel insights that can drive new hypotheses and inform future research. Expansion of this database in the treatment-naïve, newly diagnosed, controlling for treatment confounders, and through the disease progression, can be leveraged to profile and contextualize breast cancer and breast cancer survivorship, potentially leading to the development of new strategies to combat this disease and improve the quality of life for its victims. Full article
(This article belongs to the Special Issue Cancer Metabolomics 2024)
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Review

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18 pages, 1862 KiB  
Review
SMARCB1 Deficiency as a Driver of the Hallmarks of Cancer in Rhabdoid Tumours: Novel Insights into Dysregulated Energy Metabolism, Emerging Targets, and Ongoing Clinical Trials
by Abdul L. Shakerdi and Graham P. Pidgeon
Metabolites 2025, 15(5), 304; https://doi.org/10.3390/metabo15050304 - 3 May 2025
Viewed by 274
Abstract
Background: Rhabdoid tumours (RTs) are aggressive neoplasms most often characterised by biallelic loss of the SMARCB1 gene, encoding a core subunit of the SWI/SNF chromatin-remodelling complex. Despite their relative genetic stability, RTs exhibit a highly malignant phenotype and poor prognosis. Methods: This review [...] Read more.
Background: Rhabdoid tumours (RTs) are aggressive neoplasms most often characterised by biallelic loss of the SMARCB1 gene, encoding a core subunit of the SWI/SNF chromatin-remodelling complex. Despite their relative genetic stability, RTs exhibit a highly malignant phenotype and poor prognosis. Methods: This review explores the mechanisms underlying SMARCB1 aberrations, their role in driving hallmarks of cancer, and emerging therapeutic strategies for RTs. Ongoing clinical trials listed on ClinicalTrials were reviewed to evaluate the translational potential of targeted therapies in SMARCB1-deficient rhabdoid tumours. Results: Loss of SMARCB1 drives multiple cancer hallmarks by disrupting key regulatory pathways. It promotes unchecked cell proliferation through alterations in p16INK4a and Myc signalling. SMARCB1-deficient tumours possess immune-evading capabilities via PD-L1 overexpression and immune checkpoint activation. SMARCB1 deficiency also alters cellular energetics. The nucleotide biosynthesis pathway has been demonstrated to be upregulated in RT organoids, as shown by increased levels of pathway metabolites. Enzymes of the mevalonate pathway such as HMG-CoA reductase and mevalonate kinase are also dysregulated. Targeting glutathione metabolism with eprenetapopt may induce oxidative stress and apoptosis. Widespread epigenetic aberrations, including increased EZH2 activity, are being targeted with inhibitors such as tazemetostat. Conclusions: SMARCB1 loss is a central driver of cancer hallmarks in RTs, enabling proliferation, immune evasion, metabolic reprogramming, and epigenetic dysregulation. Future horizons in RT treatment include immunotherapies, epigenetic modifiers, and gene therapies. The synergy and optimal timing of targeted therapy with conventional treatment requires further characterisation for clinical translation. Full article
(This article belongs to the Special Issue Cancer Metabolomics 2024)
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