Overview of Cancer Metabolism

Topic Information

Dear Colleagues,

Cancers are characterized by a high metabolic heterogeneity, allowing cancer cells to survive and proliferate in harsh microenvironmental conditions, including hypoxia, acidosis, and limited availability of metabolic resources. In recent years, a growing body of experimental and clinical evidence has been obtained, suggesting that the metabolic plasticity of malignant cells plays a key role in cancer progression. Indeed, metabolic activities of cancer cells directly influence (epi)genetic modifications, intra- and inter-cellular signaling, metastatic processes, immune escape, and response of tumors to different anticancer therapies. Recent technical developments have allowed us to reveal the spatially and temporally resolved complexity of the metabolic networks within tumors and their role in tumor initiation and progression.

The aim of this Topic is to present new reports that advance our knowledge on tumor metabolism. We welcome the submissions of original research articles and reviews that focus on all aspects of cancer cell metabolism, with a special focus on the interactions between cancer cells and their microenvironment, as well as on the alterations of the various hallmarks of cancer. Apart from the contributions of conference participants, manuscripts are welcome from other interested research groups. All manuscripts will be peer-reviewed.

Dr. Arnaud Blomme
Dr. Cyril Corbet
Topic Editors

Keywords

Participating Journals

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Cells cells	5.2	10.5	2012	15.5 Days	CHF 2700	Submit
Organoids organoids	-	-	2022	27.8 Days	CHF 1200	Submit
Cancers cancers	4.4	8.8	2009	19.1 Days	CHF 2900	Submit
Metabolites metabolites	3.7	6.9	2011	16.7 Days	CHF 2700	Submit
Pathophysiology pathophysiology	2.6	4.6	1994	27.8 Days	CHF 1500	Submit

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Published Papers (4 papers)

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All Cells Organoids Cancers Metabolites Pathophysiology

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34 pages, 472 KB  

Open AccessReview

Lifestyle-Based Approaches to Cancer Prevention and Treatment: Diet, Physical Activity, and Integrative Strategies

by Gianpiero Greco, Alessandro Petrelli, Francesco Fischetti and Stefania Cataldi

Pathophysiology 2025, 32(4), 70; https://doi.org/10.3390/pathophysiology32040070 - 17 Dec 2025

Viewed by 1277

Abstract

Cancer remains a leading global cause of morbidity and mortality. Modifiable lifestyle factors, including avoidance of tobacco use and excessive ultraviolet radiation, healthy dietary patterns, regular physical activity, and weight management, play key roles in prevention and care. This narrative review synthesizes evidence [...] Read more.

Cancer remains a leading global cause of morbidity and mortality. Modifiable lifestyle factors, including avoidance of tobacco use and excessive ultraviolet radiation, healthy dietary patterns, regular physical activity, and weight management, play key roles in prevention and care. This narrative review synthesizes evidence on lifestyle-based interventions influencing cancer risk, treatment tolerance, and survivorship. A literature search was conducted in PubMed and Scopus, supplemented by manual screening via Google Scholar. The time frame (2001–2025) was selected to reflect evidence produced within the modern era of molecular oncology and contemporary lifestyle medicine research. Eligible publications addressed carcinogen exposure (tobacco, alcohol, ultraviolet radiation), diet and nutritional strategies, physical activity, sedentary behavior, obesity, metabolic health, complementary therapies, and cancer outcomes. Evidence indicates that reducing exposure to tobacco and ultraviolet radiation remains central to cancer prevention. Adherence to predominantly plant-based diets, regular physical activity, and maintenance of healthy body weight are consistently associated with lower incidence of several cancers, including breast, colorectal, and liver cancer. Nutritional strategies such as caloric restriction, ketogenic diets, and fasting-mimicking diets show promise in improving treatment efficacy and quality of life. Complementary and mind–body therapies may alleviate treatment-related symptoms, although high-quality evidence on long-term safety and effectiveness is limited. Integrating lifestyle medicine into oncology offers a cost-effective, sustainable strategy to reduce cancer burden and enhance survivorship. Comprehensive programs combining carcinogen avoidance, dietary regulation, structured exercise, and effective radiation risk mitigation may extend healthspan, improve treatment tolerance, and help prevent recurrence. Full article

(This article belongs to the Topic Overview of Cancer Metabolism)

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28 pages, 586 KB  

Open AccessReview

A New Look at the Role of Radiation-Related Epigenetic Mechanisms in Diagnosis and Anticancer Therapies

by Adam Jan Olichwier, Magdalena Bruzgo-Grzybko, Izabela Suwda Kalita, Natalia Bielicka, Ewa Chabielska and Anna Gromotowicz-Poplawska

Cells 2025, 14(23), 1885; https://doi.org/10.3390/cells14231885 - 27 Nov 2025

Viewed by 906

Abstract

Epigenetics encompasses heritable but reversible modifications of gene expression that occur without changes in the DNA sequence and involve mechanisms such as DNA and RNA methylation and histone modifications. These mechanisms modulate chromatin architecture, genome stability, and cellular responses to environmental stressors, and [...] Read more.

Epigenetics encompasses heritable but reversible modifications of gene expression that occur without changes in the DNA sequence and involve mechanisms such as DNA and RNA methylation and histone modifications. These mechanisms modulate chromatin architecture, genome stability, and cellular responses to environmental stressors, and their dysregulation contributes to oncogenesis and cancer progression. In parallel, radiotherapy remains a cornerstone of cancer treatment; furthermore, ionizing radiation induces epigenetic modifications alongside direct DNA double-strand breaks and oxidative damage. Radiation-induced epigenetic changes, including global or locus-specific DNA methylation shifts (e.g., genes promoter CpG islets), histone acetylation and methylation imbalances, are increasingly recognized as key contributors to molecular radioresistance. These adaptive responses may enhance tumor cell survival, affect therapeutic efficacy, and promote metastasis. Understanding the interplay between radiation exposure and epigenetic remodeling opens new perspectives for precision oncology and diagnostics. Epigenetic biomarkers hold potential for predicting treatment response and prognosis, while epigenetic modifiers may sensitize tumors to radiation. This review summarizes current evidence on radiation-induced epigenetic mechanisms and evaluates their diagnostic, prognostic, and therapeutic implications in cancer management. Full article

(This article belongs to the Topic Overview of Cancer Metabolism)

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38 pages, 1308 KB  

Open AccessReview

Mitochondrial Metabolomics in Cancer: Mass Spectrometry-Based Approaches for Metabolic Rewiring Analysis and Therapeutic Discovery

by Yuqing Gao, Zhirou Xiong and Xinyi Wei

Metabolites 2025, 15(8), 513; https://doi.org/10.3390/metabo15080513 - 31 Jul 2025

Viewed by 2114

Abstract

Mitochondria, pivotal organelles in cellular metabolism and energy production, have emerged as critical players in the pathogenesis of cancer. This review outlines the progress in mitochondrial profiling through mass spectrometry-based metabolomics and its applications in cancer research. We provide unprecedented insights into the [...] Read more.

Mitochondria, pivotal organelles in cellular metabolism and energy production, have emerged as critical players in the pathogenesis of cancer. This review outlines the progress in mitochondrial profiling through mass spectrometry-based metabolomics and its applications in cancer research. We provide unprecedented insights into the mitochondrial metabolic rewiring that fuels tumorigenesis, metastasis, and therapeutic resistance. The purpose of this review is to provide a comprehensive guide for the implementation of mitochondrial metabolomics, integrating advanced methodologies—including isolation, detection, and data integration—with insights into cancer-specific metabolic rewiring. We first summarize current methodologies for mitochondrial sample collection and pretreatment. Furthermore, we then discuss the recent advancements in mass spectrometry-based methodologies that facilitate the detailed profiling of mitochondrial metabolites, unveiling significant metabolic reprogramming associated with tumorigenesis. We emphasize how recent technological advancements have addressed longstanding challenges in the field and explore the role of mitochondrial metabolism-driven cancer development and progression for novel drug discovery and translational research applications in cancer. Collectively, this review delineates emerging opportunities for therapeutic discovery and aims to establish a foundation for future investigations into the therapeutic modulation of mitochondrial pathways in cancer, thereby paving the way for innovative diagnostic and therapeutic approaches targeting mitochondrial pathways. Full article

(This article belongs to the Topic Overview of Cancer Metabolism)

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15 pages, 2681 KB  

Open AccessArticle

Metabolomic Profiling and Bioanalysis of Chronic Myeloid Leukemia: Identifying Biomarkers for Treatment Response and Disease Monitoring

by Selim Sayın, Murat Yıldırım, Batuhan Erdoğdu, Ozan Kaplan, Emine Koç, Tuba Bulduk, Melda Cömert, Mustafa Güney, Mustafa Çelebier and Meltem Aylı

Metabolites 2025, 15(6), 376; https://doi.org/10.3390/metabo15060376 - 6 Jun 2025

Cited by 2 | Viewed by 1218

Abstract

Background: Including Chronic Myeloid Leukemia (CML) patients with deep molecular responses (MR4.5) and those with suboptimal responses provides valuable insights into treatment-associated metabolic changes. This study aimed to characterize the metabolomic alterations associated with CML and identify potential biomarkers for treatment response, particularly [...] Read more.

Background: Including Chronic Myeloid Leukemia (CML) patients with deep molecular responses (MR4.5) and those with suboptimal responses provides valuable insights into treatment-associated metabolic changes. This study aimed to characterize the metabolomic alterations associated with CML and identify potential biomarkers for treatment response, particularly in patients achieving a deeper molecular response versus those with poorer responses. Methods: Plasma samples were collected from 51 chronic-phase CML patients and 24 healthy controls. CML patients were classified into two groups based on molecular responses: T1 (BCR-ABL1 IS ≤ 0.0032%) and T2 (BCR-ABL1 IS > 0.0032%, <1%). Metabolomic profiling was conducted using quadrupole time-of-flight liquid chromatography/mass spectrometry. The data analysis involved a partial least squares discriminant analysis, variable importance in projection (VIP) scores, and a pathway enrichment analysis. Significant metabolites were identified. Results: The PLS-DA revealed distinct metabolomic profiles between CML patients and healthy controls as well as between the T1 and T2 groups. Key differentiating metabolites with VIP scores > 1.5 included glutamate, hypoxanthine, and D-galactonic acid. In the T2 group, significant increases in malate and 5-aminoimidazole-4-carboxamide ribonucleotide were observed, reflecting disruptions in purine metabolism, the tricarboxylic acid cycle, and amino acid metabolism. The pathway enrichment analysis highlighted significant alterations in CML energy metabolism, nucleotide synthesis, and amino acid biosynthesis. Conclusions: CML patients exhibit pronounced metabolic changes, particularly in energy and nucleotide metabolism, which are linked to treatment response. These findings provide novel insights into CML biology and suggest potential biomarkers for monitoring treatment efficacy and predicting outcomes and therapeutic targets for improving treatment outcomes and overcoming tyrosine kinase inhibitor resistance. Full article

(This article belongs to the Topic Overview of Cancer Metabolism)

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