Metabolic Cancer Therapy: Targeting Tumor Metabolism for Innovative Adjuvant Treatment

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

Deadline for manuscript submissions: 30 September 2024 | Viewed by 2239

Special Issue Editor


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Guest Editor
Department of Clinical and Experimental Medicine, Faculty of Medicine and Surgery, University of Foggia, Foggia, 71122 Puglia, Italy
Interests: ketogenic; diet; low-carb diet; mitochondrial dysfunction; adjuvant metabolic therapy; diabetes; obesity; cancer nutritional support

Special Issue Information

Dear Colleagues,

A possible emerging approach to cancer treatment involves the targeting of aberrant tumor metabolism. The metabolic changes that occur throughout the progression of cancer provide distinct characteristics that can be used for therapeutic purposes, specifically targeting the metabolic demands of neoplastic cells for essential nutrients. As no tumor can grow without anabolic substrates or energy, their simultaneous inhibition could ultimately reduce the viability of most, if not all, neoplastic cells. Normal eukaryotic animal cells are metabolically flexible and can generate energy using substrate-level phosphorylation or mitochondrial oxidative phosphorylation, based on the availability of oxygen. Otherwise, cancer cells are largely dependent on the substrate-level phosphorylation of glucose and glutamine through the glycolysis and glutaminolysis pathways, regardless of the presence of oxygen. Exploiting these specific energy and metabolic characteristics of neoplastic cells, it is possible to implement a nutritional and pharmacological intervention aimed at reducing the main substrate-level phosphorylation energy substrates, i.e. glucose and glutamine, in order to obtain the production of non-fermentable substrates by neoplastic cells (e.g., ketone bodies) due to cancer’s mitochondrial dysfunction. This Special Issue will explore the therapeutic possibilities that emerge from cancer-disrupted metabolism and metabolic communication, acting through nutritional, metabolic, and pharmaceutical approaches, to precisely target abnormal tumor metabolism.

Dr. Raffaele Ivan Cincione
Guest Editor

Manuscript Submission Information

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Keywords

  • cancer metabolism
  • glycolysis
  • glutaminolysis
  • ketone bodies
  • mitochondrial dysfunction

Published Papers (1 paper)

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24 pages, 2543 KiB  
Hypothesis
Mitochondrial–Stem Cell Connection: Providing Additional Explanations for Understanding Cancer
by Pierrick Martinez, Ilyes Baghli, Géraud Gourjon and Thomas N. Seyfried
Metabolites 2024, 14(4), 229; https://doi.org/10.3390/metabo14040229 - 17 Apr 2024
Viewed by 2012
Abstract
The cancer paradigm is generally based on the somatic mutation model, asserting that cancer is a disease of genetic origin. The mitochondrial–stem cell connection (MSCC) proposes that tumorigenesis may result from an alteration of the mitochondria, specifically a chronic oxidative phosphorylation (OxPhos) insufficiency [...] Read more.
The cancer paradigm is generally based on the somatic mutation model, asserting that cancer is a disease of genetic origin. The mitochondrial–stem cell connection (MSCC) proposes that tumorigenesis may result from an alteration of the mitochondria, specifically a chronic oxidative phosphorylation (OxPhos) insufficiency in stem cells, which forms cancer stem cells (CSCs) and leads to malignancy. Reviewed evidence suggests that the MSCC could provide a comprehensive understanding of all the different stages of cancer. The metabolism of cancer cells is altered (OxPhos insufficiency) and must be compensated by using the glycolysis and the glutaminolysis pathways, which are essential to their growth. The altered mitochondria regulate the tumor microenvironment, which is also necessary for cancer evolution. Therefore, the MSCC could help improve our understanding of tumorigenesis, metastases, the efficiency of standard treatments, and relapses. Full article
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