Inflammation and Metabolism of Cancers

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Tumor Microenvironment".

Deadline for manuscript submissions: closed (30 June 2024) | Viewed by 2181

Special Issue Editor


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Guest Editor
Department of Thoracic Surgery, Faculty of Medicine, Kyoto University, Kyoto 606-8303, Japan
Interests: cancer metabolism

Special Issue Information

Dear Colleagues,

Cancer cells characteristically exhibit a metabolic shift toward aerobic glycolysis, a phenomenon often referred to as the "Warburg effect", thereby creating an acidic tumor microenvironment (TME). This acidic TME and related metabolic changes not only support cancer cell survival and proliferation, but also cause inflammation and shape the immune profile of the tumor. Furthermore, these factors contribute to multidrug resistance. Understanding these complex relationships opens new therapeutic avenues, underscoring the importance of managing these metabolic changes and associated inflammatory responses to control cancer progression. Therefore, strategies addressing the key aspects of cancer-specific metabolism, such as the acidic TME, as well as anti-inflammatory approaches, could be crucial in cancer management. Further research in these areas aims to deepen our understanding of these mechanisms and their potential implications for cancer treatment.

Prof. Dr. Hiromi Wada
Guest Editor

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Keywords

  • inflammation
  • metabolism
  • cancer
  • tumor microenvironment
  • TME

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Published Papers (1 paper)

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Review

41 pages, 3561 KiB  
Review
Plasticity and Tumor Microenvironment in Pancreatic Cancer: Genetic, Metabolic, and Immune Perspectives
by Ari Hashimoto and Shigeru Hashimoto
Cancers 2024, 16(23), 4094; https://doi.org/10.3390/cancers16234094 - 6 Dec 2024
Viewed by 1622
Abstract
Cancer has long been believed to be a genetic disease caused by the accumulation of mutations in key genes involved in cellular processes. However, recent advances in sequencing technology have demonstrated that cells with cancer driver mutations are also present in normal tissues [...] Read more.
Cancer has long been believed to be a genetic disease caused by the accumulation of mutations in key genes involved in cellular processes. However, recent advances in sequencing technology have demonstrated that cells with cancer driver mutations are also present in normal tissues in response to aging, environmental damage, and chronic inflammation, suggesting that not only intrinsic factors within cancer cells, but also environmental alterations are important key factors in cancer development and progression. Pancreatic cancer tissue is mostly comprised of stromal cells and immune cells. The desmoplasmic microenvironment characteristic of pancreatic cancer is hypoxic and hypotrophic. Pancreatic cancer cells may adapt to this environment by rewiring their metabolism through epigenomic changes, enhancing intrinsic plasticity, creating an acidic and immunosuppressive tumor microenvironment, and inducing noncancerous cells to become tumor-promoting. In addition, pancreatic cancer has often metastasized to local and distant sites by the time of diagnosis, suggesting that a similar mechanism is operating from the precancerous stage. Here, we review key recent findings on how pancreatic cancers acquire plasticity, undergo metabolic reprogramming, and promote immunosuppressive microenvironment formation during their evolution. Furthermore, we present the following two signaling pathways that we have identified: one based on the small G-protein ARF6 driven by KRAS/TP53 mutations, and the other based on the RNA-binding protein Arid5a mediated by inflammatory cytokines, which promote both metabolic reprogramming and immune evasion in pancreatic cancer. Finally, the striking diversity among pancreatic cancers in the relative importance of mutational burden and the tumor microenvironment, their clinical relevance, and the potential for novel therapeutic strategies will be discussed. Full article
(This article belongs to the Special Issue Inflammation and Metabolism of Cancers)
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