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Cells
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Pathogenic Mechanisms of Chronic Inflammation-Associated Cancer
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Pathogenic Mechanisms of Chronic Inflammation-Associated Cancer

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 15 September 2025 | Viewed by 4306

Special Issue Editor

Prof. Dr. Emiko Mizoguchi

E-Mail Website
Guest Editor
Department of Immunology, Kurume University School of Medicine, Kurume-shi 830-0011, Fukuoka-ken, Japan
Interests: centered around the basic cellular and molecular mechanisms involved in the functional modulation of colonic epithelial cells during the development of inflammatory bowel disease

Special Issue Information

Dear Colleagues,

It has been largely recognized that chronic inflammation, including inflammatory bowel disease, chronic hepatitis, chronic obstructive pulmonary disease, chronic pancreatitis, and chronic gastritis, serves as a foundation for cancer development over many years. There are two major mechanisms thought to be involved in chronic inflammation-associated cancer. Primarily, chronic inflammation triggered by bacteria or viral infection causes inflammatory cell infiltration into affected organs continuously. While inflammatory cells try to eliminate them by attacking pathogens, they also attack surrounding normal cells as well. As a result, mutations may appear in cells that survive with damaged genes. Although these mutations are typically repaired in a normal state, some abnormal cells with unrepaired mutations persist due to continuous damage caused by inflammatory cells. Secondarily, inflammatory cells release soluble factors, including growth factors and cytokines, that promote cell proliferation to supplement damaged or apoptotic cells. These soluble factors are thought to act repeatedly on abnormal cells, promoting proliferation and inducing new mutations, leading to the generation of cancer cells. Additionally, some biological factors have been elucidated regarding the pathogenic mechanisms of chronic inflammation-associated cancer.

This Special Issue of Cells focuses on recent progress in our understanding of inflammation-associated cancers in several organs with the hope that this will lead to clinical applications in the near future.

We are looking forward to your contributions to this Special Issue.

Prof. Dr. Emiko Mizoguchi
Guest Editor

Manuscript Submission Information

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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. Cells is an international peer-reviewed open access semimonthly 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

  • chronic inflammation
  • dysplasia
  • neoplasia
  • oncogene
  • cytokine
  • colitis-associated cancer

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Published Papers (4 papers)

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Review

22 pages, 4324 KiB  
Review
Inflammation-Associated Carcinogenesis in Inflammatory Bowel Disease: Clinical Features and Molecular Mechanisms
by Tadakazu Hisamatsu, Jun Miyoshi, Noriaki Oguri, Hiromu Morikubo, Daisuke Saito, Akimasa Hayashi, Teppei Omori and Minoru Matsuura
Cells 2025, 14(8), 567; https://doi.org/10.3390/cells14080567 - 9 Apr 2025
Viewed by 317
Abstract
Inflammatory bowel disease (IBD), comprising ulcerative colitis (UC) and Crohn’s disease (CD), is a chronic condition marked by persistent intestinal inflammation of unknown etiology. Disease onset involves genetic predisposition and environmental factors that disrupt the intestinal immune homeostasis. The intestinal microbiome and immune [...] Read more.
Inflammatory bowel disease (IBD), comprising ulcerative colitis (UC) and Crohn’s disease (CD), is a chronic condition marked by persistent intestinal inflammation of unknown etiology. Disease onset involves genetic predisposition and environmental factors that disrupt the intestinal immune homeostasis. The intestinal microbiome and immune response play pivotal roles in disease progression. Advances in molecular therapies and early interventions have reduced surgery rates; however, colorectal cancer (CRC) remains a significant concern, driven by chronic inflammation. In UC, the risk of UC-associated neoplasia (UCAN) increases with disease duration, while CD patients face elevated risks of small intestine, anal fistula, and anal canal cancers. Endoscopic surveillance is advised for UCAN, but optimal screening intervals remain undefined, and no established guidelines exist for CD-associated cancers. UCAN morphology often complicates detection due to its flat, inflammation-blended appearance, which differs pathologically from sporadic CRC (sCRC). UCAN is frequently surrounded by dysplasia, with p53 mutations evident at the dysplasia stage. IBD-associated gastrointestinal cancers exemplify inflammation-driven carcinogenesis with distinct molecular mechanisms from the adenoma-carcinoma sequence. This review explores the epidemiology, risk factors, clinical and pathological features, current surveillance practices, and molecular pathways underlying inflammation-associated cancers in IBD. Full article
(This article belongs to the Special Issue Pathogenic Mechanisms of Chronic Inflammation-Associated Cancer)
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29 pages, 1740 KiB  
Review
The Role of Inflammation in Cancer: Mechanisms of Tumor Initiation, Progression, and Metastasis
by Atsushi Nishida and Akira Andoh
Cells 2025, 14(7), 488; https://doi.org/10.3390/cells14070488 - 25 Mar 2025
Viewed by 1214
Abstract
Inflammation is an essential component of the immune response that protects the host against pathogens and facilitates tissue repair. Chronic inflammation is a critical factor in cancer development and progression. It affects every stage of tumor development, from initiation and promotion to invasion [...] Read more.
Inflammation is an essential component of the immune response that protects the host against pathogens and facilitates tissue repair. Chronic inflammation is a critical factor in cancer development and progression. It affects every stage of tumor development, from initiation and promotion to invasion and metastasis. Tumors often create an inflammatory microenvironment that induces angiogenesis, immune suppression, and malignant growth. Immune cells within the tumor microenvironment interact actively with cancer cells, which drives progression through complex molecular mechanisms. Chronic inflammation is triggered by factors such as infections, obesity, and environmental toxins and is strongly linked to increased cancer risk. However, acute inflammatory responses can sometimes boost antitumor immunity; thus, inflammation presents both challenges and opportunities for therapeutic intervention. This review examines how inflammation contributes to tumor biology, emphasizing its dual role as a critical factor in tumorigenesis and as a potential therapeutic target. Full article
(This article belongs to the Special Issue Pathogenic Mechanisms of Chronic Inflammation-Associated Cancer)
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21 pages, 2615 KiB  
Review
Pathogenic Mechanisms of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD)-Associated Hepatocellular Carcinoma
by Toru Nakamura, Atsutaka Masuda, Dan Nakano, Keisuke Amano, Tomoya Sano, Masahito Nakano and Takumi Kawaguchi
Cells 2025, 14(6), 428; https://doi.org/10.3390/cells14060428 - 13 Mar 2025
Viewed by 1036
Abstract
Hepatocellular carcinoma (HCC) is the sixth most common cancer and the third leading cause of cancer deaths worldwide. The etiology of HCC has now dramatically changed from viral hepatitis to metabolic dysfunction-associated steatotic liver disease (MASLD). The main pathogenesis of MASLD-related HCC is [...] Read more.
Hepatocellular carcinoma (HCC) is the sixth most common cancer and the third leading cause of cancer deaths worldwide. The etiology of HCC has now dramatically changed from viral hepatitis to metabolic dysfunction-associated steatotic liver disease (MASLD). The main pathogenesis of MASLD-related HCC is the hepatic lipid accumulation of hepatocytes, which causes chronic inflammation and the subsequent progression of hepatic fibrosis. Chronic hepatic inflammation generates oxidative stress and DNA damage in hepatocytes, which contribute to genomic instability, resulting in the development of HCC. Several metabolic and molecular pathways are also linked to chronic inflammation and HCC in MASLD. In particular, the MAPK and PI3K-Akt-mTOR pathways are upregulated in MASLD, promoting the survival and proliferation of HCC cells. In addition, MASLD has been reported to enhance the development of HCC in patients with chronic viral hepatitis infection. Although there is no approved medication for MASLD besides resmetirom in the USA, there are some preventive strategies for the onset and progression of HCC. Sodium-glucose cotransporter-2 (SGLT2) inhibitor, a class of medications, has been reported to exert anti-tumor effects on HCC by regulating metabolic reprogramming. Moreover, CD34-positive cell transplantation improves hepatic fibrosis by promoting intrahepatic angiogenesis and supplying various growth factors. Furthermore, exercise improves MASLD through an increase in energy consumption as well as changes in chemokines and myokines. In this review, we summarize the recent progress made in the pathogenic mechanisms of MASLD-associated HCC. Furthermore, we introduced new therapeutic strategies for preventing the development of HCC based on the pathogenesis of MASLD. Full article
(This article belongs to the Special Issue Pathogenic Mechanisms of Chronic Inflammation-Associated Cancer)
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18 pages, 1490 KiB  
Review
Molecular Mechanisms and Clinical Aspects of Colitis-Associated Cancer in Ulcerative Colitis
by Jesus K. Yamamoto-Furusho and Fausto D. Gutierrez-Herrera
Cells 2025, 14(3), 162; https://doi.org/10.3390/cells14030162 - 22 Jan 2025
Viewed by 1328
Abstract
Inflammatory bowel diseases have long been recognized as entities with a higher risk of colorectal cancer. An increasing amount of information has been published regarding ulcerative colitis-associated colorectal cancer and its unique mechanisms in recent decades, as ulcerative colitis constitutes a chronic process [...] Read more.
Inflammatory bowel diseases have long been recognized as entities with a higher risk of colorectal cancer. An increasing amount of information has been published regarding ulcerative colitis-associated colorectal cancer and its unique mechanisms in recent decades, as ulcerative colitis constitutes a chronic process characterized by cycles of activity and remission of unpredictable durations and intensities; cumulative genomic alterations occur during active disease and mucosal healing, resulting in a special sequence of events different to the events associated with sporadic colorectal cancer. The recognition of the core differences between sporadic colorectal cancer and colitis-associated cancer is of great importance to understand and guide the directions in which new research could be performed, and how it could be applied to current clinical scenarios. A DSS/AOM murine model has allowed for a better understanding of the pathogenic mechanisms in colitis-associated cancer, as it is currently the closest model to this unique scenario. In this review, we provide a summary of the main molecular mechanisms and the clinical aspects of colitis-associated cancer in ulcerative colitis. Full article
(This article belongs to the Special Issue Pathogenic Mechanisms of Chronic Inflammation-Associated Cancer)
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