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: 31 March 2025 | Viewed by 137
Special Issue Editor
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
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Keywords
- chronic inflammation
- dysplasia
- neoplasia
- oncogene
- cytokine
- colitis-associated cancer
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