Inflammation predisposes to the development of cancer and promotes all stages of tumorigenesis. Cancer cells, as well as surrounding stromal and inflammatory cells, engage in well-orchestrated reciprocal interactions to form an inflammatory tumor microenvironment (TME). Cells within the TME are highly plastic, continuously changing their phenotypic and functional characteristics. Here, we review the origins of inflammation in tumors, and the mechanisms whereby inflammation drives tumor initiation, growth, progression, and metastasis. We discuss how tumor-promoting inflammation closely resembles inflammatory processes typically found during development, immunity, maintenance of tissue homeostasis, or tissue repair and illuminate the distinctions between tissue-protective and pro-tumorigenic inflammation, including spatiotemporal considerations. Defining the cornerstone rules of engagement governing molecular and cellular mechanisms of tumor-promoting inflammation will be essential for further development of anti-cancer therapies.
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http://dx.doi.org/10.1016/j.immuni.2019.06.025 | DOI Listing |
BMC Med
January 2025
Department of Gynaecology and Obstetrics, University and University Medical Center Schleswig-Holstein Campus Kiel, Kiel, Germany.
Ovarian cancer remains the most lethal gynecological malignancy. Despite the approval of promising targeted therapy such as bevacizumab and PARP inhibitors, 5-year survival has not improved significantly. Thus, there is an urgent need for new therapeutics.
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January 2025
Peking Union Medical College, Graduate School of Peking Union Medical College, Beijing, China.
Autophagy is a physiologically regulated cellular process orchestrated by autophagy-related genes (ATGs) that, depending on the tumor type and stage, can either promote or suppress tumor growth and progression. It can also modulate cancer stem cell maintenance and immune responses. Therefore, targeted manipulation of autophagy may inhibit tumor development by overcoming tumor-promoting mechanisms.
View Article and Find Full Text PDFCancers (Basel)
December 2024
Division of Molecular Psychoimmunology, Institute for Genetic Medicine, Hokkaido University, Sapporo 060-0818, Japan.
Cancer Res
December 2024
University of California, San Francisco, San Francisco, CA, United States.
Hepatitis B virus (HBV) infections promote liver cancer initiation by inducing inflammation and cellular stress. Despite the primarily indirect effect on oncogenesis, HBV is associated with a recurrent genomic phenotype in HCC, suggesting that it impacts the biology of established HCC. Characterization of the interaction of HBV with host proteins and the mechanistic contributions of HBV to HCC initiation and maintenance could provide insights into HCC biology and uncover therapeutic vulnerabilities.
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December 2024
NHC Key Laboratory of Human Disease Comparative Medicine, Institute of Laboratory Animal Science, PR China; Beijing Engineering Research Center for Experimental Animal Models of Human Critical Diseases, Chinese Academy of Medical Sciences&Peking Union Medical College, Beijing 100021, PR China. Electronic address:
Chronic inflammation has been recognized as one of the hallmarks of head and neck squamous cell carcinoma (HNSCC), Absent In Melanoma 2(AIM2) has emerged as important regulators of chronic inflammatory, and participated in initiation, progression of kinds of human cancers. Nonetheless, the biological functions and underlying mechanisms of AIM2 in HNSCC remain inadequately understood. Based on the bioinformatics analysis of public databases, we identified elevated AIM2 expression in HNSCC, which positively correlates with disease stage and HPV infection, thereby possessing both diagnostic and prognostic significance.
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