Mechanisms linking pathogens-associated inflammation and cancer
Chiara Porta1, Elena Riboldi, Antonio Sica
1DISCAFF, University of Piemonte Orientale A. Avogadro, via Bovio 6, Novara, Italy.
Cancer Letters
|November 25, 2010
Summary
Chronic infections from viruses, bacteria, and parasites contribute to cancer development by promoting inflammation. Tumor-associated macrophages (TAMs) play a key role in cancer progression, and infectious agents can reprogram these cells to support tumor growth.
Area of Science:
- Oncology
- Immunology
- Infectious Diseases
Background:
- Chronic infections are linked to 8-17% of the global cancer burden.
- Inflammation is a key factor in carcinogenesis and is recognized as the 7th hallmark of cancer.
- Infectious agents can trigger chronic inflammatory responses, increasing cancer susceptibility.
Purpose of the Study:
- To discuss the causal relationship between infectious agents and the pro-tumoral reprogramming of inflammatory cells.
- To highlight the significance of this phenomenon in tumor development.
- To explore implications for cancer prevention and therapy.
Main Methods:
- Review of evidence linking infectious agents to cancer.
- Analysis of the role of inflammation and tumor microenvironment in cancer progression.
- Focus on the plasticity and function of Tumor-Associated Macrophages (TAMs).
Main Results:
- Infectious agents can initiate inflammatory cascades that predispose tissues to cancer.
- Tumor-Associated Macrophages (TAMs) are crucial in orchestrating tumor progression, including immune evasion, growth, angiogenesis, and metastasis.
- TAMs in established tumors often adopt an M2 phenotype, promoting immunosuppression and metastasis.
Conclusions:
- A causal link exists between specific infectious agents and the reprogramming of inflammatory cells towards a pro-tumoral state.
- Understanding this interplay is crucial for developing novel cancer prevention and therapeutic strategies.
- Targeting the reprogramming of inflammatory cells by infectious agents offers potential avenues for cancer intervention.
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