Molecular link mechanisms between inflammation and cancer
D B Vendramini-Costa1, J E Carvalho
1Pharmacology and Toxicology Division, Chemical, Biological and Agricultural Pluridisciplinary Research Center, Campinas State University, Campinas-SP, Brazil.
Current Pharmaceutical Design
|May 29, 2012
Summary
Chronic inflammation, linked to over 25% of cancers, can promote tumor development. Non-steroidal anti-inflammatory drugs (NSAIDs) show promise in reducing cancer risk by targeting inflammatory pathways.
Area of Science:
- Oncology
- Immunology
- Molecular Biology
Background:
- Inflammation is a natural defense mechanism, but chronic inflammation contributes to various diseases, including over 25% of all cancers.
- Non-steroidal anti-inflammatory drugs (NSAIDs) have demonstrated a reduced risk for several cancer types, suggesting a link between inflammation and carcinogenesis.
- The tumor microenvironment is infiltrated by various immune cells, producing mediators that influence cancer progression.
Purpose of the Study:
- To review key mediators of inflammation within the tumor microenvironment.
- To explore the role of inflammation in the various stages of carcinogenesis.
Main Methods:
- Literature review of inflammatory mediators (cytokines, chemokines, transcription factors, eicosanoids, kinins).
- Analysis of the cellular composition of the tumor microenvironment (e.g., TAMs, mast cells, lymphocytes).
- Examination of cytotoxic mediators produced by immune cells (e.g., ROS, MMPs, TNFα, interleukins).
Main Results:
- Chronic inflammation is a significant risk factor for cancer development.
- Specific inflammatory mediators and transcription factors (NF-κB, STAT3) are implicated in cancer progression.
- NSAIDs may offer protective effects against certain cancers by modulating inflammatory responses.
Conclusions:
- Inflammation plays a critical role in multiple steps of carcinogenesis.
- Understanding tumor microenvironment mediators is crucial for developing anti-cancer strategies.
- Targeting inflammatory pathways represents a potential therapeutic avenue for cancer prevention and treatment.
Related Concept Videos
The Tumor Microenvironment
Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
Chronic Inflammation: Introduction
Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
The JAK-STAT Signaling Pathway
Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as SH2...
Mechanisms of Retrovirus-induced Cancers
Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...
Mechanisms of Retrovirus-induced Cancers
Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...
Metastasis
Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
