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. Author manuscript; available in PMC: 2011 Mar 19.
Published in final edited form as: Cell. 2010 Mar 19;140(6):883–899. doi: 10.1016/j.cell.2010.01.025

Figure 3.

Figure 3

Role of inflammation in tumor initiation and promotion

A) Tumor initiation. Reactive oxygen species (ROS) and reactive nitrogen intermediates (RNI) produced by inflammatory cells may cause mutations in neighboring epithelial cells. Also, cytokines produced by inflammatory cells can elevate intracellular ROS and RNI in pre-malignant cells. In addition, inflammation can result in epigenetic changes that favor tumor initiation. Tumor-associated inflammation contributes to further ROS, RNI and cytokine production.

B) Tumor promotion. Cytokines produced by tumor infiltrating immune cells activate key transcription factors, such as NF-κB or STAT3, in pre-malignant cells to control numerous pro-tumorigenic processes, including survival, proliferation, growth, angiogenesis, and invasion. As parts of positive feed-forward loops, NF-κB and STAT3 induce production of chemokines that attract additional immune/inflammatory cells to sustain tumor-associated inflammation.