Figure 1: Schematic illustration of the relation of cancer development originating from chronic inflammation. Legend: Inflammatory cells and a variety of mediators together establish an inflammatory microenvironment. Neutrophils and tissue mast cells are recruited (2). B lymphocytes, CD8+ cytotoxic T lymphocytes, and CD4+ T-helper lymphocytes are responsible for an adaptive immune response during the acute activation of innate immunity (3). Mast cells release inflammatory mediators that attract migratory inflammatory cells to the site. Then, monocytes migrate to the area, differentiate into macrophages, and become activated in response to local chemokine and cytokine interactions (3). These alterations in the stem cell niche are responsible for the transformation of stem or progenitor cells to tumor stem cells (4a–c). The origin of cancer stem cells and cancer cells could be tissue (4a, 4c) or bone marrow-derived (4b) stem cells. There are two possible origins for tissue progenitor cells, referred to as label-retaining cells (LRCs) or Lgr5 positive crypt base columnar (CBC) cells between Paneth cells. From Quante M, Wang TC. Inflammation and Stem Cells in Gastrointestinal Carcinogenesis. Physiology 23: 350-359, 2008.