Oxidative stress, inflammation, and cancer are closely linked. Oxidative stress can activate transcription factors such as NF-κB, AP-1, p53, HIF-1α, PPAR-γ, β-catenin/Wnt, and Nrf2, leading to the expression of over 500 genes, including those for growth factors, inflammatory cytokines, chemokines, cell cycle regulatory molecules, and anti-inflammatory molecules. Oxidative stress can lead to chronic inflammation, which is associated with various chronic diseases, including cancer. ROS are involved in a wide spectrum of diseases, including chronic inflammation and various cancers. Chronic inflammation is induced by biological, chemical, and physical factors and is associated with an increased risk of several human cancers. The link between inflammation and cancer has been suggested by epidemiological and experimental data and confirmed by anti-inflammatory therapies that show efficacy in cancer prevention and treatment. The fact that continuous irritation over long periods of time can lead to cancer had already been described in traditional Ayurvedic medical system. Virchow first noted that inflammatory cells are present within tumors and that tumors arise at sites of chronic inflammation. This inflammation is now regarded as a "secret killer" for diseases such as cancer. For example, inflammatory bowel diseases such as Crohn’s disease and ulcerative colitis are associated with increased risk of colon adenocarcinoma, and chronic pancreatitis is related to an increased rate of pancreatic cancer. The exact mechanisms by which a wound-healing process turns into cancer are topics of intense research. Possible mechanisms include induction of genomic instability, alterations in epigenetic events and subsequent inappropriate gene expression, enhanced proliferation of initiated cells, resistance to apoptosis, aggressive tumor neo-vascularization, invasion through tumor-associated basement membrane, and metastasis. How oxidative stress modulates these different stages of inflammation-induced carcinogenesis is the focus of this review. The sources of inflammation are widespread and include microbial and viral infections, exposure to allergens, radiation and toxic chemicals, autoimmune and chronic diseases, obesity, consumption of alcohol, tobacco use, and a high-calorie diet. In general, the longer the inflammation persists, the higher the risk of cancer. Two stages of inflammation exist, acute and chronic inflammation. Acute inflammation is an initial stage of inflammation (innate immunity), which is mediated through the activation of the immune system. This type of inflammation persists only for a short time and is usually beneficial for the host. If the inflammation lasts for a longer period of time, the second stage of inflammation, or chronic inflammation, sets in and may predispose the host to various chronic illnesses, including cancer. During inflammation, mast cells and leukocytes are recruited to the site of damage, which leads to a 'respiratory burst' due to an increased uptake of oxygen, and thus, an increased release and accumulation of ROS at the site of damage. On the other hand, inflammatory cells also produce soluble mediOxidative stress, inflammation, and cancer are closely linked. Oxidative stress can activate transcription factors such as NF-κB, AP-1, p53, HIF-1α, PPAR-γ, β-catenin/Wnt, and Nrf2, leading to the expression of over 500 genes, including those for growth factors, inflammatory cytokines, chemokines, cell cycle regulatory molecules, and anti-inflammatory molecules. Oxidative stress can lead to chronic inflammation, which is associated with various chronic diseases, including cancer. ROS are involved in a wide spectrum of diseases, including chronic inflammation and various cancers. Chronic inflammation is induced by biological, chemical, and physical factors and is associated with an increased risk of several human cancers. The link between inflammation and cancer has been suggested by epidemiological and experimental data and confirmed by anti-inflammatory therapies that show efficacy in cancer prevention and treatment. The fact that continuous irritation over long periods of time can lead to cancer had already been described in traditional Ayurvedic medical system. Virchow first noted that inflammatory cells are present within tumors and that tumors arise at sites of chronic inflammation. This inflammation is now regarded as a "secret killer" for diseases such as cancer. For example, inflammatory bowel diseases such as Crohn’s disease and ulcerative colitis are associated with increased risk of colon adenocarcinoma, and chronic pancreatitis is related to an increased rate of pancreatic cancer. The exact mechanisms by which a wound-healing process turns into cancer are topics of intense research. Possible mechanisms include induction of genomic instability, alterations in epigenetic events and subsequent inappropriate gene expression, enhanced proliferation of initiated cells, resistance to apoptosis, aggressive tumor neo-vascularization, invasion through tumor-associated basement membrane, and metastasis. How oxidative stress modulates these different stages of inflammation-induced carcinogenesis is the focus of this review. The sources of inflammation are widespread and include microbial and viral infections, exposure to allergens, radiation and toxic chemicals, autoimmune and chronic diseases, obesity, consumption of alcohol, tobacco use, and a high-calorie diet. In general, the longer the inflammation persists, the higher the risk of cancer. Two stages of inflammation exist, acute and chronic inflammation. Acute inflammation is an initial stage of inflammation (innate immunity), which is mediated through the activation of the immune system. This type of inflammation persists only for a short time and is usually beneficial for the host. If the inflammation lasts for a longer period of time, the second stage of inflammation, or chronic inflammation, sets in and may predispose the host to various chronic illnesses, including cancer. During inflammation, mast cells and leukocytes are recruited to the site of damage, which leads to a 'respiratory burst' due to an increased uptake of oxygen, and thus, an increased release and accumulation of ROS at the site of damage. On the other hand, inflammatory cells also produce soluble medi