The aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor that plays a critical role in maintaining homeostasis of barrier organs such as the skin, lung, and gut. Initially discovered as a receptor for environmental carcinogens like polycyclic aromatic hydrocarbons (PAHs), AhR activation by these ligands can lead to DNA damage and mutations, promoting carcinogenesis. However, recent evidence suggests that AhR also plays a role in immune regulation, influencing the development of natural killer (NK) cells, regulatory T (Treg) cells, and T helper 17 (Th17) cells, as well as the production of immunosuppressive cytokines. The role of AhR in carcinogenesis is complex, with some studies showing it promotes cancer while others suggest it acts as a tumor suppressor. Genetic studies indicate that AhR can act as a positive or negative regulator in cancer development. For example, mutations in the AhR gene have been detected in bladder cancer, and these mutations can activate the AhR pathway, promoting cell transformation. AhR expression is often altered in various cancers, and its nuclear localization is associated with poor outcomes in non-small cell lung cancer. Additionally, AhR can inhibit carcinogenesis by downregulating AhR mRNA in chronic myeloid leukemia cells and by reducing the expression of genes involved in tumor progression. Functional studies have shown that AhR plays a role in UV-associated skin carcinogenesis by activating signaling pathways that contribute to photo-carcinogenesis. AhR is also involved in PAH-associated lung carcinogenesis, where it can promote cancer growth and spread. In colorectal cancer, AhR is crucial for maintaining intestinal homeostasis and regulating immune responses. Disruption of AhR expression or activity can lead to altered intestinal homeostasis and potentially contribute to carcinogenesis. Immunological studies have shown that AhR activation can enhance antitumor immunity by promoting NK cell activity and increasing IFN-γ secretion. However, AhR can also facilitate tumor immune escape by promoting the production of immunosuppressive cells like Treg cells and Th17 cells. The dual role of AhR in promoting antitumor immunity and facilitating tumor immune escape depends on the type of immune cells involved. Several AhR agonists and antagonists have been evaluated for their efficacy in cancer chemoprevention. For example, omeprazole, a proton pump inhibitor, has been shown to suppress the proliferation and migration of cancer cells. Metformin, an oral antidiabetic drug, has been found to downregulate CYP1A1 and CYP1B1 expression in breast cancer cells. Resveratrol, a natural polyphenol, has chemopreventive and chemotherapeutic properties, while curcumin, a compound found in turmeric, has been shown to inhibit the activation of AhR and reduce toxicity induced by carcinogens. β-blockThe aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor that plays a critical role in maintaining homeostasis of barrier organs such as the skin, lung, and gut. Initially discovered as a receptor for environmental carcinogens like polycyclic aromatic hydrocarbons (PAHs), AhR activation by these ligands can lead to DNA damage and mutations, promoting carcinogenesis. However, recent evidence suggests that AhR also plays a role in immune regulation, influencing the development of natural killer (NK) cells, regulatory T (Treg) cells, and T helper 17 (Th17) cells, as well as the production of immunosuppressive cytokines. The role of AhR in carcinogenesis is complex, with some studies showing it promotes cancer while others suggest it acts as a tumor suppressor. Genetic studies indicate that AhR can act as a positive or negative regulator in cancer development. For example, mutations in the AhR gene have been detected in bladder cancer, and these mutations can activate the AhR pathway, promoting cell transformation. AhR expression is often altered in various cancers, and its nuclear localization is associated with poor outcomes in non-small cell lung cancer. Additionally, AhR can inhibit carcinogenesis by downregulating AhR mRNA in chronic myeloid leukemia cells and by reducing the expression of genes involved in tumor progression. Functional studies have shown that AhR plays a role in UV-associated skin carcinogenesis by activating signaling pathways that contribute to photo-carcinogenesis. AhR is also involved in PAH-associated lung carcinogenesis, where it can promote cancer growth and spread. In colorectal cancer, AhR is crucial for maintaining intestinal homeostasis and regulating immune responses. Disruption of AhR expression or activity can lead to altered intestinal homeostasis and potentially contribute to carcinogenesis. Immunological studies have shown that AhR activation can enhance antitumor immunity by promoting NK cell activity and increasing IFN-γ secretion. However, AhR can also facilitate tumor immune escape by promoting the production of immunosuppressive cells like Treg cells and Th17 cells. The dual role of AhR in promoting antitumor immunity and facilitating tumor immune escape depends on the type of immune cells involved. Several AhR agonists and antagonists have been evaluated for their efficacy in cancer chemoprevention. For example, omeprazole, a proton pump inhibitor, has been shown to suppress the proliferation and migration of cancer cells. Metformin, an oral antidiabetic drug, has been found to downregulate CYP1A1 and CYP1B1 expression in breast cancer cells. Resveratrol, a natural polyphenol, has chemopreventive and chemotherapeutic properties, while curcumin, a compound found in turmeric, has been shown to inhibit the activation of AhR and reduce toxicity induced by carcinogens. β-block