Iron is essential for cell proliferation and growth but can also generate reactive oxygen species (ROS) and contribute to cancer initiation and progression. Recent studies show that iron plays a role in the tumor microenvironment and metastasis. Iron metabolism is reprogrammed in cancer, with pathways of acquisition, efflux, storage, and regulation altered. Signaling through hypoxia-inducible factor (HIF) and WNT pathways may affect iron metabolism in cancer. Targeting iron metabolic pathways could provide new tools for cancer prognosis and therapy. Iron is crucial for many enzymatic functions but can also cause oxidative damage. Both beneficial and harmful effects of iron are linked to cancer. Iron may accelerate tumor initiation by increasing free radical formation and act as a nutrient for tumor cell proliferation. Studies show that excess iron and altered iron metabolism are linked to cancer, with evidence ranging from epidemiological to molecular. New proteins involved in iron metabolism have helped clarify how tumor cells reprogram iron metabolism. Proteins involved in iron metabolism may have multifunctional roles in malignancy. Recent studies provide insights into cellular and systemic iron metabolism, explaining the relationship between iron and cancer, and may offer new tools for cancer therapy and prognosis. Population-based studies suggest that increased body iron levels are associated with increased cancer risk. Dietary iron intake and genetic factors may influence cancer risk. Genetically induced iron overload is linked to cancer, with hereditary hemochromatosis increasing cancer risk. Clinically driven reduction in body iron stores reduces cancer risk. Intracellular iron regulation is modified in cancer. Iron uptake and efflux are altered in cancer, with TFR1 and STEAP family members over-expressed. Lipocalin 2 (LCN2) is involved in alternative iron uptake pathways and is associated with cancer progression. Ferritin stores iron safely but its regulation is altered in cancer, with implications for tumor survival and prognosis. Iron efflux is regulated by ferroportin and hepcidin. Ferroportin is down-regulated in breast cancer, affecting iron availability. Iron-regulatory proteins like IRP1 and IRP2 control iron homeostasis, with IRP2 promoting tumor growth. Iron-regulatory proteins are linked to cancer prognosis and therapy. Iron affects the tumor microenvironment, with macrophages contributing to tumor growth by providing iron. Tumor-associated macrophages exhibit iron efflux characteristics. Iron also influences WNT signaling, which is crucial for cancer progression. Iron chelators may target WNT signaling and offer new therapeutic strategies. Iron regulates DNA metabolism and the cell cycle, with iron-dependent enzymes involved in DNA synthesis and repair. Iron affects WNT signaling, which is important in cancer. Iron chelators may inhibit WNT signaling and offer new therapeutic approaches. Iron is a target for cancer therapy and prevention, with iron chelators showing potential in reducing tumor growth and metastasis. Iron chelators may also induce NDRG1, a metastasis suppressIron is essential for cell proliferation and growth but can also generate reactive oxygen species (ROS) and contribute to cancer initiation and progression. Recent studies show that iron plays a role in the tumor microenvironment and metastasis. Iron metabolism is reprogrammed in cancer, with pathways of acquisition, efflux, storage, and regulation altered. Signaling through hypoxia-inducible factor (HIF) and WNT pathways may affect iron metabolism in cancer. Targeting iron metabolic pathways could provide new tools for cancer prognosis and therapy. Iron is crucial for many enzymatic functions but can also cause oxidative damage. Both beneficial and harmful effects of iron are linked to cancer. Iron may accelerate tumor initiation by increasing free radical formation and act as a nutrient for tumor cell proliferation. Studies show that excess iron and altered iron metabolism are linked to cancer, with evidence ranging from epidemiological to molecular. New proteins involved in iron metabolism have helped clarify how tumor cells reprogram iron metabolism. Proteins involved in iron metabolism may have multifunctional roles in malignancy. Recent studies provide insights into cellular and systemic iron metabolism, explaining the relationship between iron and cancer, and may offer new tools for cancer therapy and prognosis. Population-based studies suggest that increased body iron levels are associated with increased cancer risk. Dietary iron intake and genetic factors may influence cancer risk. Genetically induced iron overload is linked to cancer, with hereditary hemochromatosis increasing cancer risk. Clinically driven reduction in body iron stores reduces cancer risk. Intracellular iron regulation is modified in cancer. Iron uptake and efflux are altered in cancer, with TFR1 and STEAP family members over-expressed. Lipocalin 2 (LCN2) is involved in alternative iron uptake pathways and is associated with cancer progression. Ferritin stores iron safely but its regulation is altered in cancer, with implications for tumor survival and prognosis. Iron efflux is regulated by ferroportin and hepcidin. Ferroportin is down-regulated in breast cancer, affecting iron availability. Iron-regulatory proteins like IRP1 and IRP2 control iron homeostasis, with IRP2 promoting tumor growth. Iron-regulatory proteins are linked to cancer prognosis and therapy. Iron affects the tumor microenvironment, with macrophages contributing to tumor growth by providing iron. Tumor-associated macrophages exhibit iron efflux characteristics. Iron also influences WNT signaling, which is crucial for cancer progression. Iron chelators may target WNT signaling and offer new therapeutic strategies. Iron regulates DNA metabolism and the cell cycle, with iron-dependent enzymes involved in DNA synthesis and repair. Iron affects WNT signaling, which is important in cancer. Iron chelators may inhibit WNT signaling and offer new therapeutic approaches. Iron is a target for cancer therapy and prevention, with iron chelators showing potential in reducing tumor growth and metastasis. Iron chelators may also induce NDRG1, a metastasis suppress