Insulin resistance (IR) is a condition where cells fail to respond adequately to insulin, leading to increased blood glucose levels and hyperinsulinemia. This condition is associated with metabolic impairments, particularly in obesity and type 2 diabetes mellitus (T2DM). Hyperinsulinemia, a consequence of IR, is a significant factor in the development, progression, and metastasis of several cancers. Both obesity and T2DM independently and additively increase cancer risk, with metabolic disorders in cancer patients leading to poor treatment outcomes, including higher recurrence rates and reduced survival. The mechanisms linking IR to cancer involve the dysregulation of insulin and insulin-like growth factors (IGFs), which play crucial roles in cell growth, proliferation, and survival. Insulin and IGFs bind to their respective receptors, activating signaling pathways such as PI3K-AKT-mTOR and RAS-MAPK, which are involved in cellular processes essential for cancer development. Genetic and environmental factors contribute to IR, including mutations in insulin and IGF genes, obesity, aging, and certain drugs. Obesity, characterized by excess body weight, is a major risk factor for cancer, particularly for cancers of the breast, colorectal, liver, pancreatic, endometrial, lung, hepatocellular, and prostate. Hyperinsulinemia and elevated levels of IGF-1 are common in obese individuals, and these factors are associated with increased cancer risk and poor outcomes. Studies have shown that obesity increases the risk of cancer mortality, with a 40\%-80\% higher risk for obese individuals compared to non-obese individuals. In conclusion, IR and its associated metabolic disorders are significant risk factors for cancer, influencing both the initiation and progression of various cancers. Understanding these mechanisms can help develop strategies to prevent and manage cancer in patients with metabolic disorders.Insulin resistance (IR) is a condition where cells fail to respond adequately to insulin, leading to increased blood glucose levels and hyperinsulinemia. This condition is associated with metabolic impairments, particularly in obesity and type 2 diabetes mellitus (T2DM). Hyperinsulinemia, a consequence of IR, is a significant factor in the development, progression, and metastasis of several cancers. Both obesity and T2DM independently and additively increase cancer risk, with metabolic disorders in cancer patients leading to poor treatment outcomes, including higher recurrence rates and reduced survival. The mechanisms linking IR to cancer involve the dysregulation of insulin and insulin-like growth factors (IGFs), which play crucial roles in cell growth, proliferation, and survival. Insulin and IGFs bind to their respective receptors, activating signaling pathways such as PI3K-AKT-mTOR and RAS-MAPK, which are involved in cellular processes essential for cancer development. Genetic and environmental factors contribute to IR, including mutations in insulin and IGF genes, obesity, aging, and certain drugs. Obesity, characterized by excess body weight, is a major risk factor for cancer, particularly for cancers of the breast, colorectal, liver, pancreatic, endometrial, lung, hepatocellular, and prostate. Hyperinsulinemia and elevated levels of IGF-1 are common in obese individuals, and these factors are associated with increased cancer risk and poor outcomes. Studies have shown that obesity increases the risk of cancer mortality, with a 40\%-80\% higher risk for obese individuals compared to non-obese individuals. In conclusion, IR and its associated metabolic disorders are significant risk factors for cancer, influencing both the initiation and progression of various cancers. Understanding these mechanisms can help develop strategies to prevent and manage cancer in patients with metabolic disorders.