This review explores the impact of bio-behavioural factors on cancer biology, focusing on the mechanisms linking psychological and social influences to tumour development, progression, and immune responses. Stress, chronic depression, and lack of social support are identified as potential risk factors for cancer. Biological pathways, such as the hypothalamic-pituitary-adrenal (HPA) axis and autonomic nervous system (ANS), mediate these effects through stress responses that influence hormone secretion, immune function, and cellular processes. Stress activates the HPA axis, leading to the release of corticotrophin-releasing factor and arginine vasopressin, which in turn stimulate the release of hormones like ACTH and glucocorticoids. These hormones regulate growth, metabolism, and immune function, and prolonged exposure can lead to adverse health effects, including increased cancer risk. Stress also activates the sympathetic nervous system, increasing catecholamine levels, which can promote tumour growth and metastasis. Stress-related changes in the HPA and ANS axes are associated with increased cancer risk, as seen in studies linking chronic stress, depression, and social isolation to higher cancer incidence. Animal studies show that stress can enhance tumour growth and metastasis, often through mechanisms involving immune suppression, increased angiogenesis, and altered viral oncogenesis. For example, stress increases the expression of vascular endothelial growth factor (VEGF), which promotes angiogenesis and tumour growth. Glucocorticoids, such as cortisol, can interact with catecholamines to promote cancer growth. Stress also affects other hormones, including prolactin, oxytocin, and dopamine, which can influence tumour biology. Circadian rhythm disruptions, often caused by stress or shift work, are linked to increased cancer risk, as they can alter hormone secretion and immune function. Stress also influences viral oncogenesis, with studies showing that stress can reactivate latent viruses like Epstein-Barr virus (EBV) and human papillomavirus (HPV), which are associated with various cancers. Stress can also suppress immune function, reducing the body's ability to fight cancer. Conversely, positive psychosocial factors like social support and optimism are associated with better cancer outcomes. Pharmacological interventions, such as β-blockers, may help mitigate stress-related cancer risks by reducing the effects of stress hormones. Psycho-social interventions, including stress management techniques, can improve immune function and reduce cancer risk. However, the clinical relevance of these interventions remains to be fully established. In conclusion, bio-behavioural factors significantly influence cancer biology through complex interactions involving the neuroendocrine system, immune function, and cellular processes. Understanding these mechanisms is crucial for developing effective interventions to improve cancer outcomes.This review explores the impact of bio-behavioural factors on cancer biology, focusing on the mechanisms linking psychological and social influences to tumour development, progression, and immune responses. Stress, chronic depression, and lack of social support are identified as potential risk factors for cancer. Biological pathways, such as the hypothalamic-pituitary-adrenal (HPA) axis and autonomic nervous system (ANS), mediate these effects through stress responses that influence hormone secretion, immune function, and cellular processes. Stress activates the HPA axis, leading to the release of corticotrophin-releasing factor and arginine vasopressin, which in turn stimulate the release of hormones like ACTH and glucocorticoids. These hormones regulate growth, metabolism, and immune function, and prolonged exposure can lead to adverse health effects, including increased cancer risk. Stress also activates the sympathetic nervous system, increasing catecholamine levels, which can promote tumour growth and metastasis. Stress-related changes in the HPA and ANS axes are associated with increased cancer risk, as seen in studies linking chronic stress, depression, and social isolation to higher cancer incidence. Animal studies show that stress can enhance tumour growth and metastasis, often through mechanisms involving immune suppression, increased angiogenesis, and altered viral oncogenesis. For example, stress increases the expression of vascular endothelial growth factor (VEGF), which promotes angiogenesis and tumour growth. Glucocorticoids, such as cortisol, can interact with catecholamines to promote cancer growth. Stress also affects other hormones, including prolactin, oxytocin, and dopamine, which can influence tumour biology. Circadian rhythm disruptions, often caused by stress or shift work, are linked to increased cancer risk, as they can alter hormone secretion and immune function. Stress also influences viral oncogenesis, with studies showing that stress can reactivate latent viruses like Epstein-Barr virus (EBV) and human papillomavirus (HPV), which are associated with various cancers. Stress can also suppress immune function, reducing the body's ability to fight cancer. Conversely, positive psychosocial factors like social support and optimism are associated with better cancer outcomes. Pharmacological interventions, such as β-blockers, may help mitigate stress-related cancer risks by reducing the effects of stress hormones. Psycho-social interventions, including stress management techniques, can improve immune function and reduce cancer risk. However, the clinical relevance of these interventions remains to be fully established. In conclusion, bio-behavioural factors significantly influence cancer biology through complex interactions involving the neuroendocrine system, immune function, and cellular processes. Understanding these mechanisms is crucial for developing effective interventions to improve cancer outcomes.