Prostate cancer is the most common non-skin cancer among men in most western populations and the second leading cause of cancer death among U.S. men. Despite its high morbidity, the etiology remains largely unknown. Established risk factors include age, race, and family history. Many potential risk factors, such as hormones, diet, obesity, and inflammation, have been implicated, but their roles are unclear. Genetic factors may account for up to 42% of prostate cancer risk, with various genetic pathways, including androgen biosynthesis, carcinogen metabolism, DNA repair, and chronic inflammation, being explored. However, results are inconclusive. The pathogenesis likely involves interactions between environmental and genetic factors. Large, interdisciplinary studies are needed to unravel these complex relationships. New molecular tools are enabling large-scale studies to investigate gene-gene and gene-environment interactions. These studies may lead to better detection, treatment, and prevention of prostate cancer. Prostate cancer incidence varies widely globally, with African-Americans having the highest rates. Incidence rates are lower in Asian countries but have increased more rapidly than in western countries. Mortality rates also vary, with higher rates in Western nations and Caribbean countries. Factors associated with westernization, such as diet and obesity, may contribute to prostate cancer risk. Prostate cancer disproportionately affects African-Americans and Caribbean men, suggesting a role for African ancestry. Risk factors include age, race, and family history. Hormonal factors, such as androgens and vitamin D, and lifestyle factors like diet, obesity, and physical activity, are also implicated. Chronic inflammation and sexually transmitted diseases may also play a role. Obesity is linked to aggressive tumors and increased risk. Physical activity may reduce prostate cancer risk. Occupation and exposure to certain chemicals may also increase risk. Chronic inflammation is associated with prostate cancer, and anti-inflammatory agents like aspirin may reduce risk. Sexual frequency and vasectomy have mixed associations. Benign prostatic hyperplasia may share risk profiles with prostate cancer but is not a direct precursor. Genetic factors, including family history and common low-penetrance markers, are being studied, but results are inconclusive. Future studies need to clarify the role of these factors and investigate prostate cancer etiology through large, interdisciplinary studies.Prostate cancer is the most common non-skin cancer among men in most western populations and the second leading cause of cancer death among U.S. men. Despite its high morbidity, the etiology remains largely unknown. Established risk factors include age, race, and family history. Many potential risk factors, such as hormones, diet, obesity, and inflammation, have been implicated, but their roles are unclear. Genetic factors may account for up to 42% of prostate cancer risk, with various genetic pathways, including androgen biosynthesis, carcinogen metabolism, DNA repair, and chronic inflammation, being explored. However, results are inconclusive. The pathogenesis likely involves interactions between environmental and genetic factors. Large, interdisciplinary studies are needed to unravel these complex relationships. New molecular tools are enabling large-scale studies to investigate gene-gene and gene-environment interactions. These studies may lead to better detection, treatment, and prevention of prostate cancer. Prostate cancer incidence varies widely globally, with African-Americans having the highest rates. Incidence rates are lower in Asian countries but have increased more rapidly than in western countries. Mortality rates also vary, with higher rates in Western nations and Caribbean countries. Factors associated with westernization, such as diet and obesity, may contribute to prostate cancer risk. Prostate cancer disproportionately affects African-Americans and Caribbean men, suggesting a role for African ancestry. Risk factors include age, race, and family history. Hormonal factors, such as androgens and vitamin D, and lifestyle factors like diet, obesity, and physical activity, are also implicated. Chronic inflammation and sexually transmitted diseases may also play a role. Obesity is linked to aggressive tumors and increased risk. Physical activity may reduce prostate cancer risk. Occupation and exposure to certain chemicals may also increase risk. Chronic inflammation is associated with prostate cancer, and anti-inflammatory agents like aspirin may reduce risk. Sexual frequency and vasectomy have mixed associations. Benign prostatic hyperplasia may share risk profiles with prostate cancer but is not a direct precursor. Genetic factors, including family history and common low-penetrance markers, are being studied, but results are inconclusive. Future studies need to clarify the role of these factors and investigate prostate cancer etiology through large, interdisciplinary studies.