Exposure to ionizing radiation is a well-established risk factor for cancer, but the biological mechanisms underlying this relationship remain incompletely understood. While the prevailing model emphasizes direct DNA damage and resulting genetic mutations as a central driver of radiation-induced cancer, important uncertainties remain about how fully this explanation accounts for observed disease patterns.

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Emerging research suggests that multiple complementary pathways may also contribute, including effects on immune surveillance, inflammation, cellular energetics (such as mitochondrial damage), the microbiome, epigenetic changes, viral activation, and alterations in the tissue microenvironment. These mechanisms may act alone or in combination and may vary by individual, radiation type, dose, and cancer subtype. This conference will explore these questions from experimental, clinical, and theoretical perspectives to improve understanding of radiation-related carcinogenesis and identify key directions for future research.