TU‐E‐214‐03: Preclinical and Clinical Hypoxia Imaging: Current and Emerging Methods and Technology

The definition of tumor hypoxia is multifaceted, ranging from a simple physiological absence of molecular oxygen in tumor cells to a major factor associated with aggressive tumor phenotype; therefore, imaging of tumor hypoxia is equally poorly defined. Several compounds have been synthesized for PET hypoxia imaging studies: 18 F‐fluoromisonidazole (FMISO), Cu‐diacetyl‐bis(N4‐methylthiosemicarbazone) (Cu‐ATSM), 2‐nitroimidazoles based markers such as 2‐(2‐nitroimidazol‐1[H]‐yl)‐N‐(3‐[F‐18]fluoropropyl) acetamide (EF1) and [2‐(2‐nitroimidazol‐1‐yl)‐N‐(3,3,3‐trifluoropropyl)‐acetamide], [2‐(2‐nitro‐1[H]‐imidazol‐1‐yl)‐N‐(2,2,3,3,3‐penta‐fluoropropyl)‐acetamide] (EF5), and most recently 1‐(5‐fluoro‐5‐deoxy‐alpha‐D‐arabinofuranosyl)‐2‐nitroimidazole (FAZA). All these compounds diffuse into normally oxygenated and hypoxic cells but are retained in substantially higher concentrations in hypoxic issues. Clinically most commonly used PET hypoxia tracers are FMISO and Cu‐ATSM. In this lecture, different PET hypoxia tracers will be reviewed, focusing on differences in their uptake mechanisms, which lead to differences in their clinical appearance. In addition, the most important clinical trials utilizing PET hypoxia imaging will be reviewed. Learning objectives: 1. To learn about clinical PET imaging of hypoxia 2. To learn about differences between various PET hypoxia tracers 3. To learn about clinical trials utilizing PET hypoxia imaging