Abstract
Abstract5‐Aminolevulinic acid‐based photodynamic therapy (ALA‐PDT) comprises photochemical and biological reactions, finally generating tumor destruction. Tumor selectivity of ALA‐PDT relies on the disturbed heme synthesis pathway in neoplastic cells. Tumor pretreatment with ALA induces two reactions: the first, self‐activation of the key enzyme porphobilinogen synthase and then protoporphyrin (PpIX) synthesis at low Fe++ availability. We emphasize that the toxic mechanism of ALA‐PDT triggered by 1O2 targets intracellular organelle destruction death pathways. PpIX fluorescence of tumors, particularly in glioblastoma, is used clinically for fluorescence guidance during neurosurgery. Targeting residual and metastatic cancer stem cells is a crucial challenge of ALA‐PDT, plausibly combined with other therapeutic modalities to encounter metastatic recurrences. We overview the different aspects of ALA‐PDT mechanism and future research and prospects.
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