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The process involves administration of a **photosensitizer**, which accumulates in the target tissue (most often a tumor or local vasculature)[6][2][8]. Upon illumination with light of a specific wavelength, the photosensitizer enters an excited electronic state[1][5], then transfers energy to molecular oxygen via intersystem crossing and energy transfer, generating **reactive oxygen species** (especially singlet oxygen)[1][5][7]. These ROS are potent cytotoxins, causing cell death, apoptosis, and/or damage to the vascular wall. In the vascular-targeted variant of PDT, rapid endothelial cell apoptosis and vessel occlusion leads to local infarction of the targeted region[2][4][8]. The specificity and efficacy depend on the photosensitizer used, its localization, light delivery protocol, and timing[2][6][4]. Photosensitizer examples include Photofrin, MV6401, and Tookad[2][4][8]. This method is well-established for the local treatment of solid tumors and sometimes vascular malformations, offering specific spatial and temporal control with well-characterized risks including phototoxicity, non-target tissue damage, and depth limitations.
Light activation of the photosensitizer produces an excited state that transfers energy to molecular oxygen, generating ROS (mainly singlet oxygen), resulting in localized cell damage/apoptosis and/or vascular occlusion[1][5][7][9]
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