The mechanisms of photosensitized tumor destruction during photodynamic therapy (PDT) appear to be a complex interplay of processes involving several tissular components, such as malignant cells, microvasculature, specific blood constituents and non-vascular stroma. While vascular aberrations are of major importance when PDT is performed with Photofrin II, which is the photosensitizer most frequently used in clinical PDT, the initial pattern of tumor damage can be substantially modified by factors that alter the distribution of the photosensitizer in the neoplastic tissue. Such factors include the chemical structure of the photosensitizer, its physico-chemical properties (especially, the degree of hydrophobicity), the modality of its transport in the bloodstream, and the use of delivery systems.
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