Responses of tumor tissues to photodynamic therapy

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.

[1]  K. Berg,et al.  THE PHOTODEGRADATION OF PORPHYRINS IN CELLS CAN BE USED TO ESTIMATE THE LIFETIME OF SINGLET OXYGEN , 1991, Photochemistry and photobiology.

[2]  G. Jori Far-red-absorbing photosensitizers: their use in the photodynamic therapy of tumours , 1992 .

[3]  J Moan,et al.  PHOTOCHEMOTHERAPY OF CANCER: EXPERIMENTAL RESEARCH , 1992, Photochemistry and photobiology.

[4]  C. Zhou,et al.  Mechanisms of tumor necrosis induced by photodynamic therapy. , 1989, Journal of photochemistry and photobiology. B, Biology.

[5]  T. Dougherty,et al.  HOW DOES PHOTODYNAMIC THERAPY WORK? , 1992, Photochemistry and photobiology.