Article ID: jslsm-41_0018
The main tumor killing mechanism of photodynamic therapy (PDT) is apoptosis and necrosis of tumor cells after generation of singlet oxygen species and this effect is mainly dependent on the depth of laser irradiation penetration. PDT using talaporfin sodium as a photosensitizer has already been applied clinically for high-grade glioma treatment and improvement of its further therapeutic effect is highly desired. Recently, basic research and preclinical evaluation of PDT to improve its effect while minimizing surrounding normal tissue damage has been performed, since simply raising laser power to improve PDT effect is not realistic in view of damage to surrounding normal tissue.
The main countermeasure might be the increase in accumulation of already known photosensitizers in tumor tissue. However, the search for mechanisms of tumor-specific accumulation of the photosensitizers and their interactions with key molecules of tumor cells is still underway. Using next generation photosensitizers and combination with immunotherapy, as well as increasing the tumor accumulation of existing photosensitizers, are important issues regarding basic research on and preclinical evaluation of PDT, and application of such new findings will result in the increase of the clinical role of PDT.
