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DRUG and LIGHT DOSE DEPENDENCE OF PHOTODYNAMIC THERAPY: A STUDY OF TUMOR and NORMAL TISSUE RESPONSE
Author(s) -
Fingar Victor H.,
Henderson Barbara W.
Publication year - 1987
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/j.1751-1097.1987.tb04856.x
Subject(s) - drug , photosensitivity , reciprocity (cultural anthropology) , medicine , drug response , photodynamic therapy , cancer research , pathology , chemistry , pharmacology , optics , organic chemistry , psychology , social psychology , physics
It is clinically relevant to determine drug and light dose combinations where complete tumor response is accompanied by little or no photosensitivity, and minimal damage to normal tissues. Although reciprocity of RIF tumor cell clonogenicity has been established within a range of drug and light doses, no quantitative data exist for reciprocity of tumor response. This study has examined reciprocity of drug and light doses for tumor response and normal tissue damage in two experimental mouse models. Representative tumors were examined for vascular damage after treatment. Reciprocity of drug and light doses for tumor response was observed over a range of drug/light combinations in both tumor models. Reciprocity failed when drug dose was reduced below a threshold value. For reciprocal drug/light combinations, complete vascular stasis occurred in the tumor and surrounding skin which was followed by necrosis of those tissues. In non‐reciprocal PDT combinations, there was vascular damage to the tumor but no damage to the surrounding normal tissues. Tumors responded initially, but no cure was obtained. Tumor cure was only observed under conditions where a considerable margin of normal tissue surrounding the tumor was damaged. This conclusion was supported by shielding experiments done to assess the contribution of normal tissue damage to tumor response. Reciprocity of drug and light doses for tumor response was therefore shown to exist only at high drug doses, which were not low enough to reduce skin photosensitivity in our models.

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