Abstract
Photodynamic therapy (PDT) not only causes direct cytotoxicity to malignant cells within a tumor but also appears to have both direct and indirect effects on nonmalignant components of the tumor microenvironment. A host of preclinical studies have been performed to document how PDT modulates the tumor microenvironment. This article explores the role of cellular components such as the hypoxia-inducible factor 1α, vascular endothelial growth factor, cyclooxygenase-2, matrix metalloproteinases, the antiapoptotic protein survivin, and 17-AAG (an inhibitor of heat shock proteins), with the hope that combined modality regimens targeting these processes may improve PDT tumor responsiveness.
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