Abstract
Photodynamic therapy (PDT) of cancer is a two-step drug-device combination modality, which involves the topical or systemic administration of a photosensitizer followed by light illumination of cancer site. In the presence of oxygen molecules, the light illumination of photosensitizer (PS) can lead to the generation of cytotoxic reactive oxygen species (ROS) and consequently destroy cancer. Similar to many other anticancer therapies, PDT is also subject to intrinsic cancer resistance mediated by multidrug resistance (MDR) mechanisms. This paper will review the recent progress in understanding the interaction between MDR transporters and PS uptake. The strategies that can be used in a clinical setting to overcome or bypass MDR will also be discussed.
Highlights
Photodynamic therapy (PDT) of cancer involves the administration of a photosensitizer (PS) followed by illumination of the cancer site with visible light
MDR is often attributed to the over-expression of certain members of ATP-binding cassette (ABC) transporter proteins including p-glycoprotein (P-gp/ABCB1/MDR1), multidrug resistance proteins (MRPs, e.g., MRP1-9), and breast cancer resistance proteins (BCRP/ABCG2/ MXR/ABCP).[10]
The mechanisms of resistance to PDT ascribed to the PS may be shared with the general mechanisms of MDR, and are related to altered PS uptake and e®lux rates or altered intracellular tra±cking within cancer cells.[26]
Summary
Photodynamic therapy (PDT) of cancer involves the administration of a photosensitizer (PS) followed by illumination of the cancer site with visible light. This process can lead to generation of reactive oxygen species (e.g., singlet oxygen) in the presence of oxygen molecules via photon-induced energy and/or electron transfer. PDT-mediated oxidation can cause local cytotoxicity leading to cancer cell death through apoptosis and/or necrosis pathways. Unlike other oxidant-based cancer therapies, in addition to the rapid direct oxidationdriven cytotoxic e®ects on cancer cells, PDTinduced damage to the tumor vasculature, acute in°ammatory reaction and systemic immunity play signicant roles in the anticancer e®ectiveness of PDT.[1]. The strategies that can be used in the clinical setting to overcome this particular type of resistance will be discussed
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