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Review
. 2022:2451:405-480.
doi: 10.1007/978-1-0716-2099-1_20.

Strategies for Improving Photodynamic Therapy Through Pharmacological Modulation of the Immediate Early Stress Response

Daniel J de Klerk #  1   2 , Mark J de Keijzer #  1   3 , Lionel M Dias  1   4 , Jordi Heemskerk  1 , Lianne R de Haan  1   2 , Tony G Kleijn  1   2 , Leonardo P Franchi  5   6 , Michal Heger  7   8   9 ; Photodynamic Therapy Study Group
Affiliations
Review

Strategies for Improving Photodynamic Therapy Through Pharmacological Modulation of the Immediate Early Stress Response

Daniel J de Klerk et al. Methods Mol Biol. 2022.

Abstract

Photodynamic therapy (PDT) is a minimally to noninvasive treatment modality that has emerged as a promising alternative to conventional cancer treatments. PDT induces hyperoxidative stress and disrupts cellular homeostasis in photosensitized cancer cells, resulting in cell death and ultimately removal of the tumor. However, various survival pathways can be activated in sublethally afflicted cancer cells following PDT. The acute stress response is one of the known survival pathways in PDT, which is activated by reactive oxygen species and signals via ASK-1 (directly) or via TNFR (indirectly). The acute stress response can activate various other survival pathways that may entail antioxidant, pro-inflammatory, angiogenic, and proteotoxic stress responses that culminate in the cancer cell's ability to cope with redox stress and oxidative damage. This review provides an overview of the immediate early stress response in the context of PDT, mechanisms of activation by PDT, and molecular intervention strategies aimed at inhibiting survival signaling and improving PDT outcome.

Keywords: ASK-1; Cancer cell survival; Pharmacological intervention; Photosensitizer; Tumor recalcitrance; p38 and JNK, Therapy resistance.

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References

    1. Dougherty TJ, Gomer CJ, Henderson BW et al (1998) Photodynamic therapy. JNCI 90:889–905. https://doi.org/10.1093/jnci/90.12.889 - DOI - PubMed
    1. Nowis D, Makowski M, Stokłosa T et al (2005) Direct tumor damage mechanisms of photodynamic therapy. Acta Biochim Pol 52:339–352. https://doi.org/10.18388/abp.2005_3447 - DOI - PubMed
    1. Reiniers MJ, van Golen RF, van Gulik TM, Heger M (2014) Reactive oxygen and nitrogen species in steatotic hepatocytes: a molecular perspective on the pathophysiology of ischemia-reperfusion injury in the fatty liver. Antioxid Redox Signal 21:1119–1142. https://doi.org/10.1089/ars.2013.5486 - DOI - PubMed - PMC
    1. Plaetzer K, Krammer B, Berlanda J et al (2009) Photophysics and photochemistry of photodynamic therapy: fundamental aspects. Lasers Med Sci 24. https://doi.org/10.1007/s10103-008-0539-1
    1. Dolmans DEJGJ, Fukumura D, Jain RK (2003) Photodynamic therapy for cancer. Nat Rev Cancer 3:380–387. https://doi.org/10.1038/nrc1071 - DOI - PubMed

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