Journal
PHOTOCHEMISTRY AND PHOTOBIOLOGY
Volume 97, Issue 4, Pages 837-840Publisher
WILEY
DOI: 10.1111/php.13397
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Funding
- NIH [CA 123362, DE023181, CA 23378]
- Office of the Vice President for Research
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HPV infection can enhance the efficacy of ionizing radiation for head and neck cancer treatment, while affecting the effectiveness of photodynamic therapy by promoting different cell death pathways. The explanation for these differences in PDT efficacy needs further exploration.
A concurrent human papilloma virus (HPV) infection potentiates the efficacy of ionizing radiation for treatment of head and neck cancer by promoting apoptosis. Studies in cell culture indicated an opposite effect for photodynamic therapy (PDT) when this leads to mitochondrial and ER photodamage. The explanation for this difference in PDT efficacy remains to be established. While apoptosis was impaired in HPV(-) cells, such cells can be killed via photodamage directed at the ER: this leads to a nonapoptotic death pathway termed paraptosis. No differences in photosensitizer uptake or reactive oxygen species (ROS) production were observed in HPV(+) vs. HPV(-) tumors. We now provide evidence that death pathways initiated by ER/mitochondrial photodamage leading to either paraptosis or apoptosis are impaired in an HPV(+) head and neck cell line. These results illustrate the complex determinants of PDT efficacy, a topic that has yet to be fully explored.
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