Cancer Research Infection and Cancer: Biology, Therapeutics, and Prevention  Tumor Immunology: New Perspectives
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online

[Cancer Research 46, 3348-3352, July 1, 1986]
© 1986 American Association for Cancer Research

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Gomer, C. J.
Right arrow Articles by Murphree, A. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gomer, C. J.
Right arrow Articles by Murphree, A. L.

Expression of Potentially Lethal Damage in Chinese Hamster Cells Exposed to Hematoporphyrin Derivative Photodynamic Therapy1

Charles J. Gomer2, Natalie Rucker, Angela Ferrario and A. Linn Murphree

Clayton Foundation for Ocular Oncology [C. J. G., N. R., A. F., A. L. M.], Childrens Hospital of Los Angeles, and Departments of Pediatrics (Division of Hematology-Oncology) [C. J. G.], Radiation Oncology [C. J. G.], and Ophthalmology [A. L. M.], University of Southern California School of Medicine, Los Angeles, California 90027

Experiments were performed to determine whether the expression and/or repair of potentially lethal damage could be observed in mammalian cells exposed to hemataporphyrin derivative (HPD) photodynamic therapy (PDT). Photodynamic therapy was combined with posttreatment protocols known to inhibit the repair of potentially lethal damage in cells treated with X-rays, ultraviolet radiation, or alkylating agents. Potentiation of lethal damage from photodynamic therapy was induced by hypothermia (4°C) following short (1 h) or extended (16 h) HPD incubation conditions. Caffeine potentiated the lethal effects of PDT only when cells were incubated with HPD for extended time periods. However, 3-aminobenzamide had no effect on the cytotoxic actions of PDT following either short or extended HPD incubations. Recovery from potentially lethal damage expressed by posttreatment hypothermia was complete within 1 h, while recovery from potentially lethal damage expressed by posttreatment caffeine required time periods of up to 24 h. The lack of effect of 3-aminobenzamide on expression of potentially lethal damage following photodynamic therapy may be related to direct inhibition of adenosine diphosphoribose transferase by photodynamic therapy. These results indicate that the expression and repair of potentially lethal damage can be observed in cells treated with PDT and will vary as a function of porphyrin incubation conditions.

1 This investigation was performed in conjunction with the Clayton Foundation for Research and was supported in part by USPHS Grant CA 31230 awarded by the National Cancer Institute, Department of Health and Human Services.

2 To whom requests for reprints should be addressed, at Clayton Center for Ocular Oncology, Childrens Hospital of Los Angeles, 4650 Sunset Boulevard, Los Angeles, CA 90027.

Received 1/28/86. Revised 3/24/86. Accepted 3/31/86.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1986 by the American Association for Cancer Research.