Photofrin photodynamic therapy can significantly deplete or preserve oxygenation in human basal cell carcinomas during treatment, depending on fluence rate.

At high fluence rates in animal models, photodynamic therapy (PDT) can photochemically deplete ambient tumor oxygen through the generation of singlet oxygen, causing acute hypoxia and limiting treatment effectiveness. We report that standard clinical treatment conditions (1 mg/kg Photofrin, light at 630 nm and 150 mW/cm2), which are highly effective for treating human basal cell carcinomas, significantly diminished tumor oxygen levels during initial light delivery in a majority of carcinomas. Oxygen depletion could be found during at least 40% of the total light dose, but tumors appeared well oxygenated toward the end of treatment. In contrast, initial light delivery at a lower fluence rate of 30 mW/cm2 increased tumor oxygenation in a majority of carcinomas. Laser treatment caused an intensity- and treatment time-dependent increase in tumor temperature. The data suggest that high fluence rate treatment, although effective, may be inefficient.

[1]  T. Dougherty.  Photodynamic therapy. , 1993, Photochemistry and photobiology.

[2]  G L Rosner,et al.  Pretreatment oxygenation profiles of human soft tissue sarcomas. , 1994, International journal of radiation oncology, biology, physics.

[3]  T. Foster,et al.  Oxygen consumption and diffusion effects in photodynamic therapy. , 1991, Radiation research.

[4]  J. Krosl,et al.  The role of host lymphoid populations in the response of mouse EMT6 tumor to photodynamic therapy. , 1996, Cancer research.

[5]  J. Vance,et al.  Intralesional interferon therapy for basal cell carcinoma. , 1990, Journal of the American Academy of Dermatology.

[6]  T J Dougherty,et al.  Energetics and efficiency of photoinactivation of murine tumor cells containing hematoporphyrin. , 1976, Cancer research.

[7]  B. Tromberg,et al.  In vivo TUMOR OXYGEN TENSION MEASUREMENTS FOR THE EVALUATION OF THE EFFICIENCY OF PHOTODYNAMIC THERAPY , 1990, Photochemistry and photobiology.

[8]  W. Potter,et al.  PHOTOBLEACHING OF PHOTOFRIN II AS A MEANS OF ELIMINATING SKIN PHOTOSENSITIVITY * , 1987, Photochemistry and photobiology.

[9]  M G Nichols,et al.  The Mechanism of Photofrin Photobleaching and Its Consequences for Photodynamic Dosimetry , 1997, Photochemistry and photobiology.

[10]  B W Henderson,et al.  Relationship of tumor hypoxia and response to photodynamic treatment in an experimental mouse tumor. , 1987, Cancer research.

[11]  T. Foster,et al.  Dosimetry in photodynamic therapy: oxygen and the critical importance of capillary density. , 1992, Radiation research.

[12]  P Vaupel,et al.  Oxygenation of human tumors: evaluation of tissue oxygen distribution in breast cancers by computerized O2 tension measurements. , 1991, Cancer research.

[13]  T. Dougherty,et al.  An Assay for the Quantitation of Photofrin in Tissues and Fluids , 1997, Photochemistry and photobiology.

[14]  J. P. Henning,et al.  A transient mathematical model of oxygen depletion during photodynamic therapy. , 1995, Radiation research.

[15]  P B Cerrito,et al.  The role of microvascular damage in photodynamic therapy: the effect of treatment on vessel constriction, permeability, and leukocyte adhesion. , 1992, Cancer Research.

[16]  B. Henderson,et al.  The Effect of Fluence Rate on Tumor and Normal Tissue Responses to Photodynamic Therapy , 1998, Photochemistry and photobiology.

[17]  B. Henderson,et al.  Reduction of tumour oxygenation during and after photodynamic therapy in vivo: effects of fluence rate. , 1998, British Journal of Cancer.

[18]  T. Mukherjee,et al.  Triplet excited states and semiquinone radicals of 1,4-disubstituted anthraquinones , 1990 .