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Tumor versus vascular photodamage in a rat tumor model

D Kessel1, J Hampton, V Fingar

  • 1Wayne State University, School of Medicine, Detroit, MI 48021, USA. dhkessel@med.wayne.edu

Journal of Photochemistry and Photobiology. B, Biology
|November 20, 1998
PubMed

Insights

Multidrug resistance (MDR) in rat urothelial tumors limits photosensitizer drug accumulation. This suggests that tumor regrowth delay with copper benzochlorin iminium salt is due to vascular effects, not direct cell kill.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • The [4-(5-nitro-2-furyl)-2-thiazoyl] formamide (FANFT)-induced rat urothelial tumor model is utilized.
  • This tumor model exhibits a multidrug resistance (MDR) phenotype.

Purpose of the Study:

  • To investigate the mechanism of resistance to a photosensitizer drug in FANFT-induced urothelial tumors.
  • To determine the role of MDR in the efficacy of copper benzochlorin iminium salt.

Main Methods:

  • Analysis of mdr gene expression in FANFT-induced tumors.
  • Assessment of cellular accumulation of a photosensitizer in resistant tumor cells.
  • Evaluation of tumor regrowth delay following photosensitizer treatment.

Main Results:

  • FANFT-induced urothelial tumors express the mdr gene, conferring a multidrug resistance (MDR) phenotype.
  • The MDR phenotype results in an outward transport system preventing accumulation of weakly cationic agents, including the photosensitizer.
  • FANFT tumor cells are protected from direct cell kill by the photosensitizer.

Conclusions:

  • The MDR phenotype in FANFT tumors hinders direct photosensitizer-mediated cell kill.
  • The observed delay in tumor regrowth is likely attributable to vascular effects rather than direct cytotoxicity.

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