Publications [#63238] of Mark W. Dewhirst

Papers Published

1. Vujaskovic, Z. and Anscher, M.S. and Feng, Q.-F. and Rabbani, Z.N. and Amin, K. and Samulski, T.S. and Dewhirst, M.W. and Haroon, Z.A., Radiation-induced hypoxia may perpetuate late normal tissue injury, International Journal of Radiation Oncology Biology Physics, vol. 50 no. 4 (2001), pp. 851 - 855 [S0360-3016(01)01593-0]
   (last updated on 2007/04/14)

   Abstract:
   Purpose: The purpose of this study was to determine whether or not hypoxia develops in rat lung tissue after radiation. Methods and Materials: Fisher-344 rats were irradiated to the right hemithorax using a single dose of 28 Gy. Pulmonary function was assessed by measuring the changes in respiratory rate every 2 weeks, for 6 months after irradiation. The hypoxia marker was administered 3 h before euthanasia. The tissues were harvested at 6 weeks and 6 months after irradiation and processed for immunohistochemistry. Results: A moderate hypoxia was detected in the rat lungs at 6 weeks after irradiation, before the onset of functional or histopathologic changes. The more severe hypoxia, that developed at the later time points (6 months) after irradiation, was associated with a significant increase in macrophage activity, collagen deposition, lung fibrosis, and elevation in the respiratory rate. Immunohistochemistry studies revealed an increase in TGF-β, VEGF, and CD-31 endothelial cell marker, suggesting a hypoxia-mediated activation of the profibrinogenic and proangiogenic pathways. Conclusion: A new paradigm of radiation-induced lung injury should consider postradiation hypoxia to be an important contributing factor mediating a continuous production of a number of inflammatory and fibrogenic cytokines. Copyright © 2001 Elsevier Science Inc.

   Keywords:
   Radiation;Tissue;Irradiation;Histology;Pathology;Collagen;Deposition;