Due to the radiosensitivity of the lung, toxic endpoints, in the form of radiation pneumonitis and pulmonary fibrosis, are relatively frequent outcomes following radiation treatment of thoracic neoplasms. Because of the potential lethal nature of these normal tissue reactions, they not only lead to quality-of-life issues in survivors, but also are deemed dose-limiting and thereby compromise treatment. The mitigation and treatment of lung normal tissue late effects has therefore been the goal of many investigations; however, the complexity of both the organ itself and its response to injury has resulted in little success. Nonetheless, current technology allows us to propose likely targets that are either currently being researched or should be considered in future studies.
Radiation, lung, pneumonitis, pulmonary fibrosis, pulmonary, neoplasms, bronchiole, endothelium, fibroblasts, FDA, (ROS), (SOD), Mn-SOD, (L-NAME), (iNOS), DNA damage, (SP-A), (COX-2), HMG-CoA, (MCP-1), Cytokine, (TNF), IL-1, TGF-ß, RAS, ACE
University of Rochester Medical Center, Department of Radiation Oncology, 601 Elmwood Avenue, Box 647, Rochester, NY 14642, USA