We also cannot exclude the effects of rare variants of large effect on relative EBV copy number in LCLs, as these were not studied here. It is also possible that structural variants which are poorly tagged by common SNPs may play a role. To identify the genetic factors that underpin EBV copy number, a significant increase in sample size is necessary that will become possible within on-going large-scale sequencing and genotyping projects. However, we do find that even in a relatively modest sample size, EBV copy number is correlated with LCL host-gene expression patterns, in a host genotype-independent manner. Studies using larger samples of LCLs to study host gene expression profiles may find EBV-associated changes in LCLs generate false-positive results, unless EBV copy number is controlled for. Radiotherapy, alone or in combination with chemotherapy, is a standard definitive treatment approach for patients with locally advanced NSCLC or inoperable patients with early stage disease. Over half of NSCLC patients are currently treated with RT. This rate may increase in the future with the optimal RT utilization rate being estimated to be 76%. However, local failures are a major cause for the relatively poor survival reported for patients treated with RT. A recent meta-analysis suggests that local failures still occur in up to 38% of patients. Efforts to intensify RT, however, are severely limited by the need to constrain dose to the surrounding normal lung in order to preserve function. Lung toxicity caused by RT is a real and potentially debilitating toxicity, sometimes leading to patient death. In the modern era symptomatic pneumonitis still FG-4592 808118-40-3 occurs in 29.8% of patients and fatal pneumonitis in 1.9%. Currently used RT planning constraints that were designed to limit the risk of pneumonitis are based on evidence over a decade old. These constraints apply to populations and give no indication of an individual patient’s susceptibility to lethal toxicity, beyond the fact that on average higher RT doses to larger volumes are more likely to be toxic. It is therefore imperative to establish in vivo biomarkers for prediction or early assessment of pneumonitis that will ultimately assist in avoiding RT induced lung dysfunction by individualizing treatment. The pathophysiology of radiation-induced lung toxicity is incompletely understood at present. A large body of evidence from animal models, molecular biology and clinical observations suggests that normal tissue injury is a dynamic and progressive process. A complex interaction between radiation-induced damage to parenchymal cells, supporting vasculature and associated fibrotic reactions results in acute and late radiation toxicities. In the lung, these changes can manifest themselves as reduced pulmonary function and in a chronic inflammatory cascade known as pneumonitis. There are many factors that influence the likelihood of severe respiratory toxicity including the volume of irradiated parenchyma, pre-existing lung disease and the use of radiosensitizing chemotherapy. However, the exact biological mechanisms of inflammatory cascade and eventual pulmonary fibrosis are not fully elucidated.