Genomic amplification is hypothesized to occur via the breakage-fusion-bridge cycle. A Fenton reaction causes double-stranded DNA breakage. Our results revealed that these amplifications consisted of a mixture of wide-range low-level amplifications and fragmented, narrow high-level amplifications. This suggests a mechanism of positive feedback for amplification, starting from wide-range low-level amplification. We suspect an involvement of double-minutes, and a presence of susceptible genomic loci. This hypothesis requires further study. It was interesting that two tumor suppressive genes, Cav1 and ST7, Perifosine surrounded the Met locus. This may be the reason why the Met locus was a denominator for the rat RCCs. Whole exome or genome sequencing may further reveal new findings regarding point mutation and chromosomal translocation. Finally, we compared the present rat results with corresponding human tumors by transforming data based on chromosomal synteny. It was expected that the genomic alteration of Fe-NTA-induced rat RCC was most similar to human RCC presumably because target cells are the same. However, surprisingly, human mesothelioma was the second most similar. It is now established that most human mesothelioma results from exposure to asbestos, and the primary pathogenic process involved is iron overload. The same mesodermal origin of renal tubular cells and mesothelial cells may cause the similarity of the array-based CGH profiles. Endodermal tumor, such as pancreatic ductal adenocarcinoma, and ectodermal tumor, such as glioblastoma multiforme, exhibited a significant difference in genomic profiles. In conclusion, we showed that repeated Fenton reactions in wildtype rats induced cancer that recapitulated genomic alterations similar to those in human cancers, suggesting the involvement of oxidative stress as a major factor in human carcinogenesis. In this renal carcinogenesis model, preferred alterations were deletion; Cdkn2A/2B deletion and Met amplification were the major target gene modifications. A comparative interspecies analysis would contribute to identifying candidate carcinogenic agents. Patients with chronic kidney disease suffer from complex hemostasis disorders. Both a bleeding tendency and an increased risk of accelerated atherosclerosis, with a high incidence of cardiovascular death, have been described to coexist. Moreover, these patients are known to be exposed to a chronic proinflammatory state and oxidative stress, leading to endothelial cell dysfunction. In hemodialyzed patients, humoral factors such as uremic toxics accumulated in plasma and cytokines released by cellular activation are involved in the development of these pathological processes. The vascular endothelium has been recognized as a complex endocrine organ that regulates many physiological functions such as vascular tone, vascular smooth muscle cell growth and migration, vascular permeability to solutes and blood cells, and regulation of hemostasis, among others. The endothelium is able to adapt to pathophysiological challenges. However, depending on the nature and intensity of the stimuli, the endothelium may become dysfunctional. In this regard, there is clinical and experimental evidence of endothelial activation and damage in uremia. In patients with CKD, the progression of atherothrombosis is accelerated, causing early cardiovascular complications. In this regard, mortality from cardiovascular disease is nearly tenfold higher in patients with end-stage renal disease on dialysis than in the general population.