On July 3, 2012, Mangericha, Aswin; Knutson, Charles G.; Parry, Nicola M.; Muthupalani, Sureshkumar; Ye, Wenjie; Prestwich, Erin; Cui, Liang; McFaline, Jose L.; Mobley, Melissa; Ge, Zhongming; Taghizadeh, Koli; Wishnok, John S.; Wogan, Gerald N.; Fox, James G.; Tannenbaum, Steven R.; Dedon, Peter C. published an article.SDS of cas: 55662-66-3 The title of the article was Infection-induced colitis in mice causes dynamic and tissue-specific changes in stress response and DNA damage leading to colon cancer. And the article contained the following:
Helicobacter hepaticus-infected Rag2-/- mice emulate many aspects of human inflammatory bowel disease, including the development of colitis and colon cancer. To elucidate mechanisms of inflammation-induced carcinogenesis, we undertook a comprehensive anal. of histopathol., mol. damage, and gene expression changes during disease progression in these mice. Infected mice developed severe colitis and hepatitis by 10 wk post-infection, progressing into colon carcinoma by 20 wk post-infection, with pronounced pathol. in the cecum and proximal colon marked by infiltration of neutrophils and macrophages. Transcriptional profiling revealed decreased expression of DNA repair and oxidative stress response genes in colon, but not in liver. Mass spectrometric anal. revealed higher levels of DNA and RNA damage products in liver compared to colon and infection-induced increases in 5-chlorocytosine in DNA and RNA and hypoxanthine in DNA. Paradoxically, infection was associated with decreased levels of DNA etheno adducts. Levels of nucleic acid damage from the same chem. class were strongly correlated in both liver and colon. The results support a model of inflammation-mediated carcinogenesis involving infiltration of phagocytes and generation of reactive species that cause local mol. damage leading to cell dysfunction, mutation, and cell death. There are strong correlations among histopathol., phagocyte infiltration, and damage chem. that suggest a major role for neutrophils in inflammation-associated cancer progression. Further, paradoxical changes in nucleic acid damage were observed in tissue- and chem.-specific patterns. The results also reveal features of cell stress response that point to microbial pathophysiol. and mechanisms of cell senescence as important mechanistic links to cancer. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).SDS of cas: 55662-66-3
The Article related to gene expression helicobacter infection stress dna damage colon carcinoma, Mammalian Pathological Biochemistry: Oncology and other aspects.SDS of cas: 55662-66-3
Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem