Meira, Lisiane B. et al. published their research in Journal of Clinical Investigation in 2008 |CAS: 55662-66-3

The Article related to dextran sulfate sodium colon inflammation carcinogenesis dna damage, alkyladenine dna glycosylase colon inflammation carcinogenesis dna damage, reactive oxygen species colon inflammation carcinogenesis dna damage, nitrogen reactive species colon inflammation carcinogenesis dna damage and other aspects.Application of 55662-66-3

On July 31, 2008, Meira, Lisiane B.; Bugni, James M.; Green, Stephanie L.; Lee, Chung-Wei; Pang, Bo; Borenshtein, Diana; Rickman, Barry H.; Rogers, Arlin B.; Moroski-Erkul, Catherine A.; McFaline, Jose L.; Schauer, David B.; Dedon, Peter C.; Fox, James G.; Samson, Leona D. published an article.Application of 55662-66-3 The title of the article was DNA damage induced by chronic inflammation contributes to colon carcinogenesis in mice. And the article contained the following:

Chronic inflammation increases cancer risk. While it is clear that cell signaling elicited by inflammatory cytokines promotes tumor development, the impact of DNA damage production resulting from inflammation-associated reactive oxygen and nitrogen species (RONS) on tumor development was not directly tested. RONS induce DNA damage that can be recognized by alkyladenine DNA glycosylase (Aag) to initiate base excision repair. Using a mouse model of episodic inflammatory bowel disease by repeated administration of dextran sulfate Na in the drinking water, we show that Aag-mediated DNA repair prevents colonic epithelial damage and reduces the severity of dextran sulfate sodium-induced colon tumorigenesis. Importantly, DNA base lesions expected to be induced by RONS and recognized by Aag accumulated to higher levels in Aag-deficient animals following stimulation of colonic inflammation. Finally, as a test of the generality of this effect we show that Aag-deficient animals display more severe gastric lesions that are precursors of gastric cancer after chronic infection with Helicobacter pylori. These data demonstrate that the repair of DNA lesions formed by RONS during chronic inflammation is important for protection against colon carcinogenesis. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Application of 55662-66-3

The Article related to dextran sulfate sodium colon inflammation carcinogenesis dna damage, alkyladenine dna glycosylase colon inflammation carcinogenesis dna damage, reactive oxygen species colon inflammation carcinogenesis dna damage, nitrogen reactive species colon inflammation carcinogenesis dna damage and other aspects.Application of 55662-66-3

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem