|1.||Modlin, I M: 4 articles (06/2010 - 01/2000)|
|2.||Kidd, M: 4 articles (06/2010 - 01/2000)|
|3.||Wang, Timothy C: 3 articles (04/2013 - 06/2005)|
|4.||Fossmark, Reidar: 3 articles (04/2013 - 05/2004)|
|5.||Zhao, Chun-Mei: 2 articles (04/2013 - 06/2012)|
|6.||Kidd, Mark: 2 articles (04/2013 - 06/2012)|
|7.||Chen, Duan: 2 articles (04/2013 - 06/2012)|
|8.||Vigen, Reidar Alexander: 2 articles (04/2013 - 06/2012)|
|9.||Modlin, Irvin M: 2 articles (04/2013 - 06/2012)|
|10.||Waldum, Helge L: 2 articles (09/2010 - 05/2004)|
|1.||Carcinoid Tumor (Carcinoid)
04/01/2013 - "Gastric carcinoids in Mastomys were induced by loxtidine treatment. "
09/01/2010 - "The reason why only one KO mice developed gastric neoplasia whereas the histamine-2 blocker loxtidine has previously been found to regularly induce ECL cell carcinoids in mice is not known."
05/01/1998 - "Chronic hypergastrinemia, induced by the irreversible H2-receptor antagonist loxtidine will cause carcinoid formation in Mastomys already after four to six months. "
12/01/1996 - "Generation of low acid and hypergastrinemia through irreversible H2-receptor blockade (loxtidine) in the African rodent mastomys results in gastric carcinoids (ECLomas) within 4 months. "
07/05/1996 - "Loxtidine (2g/l) was administered in drinking water for 48 weeks to allow multiple ECL cell carcinoids to develop. "
12/15/2004 - "Tumor ECL cells were obtained by hand-dissection of gastric ECL cell nodules from animals treated with loxtidine for >16 wk and from a spontaneously developed ECL cell tumor. "
01/01/2000 - "ECL cell neoplasia was generated in Mastomys by endogenous hypergastrinemia induced by H(2) blockade (loxtidine 1 g/kg/day) and tumor ECL cells prepared. "
05/01/1998 - "Long-term loxtidine treatment (seven to 21 months) results in sustained hypergastrinemia and tumor formation. "
05/01/1998 - "Subsequent to cessation of loxtidine treatment for two weeks, all parameters of histamine metabolism were normalized in tumor-bearing animals. "
05/01/1996 - "Loxtidine, an H2-receptor antagonist, did not induce DNA single-strand breaks in the pyloric mucosa at a dose of 400 mg/kg body wt. The present results together with previous information suggest that DNA single-strand scission is a good marker for tumor-initiating activity in rat stomach mucosa."
08/01/1985 - "These results support the hypothesis that the late formation of gastric carcinoids in rats receiving loxtidine is a consequence of persistent achlorhydria caused by unsurmountable blockade of parietal cell H2-receptors."
12/01/1985 - "There is no evidence that loxtidine acts as a direct carcinogen and it is suggested that the tumours were the result of prolonged achlorhydria produced by a potent unsurmountable histamine H2 receptor antagonist."
08/01/1985 - "The very late occurrence of gastric carcinoids in a life-span carcinogenicity study with loxtidine in the rat might have resulted from continuous achlorhydria induced by this long-acting unsurmountable histamine H2-antagonist. "
01/01/1988 - "The increase in carcinoid tumour incidence observed in rats and mice after loxtidine treatment was probably related to the prolonged achlorhydria produced by this potent unsurmountable histamine H2-receptor antagonist."
12/15/2004 - "Gastric mucosa (mucosal scrapping) and ECL cell-enriched fractions were obtained from untreated Mastomys (controls) and from animals treated with loxtidine for 8 wk (hyperplasia). "
01/01/2000 - "Hypergastrinemia and mucosal hyperplasia were induced by irreversible H(2) receptor blockade with loxtidine. "
01/01/1998 - "Hypergastrinemia was generated by the irreversible histamine-2 receptor antagonist loxtidine for 8 weeks (hyperplasia) and 16 weeks (neoplasia). "
09/26/1997 - "In the African rodent (mastomys) hypergastrinemia generated by the histamine-2 receptor antagonist (loxtidine) results in ECL cell hyperplasia and neoplasia at 8 and 16 weeks respectively. "
12/15/2004 - "Enterochromaffin-like (ECL) cell hyperplasia and then irreversible neoplasia can be generated in the African rodent Mastomys natalensis using the H2 receptor blocker, loxtidine, for 8-16 wk. We used a GeneChip approach complemented by standard technologies to identify gene expression alterations in the gastric mucosa during gastrin-mediated ECL cell transformation. "
|1.||Histamine (Histamine Dihydrochloride)
|3.||Adenosine Triphosphatases (ATPase)
|8.||Cholecystokinin B Receptor
|9.||Messenger RNA (mRNA)