title: The effect of celecoxib on the development of diethylnitrosamine-induced liver tumors in rats.
abstract: OBJECTIVE
  Hepatocellular carcinoma is one of the most commonly diagnosed malignant tumors in the world, and it typically has a poor prognosis. Extensive studies have examined the effects of non-steroidal anti-inflammatory drugs selective to COX-2 on the chemoprevention of various tumors. The objective of this study is to observe the effect of celecoxib on the development of liver tumors in rats.
  
  
  METHODS
  Hepatocellular carcinoma was induced in a group of 75 rats with the carcinogen diethylnitrosamine. The animals were divided into 5 groups. Three groups received various doses of celecoxib, one group received indomethacin, and a control group received no non-steroidal selective anti inflammatory drugs.
  
  
  RESULTS
  The experimental model was considered to be successful because 78% of the rats in the control group developed liver tumors. The number of neoplastic lesions was similar among the celecoxib, indomethacin and control groups, although the nodule diameter of the lesions was smaller in the celecoxib group. Better results were observed in animals that received celecoxib at doses of 6 and 9 mg/kg/ day; 4 rats in these groups did not show any neoplastic histological lesions, and a greater proportion of the nodules in the other animals in these groups were benign than in the groups that did not use celecoxib.
  
  
  CONCLUSIONS
  These results suggest that celecoxib may play a role in modifying the natural history of hepatocellular carcinoma development.
authors.affiliation: Serviço de Gastroenterologia da Irmandade Santa Casa de Misericórdia de Porto Alegre, RS, Brazil.
authors.forename: Larissa Widholzer
authors.initials: LW
authors.lastname: Galant
authors.forename: Angelo Alves
authors.initials: AA
authors.lastname: de Mattos
authors.forename: Eduardo
authors.initials: E
authors.lastname: Menti
authors.forename: Fabiana Borba
authors.initials: FB
authors.lastname: Valiatti
authors.forename: Angelo Zambam
authors.initials: AZ
authors.lastname: de Mattos
authors.forename: Marilene
authors.initials: M
authors.lastname: Porawski
authors.forename: Antônio
authors.initials: A
authors.lastname: Hartmann
authors.forename: Cláudia Ramos
authors.initials: CR
authors.lastname: Rhoden
mesh_terms: D000818:Animals; D016588:Anticarcinogenic Agents / Q000494:pharmacology*; D006528:Carcinoma, Hepatocellular / Q000139:chemically induced / Q000201:enzymology / Q000473:pathology / Q000517:prevention & control*; D000068579:Celecoxib; D002471:Cell Transformation, Neoplastic / Q000139:chemically induced / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D051546:Cyclooxygenase 2 / Q000378:metabolism; D052246:Cyclooxygenase 2 Inhibitors / Q000494:pharmacology*; D004052:Diethylnitrosamine; D007213:Indomethacin / Q000494:pharmacology; D008099:Liver / Q000187:drug effects* / Q000201:enzymology / Q000473:pathology; D008114:Liver Neoplasms, Experimental / Q000139:chemically induced / Q000201:enzymology / Q000473:pathology / Q000517:prevention & control*; D008297:Male; D011720:Pyrazoles / Q000494:pharmacology*; D051381:Rats; D013449:Sulfonamides / Q000494:pharmacology*; D013997:Time Factors
chemical_list: D016588:Anticarcinogenic Agents; D052246:Cyclooxygenase 2 Inhibitors; D011720:Pyrazoles; D013449:Sulfonamides; D004052:Diethylnitrosamine; D051546:Cyclooxygenase 2; C489691:Ptgs2 protein, rat; D000068579:Celecoxib; D007213:Indomethacin