|  Help  |  About  |  Contact Us

Publication : Lung tumors in strain A mice: application for studies in cancer chemoprevention.

First Author  Stoner GD Year  1993
Journal  J Cell Biochem Suppl Volume  17F
Pages  95-103 PubMed ID  8412213
Mgi Jnum  J:14713 Mgi Id  MGI:62876
Doi  10.1002/jcb.240531014 Citation  Stoner GD, et al. (1993) Lung tumors in strain A mice: application for studies in cancer chemoprevention. J Cell Biochem Suppl 17F:95-103
abstractText  Strain A mice develop a high incidence of spontaneous lung tumors during their lifetime. These tumors may be found in some animals as early as 3 to 4 weeks of age, increasing to nearly 100% by 24 months of age. The strain A mouse is also highly susceptible to the induction of lung tumors by several classes of chemical carcinogens and has been used extensively as a mouse lung tumor bioassay for assessing the carcinogenic activity of a variety of chemicals. In addition to its use in carcinogen detection, the strain A mouse lung tumor model has been employed extensively for the identification of inhibitors of chemical carcinogenesis. A number of chemopreventive agents including beta-naphthoflavone, butylated hydroxyanisole, ellagic acid, phenethyl isothiocyanate, phenylpropyl isothiocyanate, phenylbutyl isothiocyanate, phenylhexyl isothiocyanate, indole-3-carbinol, etc., have been shown to inhibit chemically induced lung tumors in strain A mice. In most instances, inhibition of lung tumorigenesis has been correlated with effects of the chemopreventive agent on the metabolic activation and/or detoxification of carcinogens. To date, no chemopreventive agent has been shown to inhibit lung tumorigenesis in strain A mice when administered after the carcinogen, i.e., during the promotion/progression stages of tumor development. Efforts should be made to develop a standardized protocol in strain A mice for evaluating chemopreventive agents as inhibitors of both the initiation and progression stages of lung tumor development.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

0 Bio Entities

0 Expression