| First Author | Gunning WT | Year | 1991 |
| Journal | Toxicol Pathol | Volume | 19 |
| Issue | 2 | Pages | 168-75 |
| PubMed ID | 1771369 | Mgi Jnum | J:101511 |
| Mgi Id | MGI:3604183 | Doi | 10.1177/019262339101900212 |
| Citation | Gunning WT, et al. (1991) Strain A/J mouse lung adenoma growth patterns vary when induced by different carcinogens. Toxicol Pathol 19(2):168-75 |
| abstractText | The histogenesis of mouse lung adenomas is currently being investigated in several laboratories. Based upon studies of a limited number of carcinogens in different mouse strains, some investigators suggest that all lung adenomas in mice are derived from alveolar type II cells, whereas others suggest a Clara cell origin for a majority of the tumors. This report differs from previous investigations in that 12 different carcinogens were evaluated for the types of lung tumor growth patterns they induced in a single mouse strain (strain A mice). The carcinogens aflatoxin B1 (AFB1), benzo(a)pyrene (BP), 1,2-dimethylhydrazine (DMH), 3-methylcholanthrene (MCA), 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), and N-nitrosomethylurea (MNU) induced tumors with a predominantly solid/alveolar growth pattern, whereas N-nitrosodiethylamine (NDEA) induced predominantly papillary tumors. Most of the other carcinogens induced a higher proportion of lung tumors with the solid/alveolar growth pattern than with the papillary growth pattern; however, ratios between the 2 growth patterns varied. If, as suggested by others, solid tumors are derived from alveolar type II cells and papillary tumors from Clara cells, then carcinogens may differ with respect to their ability to transform one cell type or the other. |
