Related Experiment Videos
Keratin expression in chemically induced mouse lung adenomas.
W T Gunning1, P J Goldblatt, G D Stoner
1Department of Pathology, Medical College of Ohio, Toledo 43699-0008.
The American Journal of Pathology
|January 1, 1992
Summary
Chemically induced lung tumors in A/J mice were analyzed for cytokeratin expression. Papillary tumors showed high-molecular-weight cytokeratins, suggesting derivation from bronchiolar Clara cells.
Area of Science:
- Oncology
- Cell Biology
- Toxicology
Background:
- Chemically induced lung tumors in A/J mice display distinct morphological patterns, including alveolar, solid, and papillary types.
- Understanding the cellular origin of these tumors is crucial for deciphering carcinogenesis mechanisms.
Purpose of the Study:
- To investigate the expression of low- and high-molecular-weight cytokeratins in chemically induced lung tumors in A/J mice.
- To determine the cellular origin of papillary lung tumors by analyzing cytokeratin profiles.
Main Methods:
- Induction of lung tumors in A/J mice using benzo(a)pyrene (BP) or N-nitrosoethylurea (ENU).
- Immunohistochemical examination of tumor tissues for the expression of low- and high-molecular-weight cytokeratins.
Main Results:
- Low-molecular-weight cytokeratins were present in all epithelial cells of normal lung and all tumor types.
- High-molecular-weight cytokeratins were exclusively found in normal bronchiolar cells and papillary tumor cells.
- Alveolar/solid tumors did not express high-molecular-weight cytokeratins.
Conclusions:
- The expression pattern of cytokeratins supports the hypothesis that chemically induced papillary lung tumors in A/J mice originate from bronchiolar Clara cells.
- Cytokeratin analysis serves as a valuable tool for tracing the cellular lineage of chemically induced lung tumors.