Biochemical mechanisms involved in the endotoxin-induced type II cell hyperplasia in F344 rat lung
Proliferative lesions and pulmonary epithelial neoplasms induced in the rat by plutonium inhalation have been shown to be of type II cell origin. Defining the gene changes responsible for the development of the type II proliferative lesions would help to elucidate the genetic events involved in the expansion of initiated type II cells into fully transformed tumor cells. One problem in identifying these gene alterations is dissociating changes in gene expression linked to cell replication or repair from those involved in tumor initiation and progression. The long-term goals of these investigations are to first develop and characterize a model of transient type II cell hyperplasia. Second, changes in gene expression associated with remodeling epithelium will be compared to gene changes exhibited by the {sup 239}Pu-induced hyperplastic lesions.
- Research Organization:
- Lovelace Biomedical and Environmental Research Inst., Albuquerque, NM (United States). Inhalation Toxicology Research Inst.
- DOE Contract Number:
- AC04-76EV01013
- OSTI ID:
- 54825
- Report Number(s):
- ITRI-144; ON: DE95007526; TRN: 95:012766
- Resource Relation:
- Other Information: PBD: Nov 1994; Related Information: Is Part Of Inhalation Toxicology Research Institute annual report, October 1, 1993--September 30, 1994; Belinsky, S.A.; Hoover, M.D.; Bradley, P.L. [eds.]; PB: 211 p.
- Country of Publication:
- United States
- Language:
- English
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