Biochemical mechanisms involved in the endotoxin-induced type II cell hyperplasia in F344 rat lung

Technical Report · Tue Nov 01 04:00:00 EST 1994

OSTI ID:54825

Tesfaigzi, J; Johnson, N F; Lechner, J F

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
• Country of Publication: United States
• Language: English

Related Subjects

55 BIOLOGY AND MEDICINE
BASIC STUDIES
56 BIOLOGY AND MEDICINE
APPLIED STUDIES
BIOLOGICAL MODELS
CARCINOMAS
CELL PROLIFERATION
GENE REGULATION
INHALATION
PLUTONIUM 239
PROGRESS REPORT
RATS
RESPIRATORY TRACT CELLS