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Tesfaigzi, J.; Johnson, N.F.; Lechner, J.F.
Inhalation Toxicology Research Institute annual report, October 1, 1993--September 30, 19941994
Inhalation Toxicology Research Institute annual report, October 1, 1993--September 30, 19941994
AbstractAbstract
[en] 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 239Pu-induced hyperplastic lesions
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Belinsky, S.A.; Hoover, M.D.; Bradley, P.L. (eds.); Lovelace Biomedical and Environmental Research Inst., Albuquerque, NM (United States). Inhalation Toxicology Research Inst; 211 p; Nov 1994; p. 134-136; Also available from OSTI as DE95007526; NTIS; US Govt. Printing Office Dep
Record Type
Report
Literature Type
Progress Report
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Country of publication
ACTINIDE NUCLEI, ALPHA DECAY RADIOISOTOPES, ANIMAL CELLS, ANIMALS, DISEASES, DOCUMENT TYPES, EVEN-ODD NUCLEI, HEAVY NUCLEI, INTAKE, ISOTOPES, MAMMALS, NEOPLASMS, NUCLEI, PLUTONIUM ISOTOPES, RADIOISOTOPES, RODENTS, SOMATIC CELLS, SPONTANEOUS FISSION RADIOISOTOPES, VERTEBRATES, YEARS LIVING RADIOISOTOPES
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