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Title: Individual variation in p53 and Cip1 expression profiles in normal human fibroblast strains following exposure to high-let radiation

Abstract

Exposure to {alpha}-particles emitted by radon progeny appears to be the second-leading cause of lung cancer mortality. However, individual susceptibility to the carcinogenic effects of {alpha}-particles remains poorly characterized. Variation in susceptibility to cancer produced by certian classes of DNA-damaging chemicals is suspected to involve differences in metabolic activation and detoxication. Susceptibility to {alpha}-particle-induced cancer may involve variations in capacity or opportunity to repair DNA damage. Subtle variations in DNA repair capacity would more likely explain radon-related lung cancer susceptibility. The p53 tumor suppressor protein accumulates as a cellular response to DNA damage from ionizing radiation and regulates arrest in the G{sub 1} portion of the cell cycle. Arrest in G{sub 1} portion of the cell cycle. While upstream regulation of p53 protein stability is poorly understood, variations in the ability to accumulate p53 following DNA damage represent potential variations in lung cancer susceptibility related to radon progeny. Further, transcription of the cell-cycle regulatory gene Cip1 is regulated by p53 and increases following ionizing radiation. Therefore, variations in the expression of Cip1 following {alpha}-particle exposure may also be a susceptibility factor in radon-related lung cancers. The purpose of the present investigation was to measure p53 and Cip1 protein induction followingmore » {alpha}-particle exposure of fibroblast lines from nine individuals to determine if there were significant variations. The expression of Cip1 protein indicates the differences in response are biologically relevant.« less

Authors:
; ;  [1]
  1. Univ. of New Mexico, Albuquerque, NM (United States); and others
Publication Date:
Research Org.:
Lovelace Biomedical and Environmental Research Inst., Albuquerque, NM (United States). Inhalation Toxicology Research Inst.
OSTI Identifier:
381382
Report Number(s):
ITRI-146
ON: DE96008986; TRN: 96:002767-0037
DOE Contract Number:  
AC04-76EV01013
Resource Type:
Technical Report
Resource Relation:
Other Information: PBD: Dec 1995; Related Information: Is Part Of Inhalation Toxicology Research Institute. Annual report, October 1, 1994--September 30, 1995; Bice, D.E.; Hahn, F.F.; Hoover, M.D.; Neft, R.E.; Thornton-Manning, J.R.; Bradley, P.L. [eds.]; PB: 214 p.
Country of Publication:
United States
Language:
English
Subject:
56 BIOLOGY AND MEDICINE, APPLIED STUDIES; BIOCHEMISTRY; VARIATIONS; FIBROBLASTS; BIOLOGICAL RADIATION EFFECTS; PROGRESS REPORT; ALPHA PARTICLES

Citation Formats

Carpenter, T. R., Johnson, N. F., and Gilliland, F. D. Individual variation in p53 and Cip1 expression profiles in normal human fibroblast strains following exposure to high-let radiation. United States: N. p., 1995. Web. doi:10.2172/381382.
Carpenter, T. R., Johnson, N. F., & Gilliland, F. D. Individual variation in p53 and Cip1 expression profiles in normal human fibroblast strains following exposure to high-let radiation. United States. https://doi.org/10.2172/381382
Carpenter, T. R., Johnson, N. F., and Gilliland, F. D. 1995. "Individual variation in p53 and Cip1 expression profiles in normal human fibroblast strains following exposure to high-let radiation". United States. https://doi.org/10.2172/381382. https://www.osti.gov/servlets/purl/381382.
@article{osti_381382,
title = {Individual variation in p53 and Cip1 expression profiles in normal human fibroblast strains following exposure to high-let radiation},
author = {Carpenter, T. R. and Johnson, N. F. and Gilliland, F. D.},
abstractNote = {Exposure to {alpha}-particles emitted by radon progeny appears to be the second-leading cause of lung cancer mortality. However, individual susceptibility to the carcinogenic effects of {alpha}-particles remains poorly characterized. Variation in susceptibility to cancer produced by certian classes of DNA-damaging chemicals is suspected to involve differences in metabolic activation and detoxication. Susceptibility to {alpha}-particle-induced cancer may involve variations in capacity or opportunity to repair DNA damage. Subtle variations in DNA repair capacity would more likely explain radon-related lung cancer susceptibility. The p53 tumor suppressor protein accumulates as a cellular response to DNA damage from ionizing radiation and regulates arrest in the G{sub 1} portion of the cell cycle. Arrest in G{sub 1} portion of the cell cycle. While upstream regulation of p53 protein stability is poorly understood, variations in the ability to accumulate p53 following DNA damage represent potential variations in lung cancer susceptibility related to radon progeny. Further, transcription of the cell-cycle regulatory gene Cip1 is regulated by p53 and increases following ionizing radiation. Therefore, variations in the expression of Cip1 following {alpha}-particle exposure may also be a susceptibility factor in radon-related lung cancers. The purpose of the present investigation was to measure p53 and Cip1 protein induction following {alpha}-particle exposure of fibroblast lines from nine individuals to determine if there were significant variations. The expression of Cip1 protein indicates the differences in response are biologically relevant.},
doi = {10.2172/381382},
url = {https://www.osti.gov/biblio/381382}, journal = {},
number = ,
volume = ,
place = {United States},
year = {Fri Dec 01 00:00:00 EST 1995},
month = {Fri Dec 01 00:00:00 EST 1995}
}