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Title: Host cell reactivation studies with epidermal cells of mice sensitive and resistant to carcinogenesis

Abstract

Primary epidermal cells from AKR, BALB/c, CD-1, and SENCAR mice, listed in order of least to most sensitive to epidermal carcinogenesis by initiation and promotion protocols, were found to be equally competent to ''reactivate'' herpes simplex virus type 1 irradiated by germicidal ultraviolet radiation. Nontumorigenic BALB/c epidermal cell lines selected in vitro for resistance to terminal differentiation after in vivo or in vitro treatment with initiating doses of carcinogens showed virus survival curves similar to those of primary cells. Similarly, primary cultures which were allowed to grow to confluency following a single treatment with the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (100 ng/ml) retained normal host cell reactivation. Host cell reactivation studies with mouse dermal fibroblasts could not be done because of the failure of the herpes simplex virus to infect these cells and produce plaques. These results demonstrate that survival of ultraviolet light-damaged virus in primary epidermal cells in culture is unrelated to whether the cells are derived from mice sensitive or resistant to epidermal carcinogenesis. Furthermore, virus survival is not changed by tumor promoter treatment or by treatment with initiating doses of carcinogens which results in differentiation-resistant cells.

Authors:
;
Publication Date:
Research Org.:
National Cancer Inst., Bethesda, MD
OSTI Identifier:
6408062
Resource Type:
Journal Article
Journal Name:
Cancer Res.; (United States)
Additional Journal Information:
Journal Volume: 44:3
Country of Publication:
United States
Language:
English
Subject:
63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.; EPIDERMIS; HOST-CELL REACTIVATION; HERPES SIMPLEX; CARCINOGENESIS; CARCINOGENS; INHIBITION; MICE; SENSITIVITY; TUMOR PROMOTERS; ULTRAVIOLET RADIATION; ANIMAL TISSUES; ANIMALS; BIOLOGICAL RECOVERY; BIOLOGICAL REPAIR; BODY; DISEASES; ELECTROMAGNETIC RADIATION; EPITHELIUM; INFECTIOUS DISEASES; MAMMALS; ORGANS; PATHOGENESIS; PROMOTERS; RADIATIONS; RECOVERY; REPAIR; RODENTS; SKIN; SKIN DISEASES; TISSUES; VERTEBRATES; VIRAL DISEASES; 560121* - Radiation Effects on Cells- External Source- (-1987)

Citation Formats

Strickland, J E, and Strickland, A G. Host cell reactivation studies with epidermal cells of mice sensitive and resistant to carcinogenesis. United States: N. p., 1984. Web.
Strickland, J E, & Strickland, A G. Host cell reactivation studies with epidermal cells of mice sensitive and resistant to carcinogenesis. United States.
Strickland, J E, and Strickland, A G. 1984. "Host cell reactivation studies with epidermal cells of mice sensitive and resistant to carcinogenesis". United States.
@article{osti_6408062,
title = {Host cell reactivation studies with epidermal cells of mice sensitive and resistant to carcinogenesis},
author = {Strickland, J E and Strickland, A G},
abstractNote = {Primary epidermal cells from AKR, BALB/c, CD-1, and SENCAR mice, listed in order of least to most sensitive to epidermal carcinogenesis by initiation and promotion protocols, were found to be equally competent to ''reactivate'' herpes simplex virus type 1 irradiated by germicidal ultraviolet radiation. Nontumorigenic BALB/c epidermal cell lines selected in vitro for resistance to terminal differentiation after in vivo or in vitro treatment with initiating doses of carcinogens showed virus survival curves similar to those of primary cells. Similarly, primary cultures which were allowed to grow to confluency following a single treatment with the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (100 ng/ml) retained normal host cell reactivation. Host cell reactivation studies with mouse dermal fibroblasts could not be done because of the failure of the herpes simplex virus to infect these cells and produce plaques. These results demonstrate that survival of ultraviolet light-damaged virus in primary epidermal cells in culture is unrelated to whether the cells are derived from mice sensitive or resistant to epidermal carcinogenesis. Furthermore, virus survival is not changed by tumor promoter treatment or by treatment with initiating doses of carcinogens which results in differentiation-resistant cells.},
doi = {},
url = {https://www.osti.gov/biblio/6408062}, journal = {Cancer Res.; (United States)},
number = ,
volume = 44:3,
place = {United States},
year = {Thu Mar 01 00:00:00 EST 1984},
month = {Thu Mar 01 00:00:00 EST 1984}
}