TY - JOUR
T1 - Enhancement of two-stage skin carcinogenesis by exposure of distant skin to uv radiation1, 2, 3, 4
AU - Strickland, Paul T.
AU - Creasia, Donald
AU - Kripke, Margaret L.
N1 - Funding Information:
I Received September 4, 1984; accepted January 7, 1985. 2 Research was sponsored by the National Cancer Institute, U.S. Department of Health and Human Services, under contract NOICO-23909 with Litton Bionetics, Ine. (LBI), and by the Sid W. Richardson Foundation grant 83-191. 3 The contents of this article do not necessarily reflect the views or policies of the U.S. Department of Health and Human Services nor does mention of trade names, commercial products, or organizations imply endorsement by the U.S. Government. 4 Animals were maintained under the guidelines set forth by the National Institutes of Health "Policy on Humane Care and Use of Animals" and by the Animal Welfare Act. Facilities were accredited by the American Association for Accreditation of Laboratory Animal Care. S Basic Research Program-LBI, Laboratory of Chemical and Physical Carcinogenesis, NCI-Frederick Cancer Research Facility, P.O. Box B, Frederick, MD 21701. 6 In Vivo Carcinogenesis Assessment, NCI-Frederick Cancer Research Facility. 7 Present address: Pathophysiology Department, U.S. Army Medical Research Institute of Infectious Diseases, Ft. Detrick, Frederick, MD 21701. 8 University of Texas System Cancer Center, M. D. Anderson Hospital and Tumor Institute, Houston, TX 77030. 9 Address reprint request to Dr. Kripke at Department of Immunology, University of Texas System Cancer Center, M. D. Anderson Hospital and Tumor Institute, 6723 Bertner Ave., Houston, TX 77030. 10 We thank the following from the NCI-Frederick Cancer Research Facility: Ms. Linda Brennan, Ms. Areitha Smith, Ms. Robbie Stephans, and Ms. Tammy Hoover for their skillful assistance; Mr. Charles Riggs for statistical analysis; and Warwick L. Morison, M.D., for histologic examination of the skin tumors.
PY - 1985/5/1
Y1 - 1985/5/1
N2 - Exposure of C3H/HeN mice to UV 280-320 nm (UVB) radiation induces a systemic, immunologic alteration that interferes with the rejection of highly antigenic UVB radiation-induced skin cancers. The effect of this systemic alteration, induced by ventral UVB irradiation of mice, was tested on the induction of dorsal skin tumors resulting from initiation with UVB radiation and promotion with 12-O-tetradecanoylphorbol 13-acetate (TPA). The systemic effect of UVB radiation markedly potentiated carcinogenesis at the distant site. More important, mice treated with TPA alone on the dorsal skin developed a significant number of dorsal tumors if the mice also had been exposed ventrally to UVB radiation. Treatment of dorsal skin with UVB radiation alone did not result in the development of cancers, regardless of whether the mice received ventral irradiation. These results suggest that the systemic effect of UVB radiation is exerted during the promotion phase of two-stage carcinogenesis. Furthermore, they imply that a systemic effect of UVB radiation interferes with a natural host control mechanism that ordinarily holds skin cancers in check.
AB - Exposure of C3H/HeN mice to UV 280-320 nm (UVB) radiation induces a systemic, immunologic alteration that interferes with the rejection of highly antigenic UVB radiation-induced skin cancers. The effect of this systemic alteration, induced by ventral UVB irradiation of mice, was tested on the induction of dorsal skin tumors resulting from initiation with UVB radiation and promotion with 12-O-tetradecanoylphorbol 13-acetate (TPA). The systemic effect of UVB radiation markedly potentiated carcinogenesis at the distant site. More important, mice treated with TPA alone on the dorsal skin developed a significant number of dorsal tumors if the mice also had been exposed ventrally to UVB radiation. Treatment of dorsal skin with UVB radiation alone did not result in the development of cancers, regardless of whether the mice received ventral irradiation. These results suggest that the systemic effect of UVB radiation is exerted during the promotion phase of two-stage carcinogenesis. Furthermore, they imply that a systemic effect of UVB radiation interferes with a natural host control mechanism that ordinarily holds skin cancers in check.
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U2 - 10.1093/jnci/74.5.1129
DO - 10.1093/jnci/74.5.1129
M3 - Article
C2 - 3858581
AN - SCOPUS:0021881177
SN - 0027-8874
VL - 74
SP - 1129
EP - 1134
JO - Journal of the National Cancer Institute
JF - Journal of the National Cancer Institute
IS - 5
ER -