@article{f4b9476df24e4bb0b3fd8e054532a190,
title = "Abnormal wound healing in UV-irradiated skin of sencar mice",
abstract = "Sencar mice demonstrate an unusual sensitivity to epidermal carcinogenesis by initiation-promotion or single high-dose exposure to ultraviolet radiation (UVR). These mice exhibited an exaggerated and persistent epidermal hyperplasia in response to tissue damage caused by UVR. The persistent hyperplasia was not present in similarly treated BALB/c mice, a strain that is relatively resistant to skin carcinogenesis by initiation-promotion or single-exposure UVR. Epithelial cell proliferation and migration were examined by autoradiography to determine the cellular basis for the persistence of hyperplasia in Sencar mouse skin. Twelve weeks after irradiation, the rate of epidermal basal cell proliferation was approximately 4 times greater in Sencar mice than in BALB/c mice, whereas epidermal cell transit times were similar in the two strains. This result indicated that persistent hyperplasia was due to sustained epithelial cell division rather than delayed cell maturation. Surgical incision of Sencar skin did not cause abnormal hyperplasia, nor did this procedure enhance the induction of tumors by UVR. These findings suggest that Sencar mice may possess a heritable defect that mediates both tissue regeneration and tumorigenesis in UV-irradiated skin.",
author = "Strickland, {Paul T.}",
note = "Funding Information: T he identification and clnractcrization of host factors t!ut determine susceptibi li ty to ca rcin ogenesis arc im-portant approaches to understanding the process of carcinogenesis. For this reason, animal strains tint arc unusually susceptible to carcinogenesis have been the focus of considerable investigation. SL'Ilcar mice arc selectively bred for hypersusceptibility to chemically induced skin carcinogenesis jl -3 / and arc also h ypersusceptible to ultraviolet radiatio n (UVR) carcinogenesis /41 whl'll a single high-dose exposure is used. The biologic basis for this sensitivity is unknown at present but docs not appear to involve differences in carci:wgcn metabolism j2,3j, DNA repair /5,6], epidermal growth factor receptors fTj, phorbol ester receptors j8j, or immunologic factors j9; Dr. Francis Noonan, personal communication/. Because carcinogenesis by a variety of chemical agents and at least one physica l agent is potentiated in Sencar mice, the heritable determinant that renders these mice hypersusceptible is thought to be of a general nature. The finding that Sen car mice arc hypersusceptible only ro high doses of UVll. that cause ulceration of the skin j4], suggests that ti ssue damage and subsequent wo un d healing may play a critical role in their hypersusceptibility to UVR. This report shows that after exposure ro UVR, Scncar mice exhibit abnormal wound healing that is characterized by exaggerated proliferation of epidermal cells, resulting in severe hyperplasia that persists for at least 12 weeks. In contrast, BALB/c mice, which are relatively resistant to 2-stage skin carcinogenesis Manuscript received May 15, 1985; accepted for publication August 20. 1985. Resea rch sponsored by the Natiom l Cancer Institute, Department of Health and Human Services, under contract NO 1-C0-23909 with Litton Bionetics, lnc. The contents of this publication do not necessarily reAect the views or policies of the Department of Health and Human Scrvicl's. nor docs mention of trade names , commercial products, or org:miza tions imply endorsement by the U.S. Government. Reprint requests to: Paul T. Strickbnd. Ph. D .. Photocarcinogenesis and Photoimmunology Group, NC I-Frederick Cance r Facility, P.O. Box B, Frederick, Maryland 21701. Ab breviations: TPA: 12-0-tetradccanoylphorbol-13-acetate UVR: ultraviolet radiation",
year = "1986",
month = jan,
doi = "10.1111/1523-1747.ep12283779",
language = "English (US)",
volume = "86",
pages = "37--41",
journal = "Journal of Investigative Dermatology",
issn = "0022-202X",
publisher = "Nature Publishing Group",
number = "1",
}