Fas ligand: A sensor for DNA damage critical in skin cancer etiology

Laurie L. Hill; Allal Ouhtit; Susan M. Loughlin; Margaret L. Kripke; Honnavara N. Ananthaswamy; Laurie B. Owen-Schaub

doi:10.1126/science.285.5429.898

Fas ligand: A sensor for DNA damage critical in skin cancer etiology

Laurie L. Hill, Allal Ouhtit, Susan M. Loughlin, Margaret L. Kripke, Honnavara N. Ananthaswamy, Laurie B. Owen-Schaub^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

225 Citations (Scopus)

Abstract

DNA-damaged cells can either repair the DNA or be eliminated through a homeostatic control mechanism termed 'cellular proofreading.' Elimination of DNA-damaged cells after ultraviolet radiation (UVR) through sunburn cell (apoptotic keratinocyte) formation is thought to be pivotal for the removal of precancerous skin cells. Sunburn cell formation was found to be dependent on Fas ligand (FasL), a pro-apoptotic protein induced by DNA damage. Chronic exposure to UVR caused 14 of 20 (70 percent) FasL-deficient mice and 1 of 20 (5 percent) wild-type mice to accumulate p53 mutations in the epidermis. Thus, FasL-mediated apoptosis is important for skin homeostasis, suggesting that the dysregulation of Fas-FasL interactions may be central to the development of skin cancer.

Original language	English
Pages (from-to)	898-900
Number of pages	3
Journal	Science
Volume	285
Issue number	5429
DOIs	https://doi.org/10.1126/science.285.5429.898
Publication status	Published - Aug 6 1999
Externally published	Yes

ASJC Scopus subject areas

General

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1126/science.285.5429.898

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title = "Fas ligand: A sensor for DNA damage critical in skin cancer etiology",

abstract = "DNA-damaged cells can either repair the DNA or be eliminated through a homeostatic control mechanism termed 'cellular proofreading.' Elimination of DNA-damaged cells after ultraviolet radiation (UVR) through sunburn cell (apoptotic keratinocyte) formation is thought to be pivotal for the removal of precancerous skin cells. Sunburn cell formation was found to be dependent on Fas ligand (FasL), a pro-apoptotic protein induced by DNA damage. Chronic exposure to UVR caused 14 of 20 (70 percent) FasL-deficient mice and 1 of 20 (5 percent) wild-type mice to accumulate p53 mutations in the epidermis. Thus, FasL-mediated apoptosis is important for skin homeostasis, suggesting that the dysregulation of Fas-FasL interactions may be central to the development of skin cancer.",

author = "Hill, {Laurie L.} and Allal Ouhtit and Loughlin, {Susan M.} and Kripke, {Margaret L.} and Ananthaswamy, {Honnavara N.} and Owen-Schaub, {Laurie B.}",

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TY - JOUR

T1 - Fas ligand

T2 - A sensor for DNA damage critical in skin cancer etiology

AU - Hill, Laurie L.

AU - Ouhtit, Allal

AU - Loughlin, Susan M.

AU - Kripke, Margaret L.

AU - Ananthaswamy, Honnavara N.

AU - Owen-Schaub, Laurie B.

PY - 1999/8/6

Y1 - 1999/8/6

N2 - DNA-damaged cells can either repair the DNA or be eliminated through a homeostatic control mechanism termed 'cellular proofreading.' Elimination of DNA-damaged cells after ultraviolet radiation (UVR) through sunburn cell (apoptotic keratinocyte) formation is thought to be pivotal for the removal of precancerous skin cells. Sunburn cell formation was found to be dependent on Fas ligand (FasL), a pro-apoptotic protein induced by DNA damage. Chronic exposure to UVR caused 14 of 20 (70 percent) FasL-deficient mice and 1 of 20 (5 percent) wild-type mice to accumulate p53 mutations in the epidermis. Thus, FasL-mediated apoptosis is important for skin homeostasis, suggesting that the dysregulation of Fas-FasL interactions may be central to the development of skin cancer.

AB - DNA-damaged cells can either repair the DNA or be eliminated through a homeostatic control mechanism termed 'cellular proofreading.' Elimination of DNA-damaged cells after ultraviolet radiation (UVR) through sunburn cell (apoptotic keratinocyte) formation is thought to be pivotal for the removal of precancerous skin cells. Sunburn cell formation was found to be dependent on Fas ligand (FasL), a pro-apoptotic protein induced by DNA damage. Chronic exposure to UVR caused 14 of 20 (70 percent) FasL-deficient mice and 1 of 20 (5 percent) wild-type mice to accumulate p53 mutations in the epidermis. Thus, FasL-mediated apoptosis is important for skin homeostasis, suggesting that the dysregulation of Fas-FasL interactions may be central to the development of skin cancer.

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Fas ligand: A sensor for DNA damage critical in skin cancer etiology

Abstract

ASJC Scopus subject areas

UN SDGs

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