High incidence of ultraviolet-B-or chemical-carcinogen-induced skin tumours in mice lacking the xeroderma pigmentosum group A gene

Hironobu Nakane; Seiji Takeuchi; Shunsuke Yuba; Masafumi Saijo; Yoshimichi Nakatsu; Hiroaki Murai; Yoko Nakatsuru; Takatoshi Ishikawa; Seiichi Hirota; Yukihiko Kitamura; Yoko Kato; Yukio Tsunoda; Hiroko Miyauchi; Takeshi Horio; Tomoyuki Tokunaga; Tsukasa Matsunaga; Osamu Nikaido; Yoshitake Nishimune; Yoshio Okada; Kiyoji Tanaka

doi:10.1038/377165a0

High incidence of ultraviolet-B-or chemical-carcinogen-induced skin tumours in mice lacking the xeroderma pigmentosum group A gene

Hironobu Nakane, Seiji Takeuchi, Shunsuke Yuba, Masafumi Saijo, Yoshimichi Nakatsu, Hiroaki Murai, Yoko Nakatsuru, Takatoshi Ishikawa, Seiichi Hirota, Yukihiko Kitamura, Yoko Kato, Yukio Tsunoda, Hiroko Miyauchi, Takeshi Horio, Tomoyuki Tokunaga, Tsukasa Matsunaga, Osamu Nikaido, Yoshitake Nishimune, Yoshio Okada, Kiyoji Tanaka

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Abstract

XERODERMA pigmentosum (XP) is an autosomal recessive disorder characterized by a high frequency of skin cancer on sun-exposed areas, and neurological complications. XP has a defect in the early step(s) of nucleotide-excision repair (NER) and consists of eight different genetic complementation groups (groups A–G and a variant)1. We established XPA (group-A XP) gene-deficient mice by gene targeting of mouse embryonic stem (ES) cells. The XPA-deficient mice showed neither obvious physical abnormalities nor pathological alterations, but were defective in NER and highly susceptible to ultraviolet-B- or 9, 10-dimethyl-l, 2-benz[a]anthra-cene-induced skin carcinogenesis. These findings provide in vivo evidence that the XPA protein protects mice from carcinogenesis initiated by ultraviolet or chemical carcinogen. The XP A -deficient mice may provide a good in vivo model to study the high incidence of skin carcinogenesis in group A XP patients.

Original language	English
Pages (from-to)	165-168
Number of pages	4
Journal	Nature
Volume	377
Issue number	6545
DOIs	https://doi.org/10.1038/377165a0
Publication status	Published - Sept 14 1995
Externally published	Yes

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Nakane, H., Takeuchi, S., Yuba, S., Saijo, M., Nakatsu, Y., Murai, H., Nakatsuru, Y., Ishikawa, T., Hirota, S., Kitamura, Y., Kato, Y., Tsunoda, Y., Miyauchi, H., Horio, T., Tokunaga, T., Matsunaga, T., Nikaido, O., Nishimune, Y., Okada, Y., & Tanaka, K. (1995). High incidence of ultraviolet-B-or chemical-carcinogen-induced skin tumours in mice lacking the xeroderma pigmentosum group A gene. Nature, 377(6545), 165-168. https://doi.org/10.1038/377165a0

Nakane, H, Takeuchi, S, Yuba, S, Saijo, M, Nakatsu, Y, Murai, H, Nakatsuru, Y, Ishikawa, T, Hirota, S, Kitamura, Y, Kato, Y, Tsunoda, Y, Miyauchi, H, Horio, T, Tokunaga, T, Matsunaga, T, Nikaido, O, Nishimune, Y, Okada, Y & Tanaka, K 1995, 'High incidence of ultraviolet-B-or chemical-carcinogen-induced skin tumours in mice lacking the xeroderma pigmentosum group A gene', Nature, vol. 377, no. 6545, pp. 165-168. https://doi.org/10.1038/377165a0

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title = "High incidence of ultraviolet-B-or chemical-carcinogen-induced skin tumours in mice lacking the xeroderma pigmentosum group A gene",

abstract = "XERODERMA pigmentosum (XP) is an autosomal recessive disorder characterized by a high frequency of skin cancer on sun-exposed areas, and neurological complications. XP has a defect in the early step(s) of nucleotide-excision repair (NER) and consists of eight different genetic complementation groups (groups A–G and a variant)1. We established XPA (group-A XP) gene-deficient mice by gene targeting of mouse embryonic stem (ES) cells. The XPA-deficient mice showed neither obvious physical abnormalities nor pathological alterations, but were defective in NER and highly susceptible to ultraviolet-B- or 9, 10-dimethyl-l, 2-benz[a]anthra-cene-induced skin carcinogenesis. These findings provide in vivo evidence that the XPA protein protects mice from carcinogenesis initiated by ultraviolet or chemical carcinogen. The XP A -deficient mice may provide a good in vivo model to study the high incidence of skin carcinogenesis in group A XP patients.",

author = "Hironobu Nakane and Seiji Takeuchi and Shunsuke Yuba and Masafumi Saijo and Yoshimichi Nakatsu and Hiroaki Murai and Yoko Nakatsuru and Takatoshi Ishikawa and Seiichi Hirota and Yukihiko Kitamura and Yoko Kato and Yukio Tsunoda and Hiroko Miyauchi and Takeshi Horio and Tomoyuki Tokunaga and Tsukasa Matsunaga and Osamu Nikaido and Yoshitake Nishimune and Yoshio Okada and Kiyoji Tanaka",

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doi = "10.1038/377165a0",

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AU - Nakane, Hironobu

AU - Takeuchi, Seiji

AU - Yuba, Shunsuke

AU - Saijo, Masafumi

AU - Nakatsu, Yoshimichi

AU - Murai, Hiroaki

AU - Nakatsuru, Yoko

AU - Ishikawa, Takatoshi

AU - Hirota, Seiichi

AU - Kitamura, Yukihiko

AU - Kato, Yoko

AU - Tsunoda, Yukio

AU - Miyauchi, Hiroko

AU - Horio, Takeshi

AU - Tokunaga, Tomoyuki

AU - Matsunaga, Tsukasa

AU - Nikaido, Osamu

AU - Nishimune, Yoshitake

AU - Okada, Yoshio

AU - Tanaka, Kiyoji

PY - 1995/9/14

Y1 - 1995/9/14

N2 - XERODERMA pigmentosum (XP) is an autosomal recessive disorder characterized by a high frequency of skin cancer on sun-exposed areas, and neurological complications. XP has a defect in the early step(s) of nucleotide-excision repair (NER) and consists of eight different genetic complementation groups (groups A–G and a variant)1. We established XPA (group-A XP) gene-deficient mice by gene targeting of mouse embryonic stem (ES) cells. The XPA-deficient mice showed neither obvious physical abnormalities nor pathological alterations, but were defective in NER and highly susceptible to ultraviolet-B- or 9, 10-dimethyl-l, 2-benz[a]anthra-cene-induced skin carcinogenesis. These findings provide in vivo evidence that the XPA protein protects mice from carcinogenesis initiated by ultraviolet or chemical carcinogen. The XP A -deficient mice may provide a good in vivo model to study the high incidence of skin carcinogenesis in group A XP patients.

AB - XERODERMA pigmentosum (XP) is an autosomal recessive disorder characterized by a high frequency of skin cancer on sun-exposed areas, and neurological complications. XP has a defect in the early step(s) of nucleotide-excision repair (NER) and consists of eight different genetic complementation groups (groups A–G and a variant)1. We established XPA (group-A XP) gene-deficient mice by gene targeting of mouse embryonic stem (ES) cells. The XPA-deficient mice showed neither obvious physical abnormalities nor pathological alterations, but were defective in NER and highly susceptible to ultraviolet-B- or 9, 10-dimethyl-l, 2-benz[a]anthra-cene-induced skin carcinogenesis. These findings provide in vivo evidence that the XPA protein protects mice from carcinogenesis initiated by ultraviolet or chemical carcinogen. The XP A -deficient mice may provide a good in vivo model to study the high incidence of skin carcinogenesis in group A XP patients.

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High incidence of ultraviolet-B-or chemical-carcinogen-induced skin tumours in mice lacking the xeroderma pigmentosum group A gene

Abstract

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