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Ionizing radiation, inflammation, and their interactions in colon carcinogenesis in Mlh1-deficient mice.
https://repo.qst.go.jp/records/47081
https://repo.qst.go.jp/records/47081d4f4f2f1-7cc8-46c2-870c-4b0912ea5a56
| Item type | 学術雑誌論文 / Journal Article(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2015-04-07 | |||||
| タイトル | ||||||
| タイトル | Ionizing radiation, inflammation, and their interactions in colon carcinogenesis in Mlh1-deficient mice. | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
| 資源タイプ | journal article | |||||
| アクセス権 | ||||||
| アクセス権 | metadata only access | |||||
| アクセス権URI | http://purl.org/coar/access_right/c_14cb | |||||
| 著者 |
Morioka, Takamitsu
× Morioka, Takamitsu× Miyoshi-Imamura, Tomoko× J, Blyth Benjamin× Kaminishi, Mutsumi× Kokubo, Toshiaki× Nishimura, Mayumi× Kito, Seiji× Tokairin, Yutaka× Tani, Shusuke× Murakami-Murofushi, Kimiko× Yoshimi, Naoki× Shimada, Yoshiya× Kakinuma, Shizuko× 森岡 孝満× Ｂｌｙｔｈ Ｂｅｎｊａｍｉｎ× 上西 睦美× 小久保 年章× 西村 まゆみ× 鬼頭 靖司× 東海林 裕× 谷 修祐× 吉見 直己× 島田 義也× 柿沼 志津子 |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Genetic, physiological and environmental factors are each implicated in colorectal carcinogenesis. Mutations in the mutL homolog 1 (MLH1) gene, one of the DNA mismatch repair genes, are a main cause of hereditary colon cancer syndromes such as Lynch syndrome. Long-term chronic inflammation is also a key risk factor, responsible for colitis-associated colorectal cancer; and, radiation exposure is also known to increase colorectal cancer risk. Here, we studied the effects of radiation exposure on inflammation-induced colon carcinogenesis in DNA mismatch repair-proficient and -deficient mice. Male and female Mlh1(-/-) and Mlh1(+/+) mice were irradiated with 2 Gy X-rays at 2-weeks-old or 7-weeks-old and/or treated with 1% dextran sodium sulfate (DSS) in drinking water for 7 days at 10-weeks-old to induce mild inflammatory colitis. No colon tumors developed after X-rays and/or DSS treatment in Mlh1(+/+) mice. Colon tumors developed after DSS treatment alone in Mlh1(-/-) mice, and exposure to radiation prior to DSS treatment increased the number of tumors. Histologically, colon tumors in the mice resembled the subtype of well-to-moderately differentiated adenocarcinomas with tumor-infiltrating lymphocytes of human Lynch syndrome. Immunohistochemistry revealed that expression of both p53 and β-catenin and loss of p21 and adenomatosis polyposis coli (Apc) proteins were observed at the later stages of carcinogenesis, suggesting a course of molecular pathogenesis distinct from typical sporadic or colitis-associated colon cancer in humans. In conclusion, radiation exposure could further increase the risk of colorectal carcinogenesis induced by inflammation under the conditions of Mlh1 deficiency. This article is protected by copyright. All rights reserved. | |||||
| 書誌情報 |
Cancer science 巻 106, 号 3, p. 217-226, 発行日 2015-01 |
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| 出版者 | ||||||
| 出版者 | Blackwell Publishing | |||||
| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 1347-9032 | |||||
| PubMed番号 | ||||||
| 識別子タイプ | PMID | |||||
| 関連識別子 | 25529563 | |||||
| DOI | ||||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | 10.1111/cas.12591 | |||||
