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  1. 原著論文

Ikaros is a mutational target for lymphomagenesis in Mlh1-deficient mice

https://repo.qst.go.jp/records/44867
https://repo.qst.go.jp/records/44867
d43c6147-6db9-4d8f-9b1e-b6ea695010ca
Item type 学術雑誌論文 / Journal Article(1)
公開日 2007-06-06
タイトル
タイトル Ikaros is a mutational target for lymphomagenesis 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 Kakinuma, Shizuko

× Kakinuma, Shizuko

WEKO 445544

Kakinuma, Shizuko

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Kodama, Youtarou

× Kodama, Youtarou

WEKO 445545

Kodama, Youtarou

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Amasaki, Yoshiko

× Amasaki, Yoshiko

WEKO 445546

Amasaki, Yoshiko

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Shang, Yi

× Shang, Yi

WEKO 445547

Shang, Yi

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Tokairin, Yutaka

× Tokairin, Yutaka

WEKO 445548

Tokairin, Yutaka

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Arai, Masami

× Arai, Masami

WEKO 445549

Arai, Masami

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Nishimura, Mayumi

× Nishimura, Mayumi

WEKO 445550

Nishimura, Mayumi

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Monobe, Manami

× Monobe, Manami

WEKO 445551

Monobe, Manami

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Kojima, Shuji

× Kojima, Shuji

WEKO 445552

Kojima, Shuji

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Shimada, Yoshiya

× Shimada, Yoshiya

WEKO 445553

Shimada, Yoshiya

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柿沼 志津子

× 柿沼 志津子

WEKO 445554

en 柿沼 志津子

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小玉 陽太郎

× 小玉 陽太郎

WEKO 445555

en 小玉 陽太郎

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甘崎 佳子

× 甘崎 佳子

WEKO 445556

en 甘崎 佳子

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尚 奕

× 尚 奕

WEKO 445557

en 尚 奕

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東海林 裕

× 東海林 裕

WEKO 445558

en 東海林 裕

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新井 正美

× 新井 正美

WEKO 445559

en 新井 正美

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西村 まゆみ

× 西村 まゆみ

WEKO 445560

en 西村 まゆみ

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物部 真奈美

× 物部 真奈美

WEKO 445561

en 物部 真奈美

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島田 義也

× 島田 義也

WEKO 445562

en 島田 義也

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抄録
内容記述タイプ Abstract
内容記述 Deficiencies in DNA mismatch repair (MMR) result in replication errors within key tumor suppressor genes or oncogenes, and cause hereditary nonpolyposis colorectal cancer (HNPCC). Hematological malignancy with microsatellite instability is also associated with defective MMR, but little is known about the target genes for MMR. Here we identified Ikaros, a master transcription factor of lymphoid lineage commitment and differentiation, as a mutational target in spontaneous and radiation-induced T-cell lymphomas in Mlh1-deficient mice. Three quaters of lymphomas lacked Ikaros protein expression, which resulted from a frameshift mutation that created a stop codon. Mononucleotide repeat sequences at 1029-1034(C)6 and 1567-1572(G)6 in Ikaros were mutational hot spots with a one-base deletion occurring with a frequency of 45% and 50%, respectively. Point mutations and splicing alterations were also observed. In total, 85% of the lymphomas showed aberrations in Ikaros. The characteristics of Mlh1-deficient lymphomas is harboring of multiple mutations simultaneously in the same tumor, displaying a combination of two frameshift mutations at different repeats, frameshift and point mutations, and/or deletion mutations. This is the first report of Ikaros mutations coupled with Mlh1 deficiency in lymphomagenesis.
書誌情報 Oncogene

巻 26, 号 20, p. 2945-2949, 発行日 2006-11
ISSN
収録物識別子タイプ ISSN
収録物識別子 0950-9232
DOI
識別子タイプ DOI
関連識別子 10.1038/sj.onc.1210100
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