Roles of AML1/RUNX1 in T-cell malignancy induced by loss of p53

Kimiko Shimizu, Kazutsune Yamagata, Mineo Kurokawa, Shuki Mizutani, Yukiko Tsunematsu, Issay Kitabayashi

研究成果: ジャーナルへの寄稿学術論文査読

13 被引用数 (Scopus)

抄録

AML1/RUNX1 is a frequent target of chromosome translocations and mutations in myeloid and B-cell leukemias, and upregulation of AML1 is also observed in some cases of T-cell leukemias and lymphomas. This study shows that the incidence of thymic lymphoma in p53-null mice is less frequent in the Aml1+/- than in the Aml1+/+ background. AML1 is upregulated in p53-null mouse bone-marrow cells and embryonic fibroblasts. In the steady state, p53 binds to and inhibits the distal AML1 promoter. When the cells are exposed to stresses, p53 is released from the distal AML1 promoter, resulting in upregulation of AML1. Overexpression of AML1 stimulates T-lymphocyte proliferation. These results suggest that upregulation of AML1 induced by loss of p53 promotes lymphoid-cell proliferation, thereby inducing lymphoma development.

本文言語英語
ページ(範囲)1033-1038
ページ数6
ジャーナルCancer science
104
8
DOI
出版ステータス出版済み - 08-2013
外部発表はい

All Science Journal Classification (ASJC) codes

  • 腫瘍学
  • 癌研究

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