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Pubmed ID :24509477
Publication Date : //

Identification of functional cooperative mutations of SETD2 in human acute leukemia.


Acute leukemia characterized by chromosomal rearrangements requires additional molecular disruptions to develop into full-blown malignancy, yet the cooperative mechanisms remain elusive. Using whole-genome sequencing of a pair of monozygotic twins discordant for MLL (also called KMT2A) gene-rearranged leukemia, we identified a transforming MLL-NRIP3 fusion gene and biallelic mutations in SETD2 (encoding a histone H3K36 methyltransferase). Moreover, loss-of-function point mutations in SETD2 were recurrent (6.2%) in 241 patients with acute leukemia and were associated with multiple major chromosomal aberrations. We observed a global loss of H3K36 trimethylation (H3K36me3) in leukemic blasts with mutations in SETD2. In the presence of a genetic lesion, downregulation of SETD2 contributed to both initiation and progression during leukemia development by promoting the self-renewal potential of leukemia stem cells. Therefore, our study provides compelling evidence for SETD2 as a new tumor suppressor. Disruption of the SETD2-H3K36me3 pathway is a distinct epigenetic mechanism for leukemia development.

Authors : Zhu Xiaofan , He Fuhong , Zeng Huimin , Ling Shaoping , Chen Aili , Wang Yaqin , Yan Xiaomei , Wei Wei , Pang Yakun , Cheng Hui , Hua Chunlan , Zhang Yue , Yang Xuejing , Lu Xin , Cao Lihua , Hao Lingtong , Dong Lili , Zou Wei , Wu Jun , Li Xia , Zheng Si , Yan Jin , Zhou Jing , Zhang Lixia , Mi Shuangli , Wang Xiaojuan , Zhang Li , Zou Yao , Chen Yumei , Geng Zhe , Wang Jianmin , Zhou Jianfeng , Liu Xin , Wang Jianxiang , Yuan Weiping , Huang Gang , Cheng Tao , Wang Qian-Fei ,

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