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Acute loss of TET function results in aggressive myeloid cancer in mice

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Title
Acute loss of TET function results in aggressive myeloid cancer in mice
Author(s)
Jungeun An; González-Avalos, E.; Chawla, A.; Jeong, M.; López-Moyado, I.F.; Li, W.; Goodell, M.A.; Chavez, L.; Ko, M.; Rao, A.
Publication Date
2015-11
Journal
NATURE COMMUNICATIONS, v.6, no., pp.10071 -
Publisher
NATURE PUBLISHING GROUP
Abstract
TET-family dioxygenases oxidize 5-methylcytosine (5mC) in DNA, and exert tumour suppressor activity in many types of cancers. Even in the absence of TET coding region mutations, TET loss-of-function is strongly associated with cancer. Here we show that acute elimination of TET function induces the rapid development of an aggressive, fully-penetrant and cell-autonomous myeloid leukaemia in mice, pointing to a causative role for TET loss-of-function in this myeloid malignancy. Phenotypic and transcriptional profiling shows aberrant differentiation of haematopoietic stem/progenitor cells, impaired erythroid and lymphoid differentiation and strong skewing to the myeloid lineage, with only a mild relation to changes in DNA modification. We also observe progressive accumulation of phospho-H2AX and strong impairment of DNA damage repair pathways, suggesting a key role for TET proteins in maintaining genome integrity.
URI
http://pr.ibs.re.kr/handle/8788114/2248
DOI
10.1038/ncomms10071
ISSN
2041-1723
Appears in Collections:
Center for Genomic Integrity(유전체 항상성 연구단) > Journal Papers (저널논문)
Files in This Item:
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