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| Home > Publications database > Acute loss of TET function results in aggressive myeloid cancer in mice. |
| Home > Publications database > Acute loss of TET function results in aggressive myeloid cancer in mice. |
| Journal Article | DKFZ-2017-02160 |
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2015
Nature Publishing Group
London
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Please use a persistent id in citations: doi:10.1038/ncomms10071
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.
Keyword(s): DNA-Binding Proteins ; Histones ; Proto-Oncogene Proteins ; RNA, Messenger ; Tet2 protein, mouse ; Tet3 protein, mouse
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