Abstract
Transgenic knockin mice expressing a common loss-of-function mutation in human TET2 exhibit aging-related accelerated myeloid leukemia development and skewing of myelopoiesis toward the production of proinflammatory MHC-IIhi monocytes that may contribute to disease. See related article by Yeaton et al., p. 2392 (2).
©2022 American Association for Cancer Research.
Publication types
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Editorial
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Research Support, Non-U.S. Gov't
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Research Support, N.I.H., Extramural
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Comment
MeSH terms
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Animals
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Carcinogenesis
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DNA-Binding Proteins / genetics
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Dioxygenases* / genetics
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Humans
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Inflammation / genetics
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Leukemia* / genetics
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Mice
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Monocytes
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Mutation
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Neoplasms*
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Proto-Oncogene Proteins / genetics
Substances
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DNA-Binding Proteins
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Proto-Oncogene Proteins
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Dioxygenases
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TET2 protein, human
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Tet2 protein, mouse