Dangerous Liaisons between Tet2 Mutation, Inflammatory Monocytes, and Leukemogenesis

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.