Loss of Asxl1 leads to myelodysplastic syndrome-like disease in mice.

@article{Wang2014LossOA,
  title={Loss of Asxl1 leads to myelodysplastic syndrome-like disease in mice.},
  author={Jiapeng Wang and Zhaomin Li and Yongzheng He and Feng Pan and Shi Chen and Steven D. Rhodes and Lihn Nguyen and Jin Yuan and Li Jiang and Xianlin Yang and Ophelia I. Weeks and Ziyue Liu and Jiehao Zhou and Hongyu Ni and Chen-leng Cai and Mingjiang Xu and Fengchun Yang},
  journal={Blood},
  year={2014},
  volume={123 4},
  pages={541-53}
}
ASXL1 is mutated/deleted with high frequencies in multiple forms of myeloid malignancies, and its alterations are associated with poor prognosis. De novo ASXL1 mutations cause Bohring-Opitz syndrome characterized by multiple congenital malformations. We show that Asxl1 deletion in mice led to developmental abnormalities including dwarfism, anophthalmia, and 80% embryonic lethality. Surviving Asxl1(-/-) mice lived for up to 42 days and developed features of myelodysplastic syndrome (MDS… CONTINUE READING
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