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Paper Details

Molecular pathogenesis of progression to myeloid leukemia from TET-insufficient status.
Blood Adv
10
2020
AML, HSCs, Mx1-Cre, T2T3, T2T3), TET, TET-insufficient, TET2, TET3, TET3 mutations, Tet, Tet deficiency, Tet insufficiency, Tet2, Tet2 or Tet3 alleles, Tet2f/f, Tet2f/fTet3f/fMx-Cre+, Tet2f/fTet3f/wtMx-Cre+, Tet2f/wtTet3f/fMx-Cre+, Tet3, Tet3 allele, Tet3 alleles, Tet3f/f, acute myeloid leukemia, mice, myeloid leukemia, nontargeted Tet2 or Tet3 allele, preleukemic hematopoietic stem cells, ten, ten-eleven translocation-2
Author NameAffiliation
Seishi OgawaKyoto University
Seishi OgawaCenter for Hematology and Regenerative Medicine, Karolinska Institute
Seishi OgawaInstitute for the Advanced Study of Human Biology (WPI ASHBi), Kyoto University
Satoru MiyanoHuman Genome Center, Institute of Medical Science, University of Tokyo
Haruhiko KosekiRIKEN Research Center for Allergy and Immunology
Atsushi IwamaGraduate School of Medicine, Chiba University
Atsushi IwamaCenter for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, University of Tokyo
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