Differential role of Id1 in MLL-AF9–driven leukemia based on cell of origin

Author:

Man Na1,Sun Xiao-Jian12,Tan Yurong1,García-Cao Marta3,Liu Fan14,Cheng Guoyan1,Hatlen Megan3,Xu Haiming3,Shah Ronit1,Chastain Nolan1,Liu Na5,Huang Gang6,Zhou Yuan7,Sheng Mengyao7,Song Junhong8,Yang Feng-Chun14,Benezra Robert3,Nimer Stephen D.149,Wang Lan1245

Affiliation:

1. Sylvester Comprehensive Cancer Center, Miller School of Medicine, University of Miami, Miami, FL;

2. State Key Laboratory of Medical Genomics, Shanghai Institute of Hematology, Rui Jin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China;

3. Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY;

4. Department of Biochemistry and Molecular Biology, Miller School of Medicine, University of Miami, Miami, FL;

5. Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences/School of Medicine, Shanghai Jiao Tong University, Shanghai, China;

6. Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH;

7. State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences/Peking Union Medical College, Tianjin, China;

8. Pediatric Hematology and Oncology, Shanghai Children’s Medical Center, Shanghai, China; and

9. Department of Medicine, Miller School of Medicine, University of Miami, Miami, FL

Abstract

Key Points Loss of Id1 delays leukemogenesis in fetal MLL-AF9 leukemia model, but accelerates leukemogenesis in postnatal MLL-AF9 leukemia model. Deletion of Cdkn1a (p21) rescues the loss of Id1 in both MLL-AF9 mouse models.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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