Nature Communications (Feb 2023)
Loss of phosphatase CTDNEP1 potentiates aggressive medulloblastoma by triggering MYC amplification and genomic instability
- Zaili Luo,
- Dazhuan Xin,
- Yunfei Liao,
- Kalen Berry,
- Sean Ogurek,
- Feng Zhang,
- Liguo Zhang,
- Chuntao Zhao,
- Rohit Rao,
- Xinran Dong,
- Hao Li,
- Jianzhong Yu,
- Yifeng Lin,
- Guoying Huang,
- Lingli Xu,
- Mei Xin,
- Ryuichi Nishinakamura,
- Jiyang Yu,
- Marcel Kool,
- Stefan M. Pfister,
- Martine F. Roussel,
- Wenhao Zhou,
- William A. Weiss,
- Paul Andreassen,
- Q. Richard Lu
Affiliations
- Zaili Luo
- Brain Tumor Center, Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center
- Dazhuan Xin
- Brain Tumor Center, Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center
- Yunfei Liao
- Brain Tumor Center, Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center
- Kalen Berry
- Brain Tumor Center, Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center
- Sean Ogurek
- Brain Tumor Center, Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center
- Feng Zhang
- Brain Tumor Center, Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center
- Liguo Zhang
- Brain Tumor Center, Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center
- Chuntao Zhao
- Brain Tumor Center, Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center
- Rohit Rao
- Brain Tumor Center, Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center
- Xinran Dong
- Key Laboratory of Birth Defects, Children’s Hospital, Fudan University and Institutes of Biomedical Sciences, Fudan University
- Hao Li
- Key Laboratory of Birth Defects, Children’s Hospital, Fudan University and Institutes of Biomedical Sciences, Fudan University
- Jianzhong Yu
- Key Laboratory of Birth Defects, Children’s Hospital, Fudan University and Institutes of Biomedical Sciences, Fudan University
- Yifeng Lin
- Key Laboratory of Birth Defects, Children’s Hospital, Fudan University and Institutes of Biomedical Sciences, Fudan University
- Guoying Huang
- Key Laboratory of Birth Defects, Children’s Hospital, Fudan University and Institutes of Biomedical Sciences, Fudan University
- Lingli Xu
- Brain Tumor Center, Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center
- Mei Xin
- Brain Tumor Center, Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center
- Ryuichi Nishinakamura
- Institute of Molecular Embryology and Genetics, Kumamoto University
- Jiyang Yu
- Department of Computational Biology, St. Jude Children’s Research Hospital
- Marcel Kool
- Hopp Children’s Cancer Center Heidelberg (KiTZ); Division of Pediatric Neurooncology, German Cancer Research Center (DKFZ) and German Cancer Consortium (DKTK)
- Stefan M. Pfister
- Hopp Children’s Cancer Center Heidelberg (KiTZ); Division of Pediatric Neurooncology, German Cancer Research Center (DKFZ) and German Cancer Consortium (DKTK)
- Martine F. Roussel
- Department of Tumor Cell Biology, St. Jude Children’s Research Hospital
- Wenhao Zhou
- Key Laboratory of Birth Defects, Children’s Hospital, Fudan University and Institutes of Biomedical Sciences, Fudan University
- William A. Weiss
- Department of Neurology, Pediatrics, and Surgery, Helen Diller Family Comprehensive Cancer Center, University of California San Francisco
- Paul Andreassen
- Brain Tumor Center, Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center
- Q. Richard Lu
- Brain Tumor Center, Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center
- DOI
- https://doi.org/10.1038/s41467-023-36400-8
- Journal volume & issue
-
Vol. 14,
no. 1
pp. 1 – 19
Abstract
Group 3 medulloblastomas (MBs) have the worst prognosis amongst the subtypes of MBs and are associated with MYC amplifications. Here the authors identify that mutations in CTDNEP1 cause MYC activation, amplification, and genomic instability in this subtype of MBs.
