Nature Communications (Sep 2019)
YAP1 subgroup supratentorial ependymoma requires TEAD and nuclear factor I-mediated transcriptional programmes for tumorigenesis
- Kristian W. Pajtler,
- Yiju Wei,
- Konstantin Okonechnikov,
- Patricia B. G. Silva,
- Mikaella Vouri,
- Lei Zhang,
- Sebastian Brabetz,
- Laura Sieber,
- Melissa Gulley,
- Monika Mauermann,
- Tatjana Wedig,
- Norman Mack,
- Yuka Imamura Kawasawa,
- Tanvi Sharma,
- Marc Zuckermann,
- Felipe Andreiuolo,
- Eric Holland,
- Kendra Maass,
- Huiqin Körkel-Qu,
- Hai-Kun Liu,
- Felix Sahm,
- David Capper,
- Jens Bunt,
- Linda J. Richards,
- David T. W. Jones,
- Andrey Korshunov,
- Lukas Chavez,
- Peter Lichter,
- Mikio Hoshino,
- Stefan M. Pfister,
- Marcel Kool,
- Wei Li,
- Daisuke Kawauchi
Affiliations
- Kristian W. Pajtler
- Hopp-Children’s Cancer Center Heidelberg (KiTZ)
- Yiju Wei
- Division of Pediatric Hematology and Oncology, Department of Pediatrics, Penn State Health Hershey Medical Center, Penn State College of Medicine
- Konstantin Okonechnikov
- Hopp-Children’s Cancer Center Heidelberg (KiTZ)
- Patricia B. G. Silva
- Hopp-Children’s Cancer Center Heidelberg (KiTZ)
- Mikaella Vouri
- Hopp-Children’s Cancer Center Heidelberg (KiTZ)
- Lei Zhang
- Division of Pediatric Hematology and Oncology, Department of Pediatrics, Penn State Health Hershey Medical Center, Penn State College of Medicine
- Sebastian Brabetz
- Hopp-Children’s Cancer Center Heidelberg (KiTZ)
- Laura Sieber
- Hopp-Children’s Cancer Center Heidelberg (KiTZ)
- Melissa Gulley
- Division of Pediatric Hematology and Oncology, Department of Pediatrics, Penn State Health Hershey Medical Center, Penn State College of Medicine
- Monika Mauermann
- Hopp-Children’s Cancer Center Heidelberg (KiTZ)
- Tatjana Wedig
- Hopp-Children’s Cancer Center Heidelberg (KiTZ)
- Norman Mack
- Hopp-Children’s Cancer Center Heidelberg (KiTZ)
- Yuka Imamura Kawasawa
- Department of Biochemistry and Molecular Biology, Penn State Health Hershey Medical Center, Penn State College of Medicine
- Tanvi Sharma
- Hopp-Children’s Cancer Center Heidelberg (KiTZ)
- Marc Zuckermann
- Hopp-Children’s Cancer Center Heidelberg (KiTZ)
- Felipe Andreiuolo
- Department of Neuropathology, Ste. Anne Hospital
- Eric Holland
- Human Biology Division, Fred Hutchinson Cancer Research Center
- Kendra Maass
- Hopp-Children’s Cancer Center Heidelberg (KiTZ)
- Huiqin Körkel-Qu
- Division of Molecular Neurogenetics, German Cancer Research Center (DKFZ)
- Hai-Kun Liu
- Division of Molecular Neurogenetics, German Cancer Research Center (DKFZ)
- Felix Sahm
- Clinical Cooperation Unit Neuropathology, German Cancer Research Center (DKFZ)
- David Capper
- Charité – Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Neuropathology, Partner Site Berlin, German Cancer Research Center (DKFZ)
- Jens Bunt
- Queensland Brain Institute, The University of Queensland
- Linda J. Richards
- Queensland Brain Institute, The University of Queensland
- David T. W. Jones
- Hopp-Children’s Cancer Center Heidelberg (KiTZ)
- Andrey Korshunov
- Clinical Cooperation Unit Neuropathology, German Cancer Research Center (DKFZ)
- Lukas Chavez
- Hopp-Children’s Cancer Center Heidelberg (KiTZ)
- Peter Lichter
- Division of Molecular Genetics, German Cancer Research Center (DKFZ)
- Mikio Hoshino
- Department of Biochemistry and Cellular Biology, National Institute of Neuroscience, NCNP
- Stefan M. Pfister
- Hopp-Children’s Cancer Center Heidelberg (KiTZ)
- Marcel Kool
- Hopp-Children’s Cancer Center Heidelberg (KiTZ)
- Wei Li
- Division of Pediatric Hematology and Oncology, Department of Pediatrics, Penn State Health Hershey Medical Center, Penn State College of Medicine
- Daisuke Kawauchi
- Hopp-Children’s Cancer Center Heidelberg (KiTZ)
- DOI
- https://doi.org/10.1038/s41467-019-11884-5
- Journal volume & issue
-
Vol. 10,
no. 1
pp. 1 – 16
Abstract
The molecular mechanisms driving proliferation in the pediatric brain cancer epdendymoma are poorly understood. Here the authors show that a YAP1- MAMLD1 fusion drives tumor formation in mice and show that the fusion protein can collaborate with the TEAD and NFI transcription factors.
