Nature Communications (Aug 2018)
A PDGFRα-driven mouse model of glioblastoma reveals a stathmin1-mediated mechanism of sensitivity to vinblastine
- Hyun Jung Jun,
- Vicky A. Appleman,
- Hua-Jun Wu,
- Christopher M. Rose,
- Javier J. Pineda,
- Alan T. Yeo,
- Bethany Delcuze,
- Charlotte Lee,
- Aron Gyuris,
- Haihao Zhu,
- Steve Woolfenden,
- Agnieszka Bronisz,
- Ichiro Nakano,
- Ennio A. Chiocca,
- Roderick T. Bronson,
- Keith L. Ligon,
- Jann N. Sarkaria,
- Steve P. Gygi,
- Franziska Michor,
- Timothy J. Mitchison,
- Al Charest
Affiliations
- Hyun Jung Jun
- Cancer Research Institute, Beth Israel Deaconess Medical Center
- Vicky A. Appleman
- Cancer Research Institute, Beth Israel Deaconess Medical Center
- Hua-Jun Wu
- Department of Biostatistics and Computational Biology, Dana-Farber Cancer Institute
- Christopher M. Rose
- Department of Cell Biology, Harvard Medical School
- Javier J. Pineda
- Department of Systems Biology, Harvard Medical School
- Alan T. Yeo
- Sackler School of Graduate Studies, Tufts University School of Medicine
- Bethany Delcuze
- Sackler School of Graduate Studies, Tufts University School of Medicine
- Charlotte Lee
- Department of Biostatistics and Computational Biology, Dana-Farber Cancer Institute
- Aron Gyuris
- Cancer Research Institute, Beth Israel Deaconess Medical Center
- Haihao Zhu
- Molecular Oncology Research Institute, Tufts Medical Center
- Steve Woolfenden
- Molecular Oncology Research Institute, Tufts Medical Center
- Agnieszka Bronisz
- Harvey Cushing Neuro-Oncology Laboratories, Department of Neurosurgery, Brigham and Women’s Hospital, Harvard Medical School
- Ichiro Nakano
- Department of Neurosurgery and Comprehensive Cancer Center, University of Alabama at Birmingham
- Ennio A. Chiocca
- Harvey Cushing Neuro-Oncology Laboratories, Department of Neurosurgery, Brigham and Women’s Hospital, Harvard Medical School
- Roderick T. Bronson
- Rodent Histopathology Core, Dana-Farber/Harvard Cancer Center
- Keith L. Ligon
- Department of Oncologic Pathology, Dana-Farber Cancer Institute
- Jann N. Sarkaria
- Department of Radiation Oncology, Mayo Clinic
- Steve P. Gygi
- Department of Cell Biology, Harvard Medical School
- Franziska Michor
- Department of Biostatistics and Computational Biology, Dana-Farber Cancer Institute
- Timothy J. Mitchison
- Department of Systems Biology, Harvard Medical School
- Al Charest
- Cancer Research Institute, Beth Israel Deaconess Medical Center
- DOI
- https://doi.org/10.1038/s41467-018-05036-4
- Journal volume & issue
-
Vol. 9,
no. 1
pp. 1 – 13
Abstract
Amplification of PDGFRα is a common alteration in glioblastoma. In this study, the authors develop a genetically engineered mouse model of GBM based on autocrine, chronic stimulation of overexpressed PDGFR and discover Stathmin1 as an important PDGFRα regulated-protein involved in the response to vinstabline.
