A PDGFRα-driven mouse model of glioblastoma reveals a stathmin1-mediated mechanism of sensitivity to vinblastine

A PDGFRα-driven mouse model of glioblastoma reveals a stathmin1-mediated mechanism of sensitivity to vinblastine

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 vi...

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Main Authors: 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
Format: Article
Language:English
Published: Nature Publishing Group 2018-08-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-018-05036-4
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spelling doaj-e36e588f60e24fb6aa72e07d8947fc7d2021-05-11T09:47:00ZengNature Publishing GroupNature Communications2041-17232018-08-019111310.1038/s41467-018-05036-4A PDGFRα-driven mouse model of glioblastoma reveals a stathmin1-mediated mechanism of sensitivity to vinblastineHyun Jung Jun0Vicky A. Appleman1Hua-Jun Wu2Christopher M. Rose3Javier J. Pineda4Alan T. Yeo5Bethany Delcuze6Charlotte Lee7Aron Gyuris8Haihao Zhu9Steve Woolfenden10Agnieszka Bronisz11Ichiro Nakano12Ennio A. Chiocca13Roderick T. Bronson14Keith L. Ligon15Jann N. Sarkaria16Steve P. Gygi17Franziska Michor18Timothy J. Mitchison19Al Charest20Cancer Research Institute, Beth Israel Deaconess Medical CenterCancer Research Institute, Beth Israel Deaconess Medical CenterDepartment of Biostatistics and Computational Biology, Dana-Farber Cancer InstituteDepartment of Cell Biology, Harvard Medical SchoolDepartment of Systems Biology, Harvard Medical SchoolSackler School of Graduate Studies, Tufts University School of MedicineSackler School of Graduate Studies, Tufts University School of MedicineDepartment of Biostatistics and Computational Biology, Dana-Farber Cancer InstituteCancer Research Institute, Beth Israel Deaconess Medical CenterMolecular Oncology Research Institute, Tufts Medical CenterMolecular Oncology Research Institute, Tufts Medical CenterHarvey Cushing Neuro-Oncology Laboratories, Department of Neurosurgery, Brigham and Women’s Hospital, Harvard Medical SchoolDepartment of Neurosurgery and Comprehensive Cancer Center, University of Alabama at BirminghamHarvey Cushing Neuro-Oncology Laboratories, Department of Neurosurgery, Brigham and Women’s Hospital, Harvard Medical SchoolRodent Histopathology Core, Dana-Farber/Harvard Cancer CenterDepartment of Oncologic Pathology, Dana-Farber Cancer InstituteDepartment of Radiation Oncology, Mayo ClinicDepartment of Cell Biology, Harvard Medical SchoolDepartment of Biostatistics and Computational Biology, Dana-Farber Cancer InstituteDepartment of Systems Biology, Harvard Medical SchoolCancer Research Institute, Beth Israel Deaconess Medical CenterAmplification 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.https://doi.org/10.1038/s41467-018-05036-4
collection DOAJ
language English
format Article
sources DOAJ
author 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
spellingShingle 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
A PDGFRα-driven mouse model of glioblastoma reveals a stathmin1-mediated mechanism of sensitivity to vinblastine
Nature Communications
author_facet 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
author_sort Hyun Jung Jun
title A PDGFRα-driven mouse model of glioblastoma reveals a stathmin1-mediated mechanism of sensitivity to vinblastine
title_short A PDGFRα-driven mouse model of glioblastoma reveals a stathmin1-mediated mechanism of sensitivity to vinblastine
title_full A PDGFRα-driven mouse model of glioblastoma reveals a stathmin1-mediated mechanism of sensitivity to vinblastine
title_fullStr A PDGFRα-driven mouse model of glioblastoma reveals a stathmin1-mediated mechanism of sensitivity to vinblastine
title_full_unstemmed A PDGFRα-driven mouse model of glioblastoma reveals a stathmin1-mediated mechanism of sensitivity to vinblastine
title_sort pdgfrα-driven mouse model of glioblastoma reveals a stathmin1-mediated mechanism of sensitivity to vinblastine
publisher Nature Publishing Group
series Nature Communications
issn 2041-1723
publishDate 2018-08-01
description 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.
url https://doi.org/10.1038/s41467-018-05036-4
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