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Chang Jie Chen
Researcher at Harvard University
Publications - 7
Citations - 6856
Chang Jie Chen is an academic researcher from Harvard University. The author has contributed to research in topics: Gastrointestinal stromal tumors (GISTs) & PDGFRA. The author has an hindex of 7, co-authored 7 publications receiving 6521 citations. Previous affiliations of Chang Jie Chen include Brigham and Women's Hospital.
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Journal ArticleDOI
PDGFRA Activating Mutations in Gastrointestinal Stromal Tumors
Michael Heinrich,Christopher L. Corless,Anette Duensing,Laura McGreevey,Chang Jie Chen,Nora E. Joseph,Samuel Singer,Diana J. Griffith,Andrea Haley,Ajia Town,George D. Demetri,Christopher D.M. Fletcher,Jonathan A. Fletcher,Jonathan A. Fletcher +13 more
TL;DR: Tumors expressing KIT or PDGFRA oncoproteins were indistinguishable with respect to activation of downstream signaling intermediates and cytogenetic changes associated with tumor progression, suggesting KIT and PDGFra mutations appear to be alternative and mutually exclusive oncogenic mechanisms in GISTs.
Journal ArticleDOI
Kinase Mutations and Imatinib Response in Patients With Metastatic Gastrointestinal Stromal Tumor
Michael Heinrich,Christopher L. Corless,George D. Demetri,Charles D. Blanke,Margaret von Mehren,Heikki Joensuu,Laura McGreevey,Chang Jie Chen,Annick D. Van den Abbeele,Brian J. Druker,Beate Kiese,Burton L. Eisenberg,Peter J. Roberts,Samuel Singer,Christopher D.M. Fletcher,Sandra Silberman,Sasa Dimitrijevic,Jonathan A. Fletcher +17 more
TL;DR: Activating mutations of KIT or PDGFRA are found in the vast majority of GISTs, and the mutational status of these oncoproteins is predictive of clinical response to imatinib.
Journal ArticleDOI
Molecular Correlates of Imatinib Resistance in Gastrointestinal Stromal Tumors
Michael Heinrich,Christopher L. Corless,Charles D. Blanke,George D. Demetri,Heikki Joensuu,Peter J. Roberts,Burton L. Eisenberg,Margaret von Mehren,Christopher D.M. Fletcher,Katrin Sandau,Karen McDougall,Wen-Bin Ou,Chang Jie Chen,Jonathan A. Fletcher +13 more
TL;DR: Using RNAi technology, it is demonstrated that imatinib-resistant GIST cells remain dependent on KIT kinase activity for activation of critical downstream signaling pathways, which has implications for future approaches to the growing problem ofImatinib resistance in patients with advanced GISTs.
Journal ArticleDOI
KIT extracellular and kinase domain mutations in gastrointestinal stromal tumors.
Marcia L. Lux,Brian P. Rubin,Tara L. Biase,Chang Jie Chen,Timothy Maclure,George D. Demetri,Sheng Xiao,Samuel Singer,Samuel Singer,Christopher D.M. Fletcher,Christopher D.M. Fletcher,Jonathan A. Fletcher,Jonathan A. Fletcher +12 more
TL;DR: Findings indicate that KIT may be activated by mutations in at least three domains-extracellular, juxtamembrane, and kinase-in GISTs.
Journal ArticleDOI
Prognostic Value of KIT Mutation Type, Mitotic Activity, and Histologic Subtype in Gastrointestinal Stromal Tumors
Samuel Singer,Brian P. Rubin,Marcia L. Lux,Chang Jie Chen,George D. Demetri,Christopher D.M. Fletcher,Jonathan A. Fletcher +6 more
TL;DR: The results suggest that KIT mutation and activation are important in GIST pathogenesis and also may provide important prognostic information.