Antitumor effect of FGFR inhibitors on a novel cholangiocarcinoma patient derived xenograft mouse model endogenously expressing an FGFR2-CCDC6 fusion protein
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- 作者：Yu Wanga ; b ; 1 ; Xiwei Dingb ; c ; 1 ; Shaoqing Wangb ; d ; 1 ; Catherine D. Moserb ; 1 ; Hassan M. Shalehb ; Essa A. Mohamedb ; Roongruedee Chaiteerakijb ; Loretta K. Alloteyb ; Gang Chenb ; Katsuyuki Miyabeb ; Melissa S. McNultye ; Albert Ndzengueb ; Emily G. Barr Fritcherf ; Ryan A. Knudsonf ; Patricia T. Greippf ; Karl J. Clarke ; Michael S. Torbensonf ; Benjamin R. Kippf ; Jie Zhoua ; Michael T. Barrettg ; Michael P. Gustafsonf ; Steven R. Albertsh ; Mitesh J. Boradg ; Lewis R. Robertsb ; roberts.lewis@mayo.edu" class="auth_mail" title="E-mail the corresponding author
- 关键词：Intrahepatic cholangiocarcinoma ; FGFR2 fusion ; Ponatinib ; Dovitinib ; BGJ398
- 刊名：Cancer Letters
- 出版年：2016
- 出版时间：28 September 2016
- 年：2016
- 卷：380
- 期：1
- 页码：163-173
- 全文大小：7498 K
文摘
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We established a new PDX mouse model bearing an FGFR2-CCDC6 fusion protein from a metastatic lung nodule of an iCCA patient.
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FGFR inhibitors, ponatinib, dovitinib and BGJ398, inhibit FGFR signaling, and tumor growth in iCCAs harboring FGFR2 fusions.
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Ponatinib was not additive or synergistic with standard gemcitabine and cisplatin chemotherapy on this PDX model.
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There was a potential therapeutic advantage of BGJ398 over dovitinib and ponatinib in this model.