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Dual Inhibition of Hedgehog and c-Met Pathways for Pancreatic Cancer Treatment

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机构： [1]Johns Hopkins Univ, Sch Med, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD 21231 USA; [2]Johns Hopkins Univ, Sch Med, Dept Oncol, Baltimore, MD 21231 USA; [3]Johns Hopkins Univ, Sch Med, Grad Program Cellular & Mol Med, Baltimore, MD 21231 USA; [4]Zhejiang Univ, Affiliated Hosp 2, Dept Surg Oncol, Sch Med, Hangzhou, Zhejiang, Peoples R China; [5]Univ Sch Med, Canc Inst, Hangzhou, Zhejiang, Peoples R China; [6]Sun Yat Sen Univ, Dept Hepatobiliary Oncol, Canc Ctr, State Key Lab Southern China,Collaborat Innovat C, Guangzhou, Guangdong, Peoples R China; [7]Chinese Acad Med Sci, Canc Hosp, Pancreat & Gastr Surg Dept, Peking Union Med Coll, Beijing, Peoples R China; [8]Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21231 USA; [9]Johns Hopkins Univ, Sch Med, Dept Surg, Baltimore, MD 21231 USA; [10]Johns Hopkins Univ, Sch Med, Skip Viragh Ctr Pancreat Canc, Baltimore, MD 21231 USA; [11]Johns Hopkins Univ, Dept Oncol, Sidney Kimmel Canc Ctr, Sch Med, 1650 Orleans St,CRB1,Room 488, Baltimore, MD 21231 USA

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Pancreatic ductal adenocarcinoma (PDAC) is one of the most chemotherapy-and radiotherapy-resistant tumors. The c-Met and Hedgehog (Hh) pathways have been shown previously by our group to be key regulatory pathways in the primary tumor growth and metastases formation. Targeting both the HGF/c-Met and Hh pathways has shown promising results in preclinical studies; however, the benefits were not readily translated into clinical trials with PDAC patients. In this study, utilizing mouse models of PDAC, we showed that inhibition of either HGF/c-Met or Hh pathways sensitize the PDAC tumors to gemcitabine, resulting in decreased primary tumor volume as well as significant reduction of metastatic tumor burden. However, prolonged treatment of single HGF/c-Met or Hh inhibitor leads to resistance to these single inhibitors, likely because the single c-Met treatment leads to enhanced expression of Shh, and vice versa. Targeting both the HGF/c-Met and Hh pathways simultaneously overcame the resistance to the single-inhibitor treatment and led to a more potent antitumor effect in combination with the chemotherapy treatment. (C) 2017 AACR.

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出版当年[2017]版：

大类 | 2 区医学

小类 | 2 区肿瘤学

最新[2023]版：

大类 | 2 区医学

小类 | 2 区肿瘤学

第一作者：

第一作者机构： [1]Johns Hopkins Univ, Sch Med, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD 21231 USA; [2]Johns Hopkins Univ, Sch Med, Dept Oncol, Baltimore, MD 21231 USA; [3]Johns Hopkins Univ, Sch Med, Grad Program Cellular & Mol Med, Baltimore, MD 21231 USA;

通讯作者：

通讯机构： [1]Johns Hopkins Univ, Sch Med, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD 21231 USA; [2]Johns Hopkins Univ, Sch Med, Dept Oncol, Baltimore, MD 21231 USA; [3]Johns Hopkins Univ, Sch Med, Grad Program Cellular & Mol Med, Baltimore, MD 21231 USA; [9]Johns Hopkins Univ, Sch Med, Dept Surg, Baltimore, MD 21231 USA; [10]Johns Hopkins Univ, Sch Med, Skip Viragh Ctr Pancreat Canc, Baltimore, MD 21231 USA; [11]Johns Hopkins Univ, Dept Oncol, Sidney Kimmel Canc Ctr, Sch Med, 1650 Orleans St,CRB1,Room 488, Baltimore, MD 21231 USA

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