Crizotinib inhibits metabolic inactivation of gemcitabine in ortothopic pancreatic tumors derived from primary cells with c-Met overexpression

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) remains a major unsolved health problem. Most drugs that pass preclinical tests fail in these patients, emphasizing the need of appropriate preclinical models to test novel anticancer strategies. We developed four orthotopic mouse models employing primary human PDAC cells expressing Firefly and Gaussia luciferases, enabling bioluminescence monitoring of tumor growth and metastasis formation. Additional tumor characterization was performed using MR and high frequency ultrasound imaging. Genomic and immunohistochemical analysis revealed c-Met amplification and overexpression in one of four models. Analysis of c-Met inhibitors in vitro showed that crizotinib had the most potent effect. Moreover, we demonstrated synergistic effects between crizotinib and

ORGANISM(S): Homo sapiens

SUBMITTER: Amir Avan 

PROVIDER: E-GEOD-44587 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress