Randomized Phase Ib/II Study of Gemcitabine Plus Placebo or Vismodegib, a Hedgehog Pathway Inhibitor, in Patients With Metastatic Pancreatic Cancer

Daniel V.T. Catenacci(St James's University Hospital), Melissa R. Junttila(St James's University Hospital), Theodore Karrison(St James's University Hospital), Nathan Bahary(St James's University Hospital), M. Naomi Horiba(St James's University Hospital), Sreenivasa Nattam(St James's University Hospital), Robert Marsh(St James's University Hospital), James A. Wallace(Ingalls Memorial Hospital), Mark Kozloff(Ingalls Memorial Hospital), Lakshmi Rajdev(St James's University Hospital), Deirdre Jill Cohen(St James's University Hospital), James L. Wade(St James's University Hospital), Bethany Sleckman(St James's University Hospital), Heinz‐Josef Lenz(St James's University Hospital), Patrick J. Stiff(St James's University Hospital), Pankaj Kumar(St James's University Hospital), Peng Xu(St James's University Hospital), Les Henderson(St James's University Hospital), Naoko Takebe(St James's University Hospital), Ravi Salgia(St James's University Hospital), Xi Wang(St James's University Hospital), Walter M. Stadler(St James's University Hospital), Frédéric J. de Sauvage(St James's University Hospital), Hedy L. Kindler(St James's University Hospital)
Journal of Clinical Oncology
November 3, 2015
Cited by 538

Abstract

PURPOSE: Sonic hedgehog (SHH), an activating ligand of smoothened (SMO), is overexpressed in > 70% of pancreatic cancers (PCs). We investigated the impact of vismodegib, an SHH antagonist, plus gemcitabine (GV) or gemcitabine plus placebo (GP) in a multicenter phase Ib/randomized phase II trial and preclinical PC models. PATIENTS AND METHODS: Patients with PC not amenable to curative therapy who had received no prior therapy for metastatic disease and had Karnofsky performance score ≥ 80 were enrolled. Patients were randomly assigned in a one-to-one ratio to GV or GP. The primary end point was progression-free-survival (PFS). Exploratory correlative studies included serial SHH serum levels and contrast perfusion computed tomography imaging. To further investigate putative biologic mechanisms of SMO inhibition, two autochthonous pancreatic cancer models (Kras(G12D); p16/p19(fl/fl); Pdx1-Cre and Kras(G12D); p53(R270H/wt); Pdx1-Cre) were studied. RESULTS: No safety issues were identified in the phase Ib portion (n = 7), and the phase II study enrolled 106 evaluable patients (n = 53 in each arm). Median PFS was 4.0 and 2.5 months for GV and GP arms, respectively (95% CI, 2.5 to 5.3 and 1.9 to 3.8, respectively; adjusted hazard ratio, 0.81; 95% CI, 0.54 to 1.21; P = .30). Median overall survival (OS) was 6.9 and 6.1 months for GV and GP arms, respectively (95% CI, 5.8 to 8.0 and 5.0 to 8.0, respectively; adjusted hazard ratio, 1.04; 95% CI, 0.69 to 1.58; P = .84). Response rates were not significantly different. There were no significant associations between correlative markers and overall response rate, PFS, or OS. Preclinical trials revealed no significant differences with vismodegib in drug delivery, tumor growth rate, or OS in either model. CONCLUSION: The addition of vismodegib to gemcitabine in an unselected cohort did not improve overall response rate, PFS, or OS in patients with metastatic PC. Our preclinical and clinical results revealed no statistically significant differences with respect to drug delivery or treatment efficacy using vismodegib.


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