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Invited Commentary
July 18, 2019

Dual Checkpoint Inhibition in Pancreatic Cancer: Revealing the Limitations of Synergy and the Potential of Novel Combinations

Author Affiliations
  • 1Skip Viragh Center for Pancreatic Cancer Research and Clinical Care, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland
JAMA Oncol. Published online July 18, 2019. doi:10.1001/jamaoncol.2019.1583

Immunotherapy has profoundly altered the treatment landscape in oncology. Immune checkpoint inhibition (ICI) using anti–programmed cell death protein (PD-1) and/or anti–programmed death-ligand 1 (PD-L1) and anti–cytotoxic T-lymphocyte-associated protein 4 (CLTA-4) has led to significant achievements in numerous malignant diseases. Yet, the success of checkpoint inhibition has not translated to every tumor type. With the notable exception of the 1% to 2% of patients with mismatch repair-deficient metastatic pancreatic cancer where anti–PD-1 therapy alone can lead to significant and durable responses,1 pancreatic ductal adenocarcinoma (PDAC) has remained refractory to single-agent immunotherapy.

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