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Cancer Immunology Research

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Research Article

Soluble PD-L1 as a biomarker in malignant melanoma and checkpoint blockade

Jun Zhou, Kathleen M. Mahoney, Anita Giobbie-Hurder, Fengmin Zhao, Sandra Lee, Xiaoyun Liao, Scott Rodig, Jingjing Li, Xinqi Wu, Lisa H. Butterfield, Matthias Piesche, Michael P. Manos, Lauren M. Eastman, Glenn Dranoff, Gordon J. Freeman and F. Stephen Hodi
Jun Zhou
Medical Oncology, Dana-Farber Cancer Institute
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Kathleen M. Mahoney
Medical Oncology, Dana-Farber Cancer Institute
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Anita Giobbie-Hurder
Biostatistics & Computational Biology, Dana-Farber Cancer Institute
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Fengmin Zhao
Biostatistics & Computational Biology, Dana-Farber Cancer Institute
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Sandra Lee
Dana-Farber Cancer Institute
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Xiaoyun Liao
Medical Oncology, Dana-Farber Cancer Institute
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Scott Rodig
Pathology, Brigham and Women's Hospital
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Jingjing Li
Medical Oncology, Dana-Farber Cancer Institute
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Xinqi Wu
Medical Oncology, Dana-Farber Cancer Institute
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Lisa H. Butterfield
University of Pittsburgh Cancer Institute, University of Pittsburgh
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Matthias Piesche
Biomedical Research Laboratories, Medicine Faculty, Catholic University of Maule
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Michael P. Manos
Center for Immuno-Oncology, Dana-Farber Cancer Institute
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Lauren M. Eastman
Center for Immuno-Oncology, Dana-Farber Cancer Institute
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Glenn Dranoff
Novartis Institutes for BioMedical Research
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Gordon J. Freeman
Center for Immuno-Oncology, Dana-Farber Cancer Institute
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F. Stephen Hodi
Medical Oncology, Dana-Farber Cancer Institute
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  • For correspondence: stephen_hodi@dfci.harvard.edu
DOI: 10.1158/2326-6066.CIR-16-0329
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Abstract

Blockade of the pathway including Programmed death-ligand 1 (PD-L1) and its receptor Programmed cell death protein 1 (PD-1) has produced clinical benefits in patients with a variety of cancers.  Elevated levels of soluble PD-L1 (sPD-L1) have been associated with worse prognosis in renal cell carcinoma and multiple myeloma.  However, the regulatory roles and function of sPD-L1 particularly in connection with immune checkpoint blockade treatment are not fully understood.  We identified four splice variants of PD-L1 in melanoma cells, and all of them are secreted.  Secretion of sPD-L1 resulted from alternate splicing activities, cytokine induction, cell stress, cell injury and cell death in melanoma cells.  Pretreatment levels of sPD-L1 were elevated in stage IV melanoma patient sera compared to healthy donors.  High pre-treatment levels of sPD-L1 were associated with increased likelihood of progressive disease in patients treated by CTLA-4 or PD-1 blockade.  Although changes in circulating sPD-L1 early after treatment could not distinguish responders from those with progressive disease, after five months of treatment by CTLA-4 or PD-1 blockade patients who had increased circulating sPD-L1 had greater likelihood of developing a partial response.  Induction of sPD-L1 was associated with increased circulating cytokines after CTLA-4 blockade but not following PD-1 blockade.  Circulating sPD-L1 is a prognostic biomarker that may predict outcomes for subgroups of patients receiving checkpoint inhibitors.

  • Received November 16, 2016.
  • Revision received March 13, 2017.
  • Accepted May 2, 2017.
  • Copyright ©2017, American Association for Cancer Research.
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Published OnlineFirst May 18, 2017
doi: 10.1158/2326-6066.CIR-16-0329

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Soluble PD-L1 as a biomarker in malignant melanoma and checkpoint blockade
Jun Zhou, Kathleen M. Mahoney, Anita Giobbie-Hurder, Fengmin Zhao, Sandra Lee, Xiaoyun Liao, Scott Rodig, Jingjing Li, Xinqi Wu, Lisa H. Butterfield, Matthias Piesche, Michael P. Manos, Lauren M. Eastman, Glenn Dranoff, Gordon J. Freeman and F. Stephen Hodi
Cancer Immunol Res May 18 2017 DOI: 10.1158/2326-6066.CIR-16-0329

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Soluble PD-L1 as a biomarker in malignant melanoma and checkpoint blockade
Jun Zhou, Kathleen M. Mahoney, Anita Giobbie-Hurder, Fengmin Zhao, Sandra Lee, Xiaoyun Liao, Scott Rodig, Jingjing Li, Xinqi Wu, Lisa H. Butterfield, Matthias Piesche, Michael P. Manos, Lauren M. Eastman, Glenn Dranoff, Gordon J. Freeman and F. Stephen Hodi
Cancer Immunol Res May 18 2017 DOI: 10.1158/2326-6066.CIR-16-0329
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