PD-L1 (CD274) promoter hypomethylation predicts immunotherapy response in metastatic urothelial carcinoma

PD-L1 status assessed by immunohistochemistry (IHC) has failed to reliably predict outcomes for patients with metastatic urothelial carcinoma (mUC) on immune checkpoint blockade (ICB). PD-L1 promoter methylation is an epigenetic mechanism that has been shown to regulate PD-L1 mRNA expression in vari...

Full description

Saved in:
Bibliographic Details
Main Authors: Niklas Klümper, Lennert Wüst, Jonas Saal, Damian J. Ralser, Romina Zarbl, Jonas Jarczyk, Johannes Breyer, Danijel Sikic, Bernd Wullich, Christian Bolenz, Florian Roghmann, Michael Hölzel, Manuel Ritter, Sebastian Strieth, Arndt Hartmann, Philipp Erben, Ralph M. Wirtz, Jennifer Landsberg, Dimo Dietrich, Markus Eckstein
Format: Article
Language:English
Published: Taylor & Francis Group 2023-12-01
Series:OncoImmunology
Subjects:
Online Access:https://www.tandfonline.com/doi/10.1080/2162402X.2023.2267744
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1850238360788926464
author Niklas Klümper
Lennert Wüst
Jonas Saal
Damian J. Ralser
Romina Zarbl
Jonas Jarczyk
Johannes Breyer
Danijel Sikic
Bernd Wullich
Christian Bolenz
Florian Roghmann
Michael Hölzel
Manuel Ritter
Sebastian Strieth
Arndt Hartmann
Philipp Erben
Ralph M. Wirtz
Jennifer Landsberg
Dimo Dietrich
Markus Eckstein
author_facet Niklas Klümper
Lennert Wüst
Jonas Saal
Damian J. Ralser
Romina Zarbl
Jonas Jarczyk
Johannes Breyer
Danijel Sikic
Bernd Wullich
Christian Bolenz
Florian Roghmann
Michael Hölzel
Manuel Ritter
Sebastian Strieth
Arndt Hartmann
Philipp Erben
Ralph M. Wirtz
Jennifer Landsberg
Dimo Dietrich
Markus Eckstein
author_sort Niklas Klümper
collection DOAJ
description PD-L1 status assessed by immunohistochemistry (IHC) has failed to reliably predict outcomes for patients with metastatic urothelial carcinoma (mUC) on immune checkpoint blockade (ICB). PD-L1 promoter methylation is an epigenetic mechanism that has been shown to regulate PD-L1 mRNA expression in various malignancies. The aim of our present study was to evaluate the predictive potential of PD-L1 promoter methylation status (mPD-L1) in ICB-treated mUC compared to conventional IHC-based PD-L1 assessment. We quantified mPD-L1 in formalin-fixed and paraffin-embedded tissue sections using an established quantitative methylation-specific PCR assay (qMSP) in a well-characterized multicenter ICB-treated cohort comprising N = 107 patients with mUC. Additionally, PD-L1 protein expression in tumor tissues was assessed using regulatory approved IHC protocols. The effect of pharmacological hypomethylation by the DNA methyltransferase inhibitor decitabine in combination with interferon-γ stimulation in urothelial carcinoma cell lines was investigated by IHC and FACS. mPD-L1 hypomethylation predicted objective response rate at the first staging on ICB. Patients with tumors categorized as PD-L1 hypomethylated (lower quartile) showed significantly prolonged progression-free (PFS) and overall survival (OS) after ICB initiation. In contrast, PD-L1 protein expression status neither correlated with response nor survival. In multivariable Cox regression analyses, PD-L1 promoter hypermethylation remained an independent predictor of unfavorable PFS and OS. In urothelial carcinoma cell lines, pharmacological demethylation led to an upregulation of membranous PD-L1 expression and an enhanced inducibility of PD-L1 expression by interferon γ. Hypomethylation of the PD-L1 promoter is a promising predictive biomarker for response to ICB in patients with mUC.
format Article
id doaj-art-db84a83835784401bcaeca4a8df3487d
institution OA Journals
issn 2162-402X
language English
publishDate 2023-12-01
publisher Taylor & Francis Group
record_format Article
series OncoImmunology
spelling doaj-art-db84a83835784401bcaeca4a8df3487d2025-08-20T02:01:29ZengTaylor & Francis GroupOncoImmunology2162-402X2023-12-0112110.1080/2162402X.2023.2267744PD-L1 (CD274) promoter hypomethylation predicts immunotherapy response in metastatic urothelial carcinomaNiklas Klümper0Lennert Wüst1Jonas Saal2Damian J. Ralser3Romina Zarbl4Jonas Jarczyk5Johannes Breyer6Danijel Sikic7Bernd Wullich8Christian Bolenz9Florian Roghmann10Michael Hölzel11Manuel Ritter12Sebastian Strieth13Arndt Hartmann14Philipp Erben15Ralph M. Wirtz16Jennifer Landsberg17Dimo Dietrich18Markus Eckstein19Department of Urology and Pediatric Urology, University Medical Center Bonn (UKB), Bonn, GermanyCenter for Integrated Oncology, Aachen/Bonn/Cologne/Düsseldorf (CIO-ABCD), GermanyCenter for Integrated Oncology, Aachen/Bonn/Cologne/Düsseldorf (CIO-ABCD), GermanyInstitute of Experimental Oncology, University Medical Center Bonn (UKB), Bonn, GermanyCenter for Integrated Oncology, Aachen/Bonn/Cologne/Düsseldorf (CIO-ABCD), GermanyDepartment of Urology and Urosurgery, Medical Faculty Mannheim, University of Heidelberg, Mannheim, GermanyDepartment of Urology, Caritas Hospital St. Josef, University of Regensburg, Regensburg, GermanyCenter for Integrated Oncology, Bavarian Center for Cancer Research (Bayerisches Zentrum für Krebsforschung, BZKF), Erlangen, GermanyCenter for Integrated Oncology, Bavarian Center for Cancer Research (Bayerisches Zentrum für Krebsforschung, BZKF), Erlangen, GermanyDepartment of Urology, University Hospital Ulm, Ulm, GermanyDepartment of Urology, Ruhr-University Bochum, Herne, GermanyInstitute of Experimental Oncology, University Medical Center Bonn (UKB), Bonn, GermanyDepartment of Urology and Pediatric Urology, University Medical Center Bonn (UKB), Bonn, GermanyCenter for Integrated Oncology, Aachen/Bonn/Cologne/Düsseldorf (CIO-ABCD), GermanyCenter for Integrated Oncology, Bavarian Center for Cancer Research (Bayerisches Zentrum für Krebsforschung, BZKF), Erlangen, GermanyDepartment of Urology and Urosurgery, Medical Faculty Mannheim, University of Heidelberg, Mannheim, GermanyCenter for Integrated Oncology, STRATIFYER Molecular Pathology GmbH, Cologne, GermanyCenter for Integrated Oncology, Aachen/Bonn/Cologne/Düsseldorf (CIO-ABCD), GermanyCenter for Integrated Oncology, Aachen/Bonn/Cologne/Düsseldorf (CIO-ABCD), GermanyCenter for Integrated Oncology, Bavarian Center for Cancer Research (Bayerisches Zentrum für Krebsforschung, BZKF), Erlangen, GermanyPD-L1 status assessed by immunohistochemistry (IHC) has failed to reliably predict outcomes for patients with metastatic urothelial carcinoma (mUC) on immune checkpoint blockade (ICB). PD-L1 promoter methylation is an epigenetic mechanism that has been shown to regulate PD-L1 mRNA expression in various malignancies. The aim of our present study was to evaluate the predictive potential of PD-L1 promoter methylation status (mPD-L1) in ICB-treated mUC compared to conventional IHC-based PD-L1 assessment. We quantified mPD-L1 in formalin-fixed and paraffin-embedded tissue sections using an established quantitative methylation-specific PCR assay (qMSP) in a well-characterized multicenter ICB-treated cohort comprising N = 107 patients with mUC. Additionally, PD-L1 protein expression in tumor tissues was assessed using regulatory approved IHC protocols. The effect of pharmacological hypomethylation by the DNA methyltransferase inhibitor decitabine in combination with interferon-γ stimulation in urothelial carcinoma cell lines was investigated by IHC and FACS. mPD-L1 hypomethylation predicted objective response rate at the first staging on ICB. Patients with tumors categorized as PD-L1 hypomethylated (lower quartile) showed significantly prolonged progression-free (PFS) and overall survival (OS) after ICB initiation. In contrast, PD-L1 protein expression status neither correlated with response nor survival. In multivariable Cox regression analyses, PD-L1 promoter hypermethylation remained an independent predictor of unfavorable PFS and OS. In urothelial carcinoma cell lines, pharmacological demethylation led to an upregulation of membranous PD-L1 expression and an enhanced inducibility of PD-L1 expression by interferon γ. Hypomethylation of the PD-L1 promoter is a promising predictive biomarker for response to ICB in patients with mUC.https://www.tandfonline.com/doi/10.1080/2162402X.2023.2267744biomarkerbladder cancerCD274DNA methylationimmune checkpoint blockadeimmunotherapy
spellingShingle Niklas Klümper
Lennert Wüst
Jonas Saal
Damian J. Ralser
Romina Zarbl
Jonas Jarczyk
Johannes Breyer
Danijel Sikic
Bernd Wullich
Christian Bolenz
Florian Roghmann
Michael Hölzel
Manuel Ritter
Sebastian Strieth
Arndt Hartmann
Philipp Erben
Ralph M. Wirtz
Jennifer Landsberg
Dimo Dietrich
Markus Eckstein
PD-L1 (CD274) promoter hypomethylation predicts immunotherapy response in metastatic urothelial carcinoma
OncoImmunology
biomarker
bladder cancer
CD274
DNA methylation
immune checkpoint blockade
immunotherapy
title PD-L1 (CD274) promoter hypomethylation predicts immunotherapy response in metastatic urothelial carcinoma
title_full PD-L1 (CD274) promoter hypomethylation predicts immunotherapy response in metastatic urothelial carcinoma
title_fullStr PD-L1 (CD274) promoter hypomethylation predicts immunotherapy response in metastatic urothelial carcinoma
title_full_unstemmed PD-L1 (CD274) promoter hypomethylation predicts immunotherapy response in metastatic urothelial carcinoma
title_short PD-L1 (CD274) promoter hypomethylation predicts immunotherapy response in metastatic urothelial carcinoma
title_sort pd l1 cd274 promoter hypomethylation predicts immunotherapy response in metastatic urothelial carcinoma
topic biomarker
bladder cancer
CD274
DNA methylation
immune checkpoint blockade
immunotherapy
url https://www.tandfonline.com/doi/10.1080/2162402X.2023.2267744
work_keys_str_mv AT niklasklumper pdl1cd274promoterhypomethylationpredictsimmunotherapyresponseinmetastaticurothelialcarcinoma
AT lennertwust pdl1cd274promoterhypomethylationpredictsimmunotherapyresponseinmetastaticurothelialcarcinoma
AT jonassaal pdl1cd274promoterhypomethylationpredictsimmunotherapyresponseinmetastaticurothelialcarcinoma
AT damianjralser pdl1cd274promoterhypomethylationpredictsimmunotherapyresponseinmetastaticurothelialcarcinoma
AT rominazarbl pdl1cd274promoterhypomethylationpredictsimmunotherapyresponseinmetastaticurothelialcarcinoma
AT jonasjarczyk pdl1cd274promoterhypomethylationpredictsimmunotherapyresponseinmetastaticurothelialcarcinoma
AT johannesbreyer pdl1cd274promoterhypomethylationpredictsimmunotherapyresponseinmetastaticurothelialcarcinoma
AT danijelsikic pdl1cd274promoterhypomethylationpredictsimmunotherapyresponseinmetastaticurothelialcarcinoma
AT berndwullich pdl1cd274promoterhypomethylationpredictsimmunotherapyresponseinmetastaticurothelialcarcinoma
AT christianbolenz pdl1cd274promoterhypomethylationpredictsimmunotherapyresponseinmetastaticurothelialcarcinoma
AT florianroghmann pdl1cd274promoterhypomethylationpredictsimmunotherapyresponseinmetastaticurothelialcarcinoma
AT michaelholzel pdl1cd274promoterhypomethylationpredictsimmunotherapyresponseinmetastaticurothelialcarcinoma
AT manuelritter pdl1cd274promoterhypomethylationpredictsimmunotherapyresponseinmetastaticurothelialcarcinoma
AT sebastianstrieth pdl1cd274promoterhypomethylationpredictsimmunotherapyresponseinmetastaticurothelialcarcinoma
AT arndthartmann pdl1cd274promoterhypomethylationpredictsimmunotherapyresponseinmetastaticurothelialcarcinoma
AT philipperben pdl1cd274promoterhypomethylationpredictsimmunotherapyresponseinmetastaticurothelialcarcinoma
AT ralphmwirtz pdl1cd274promoterhypomethylationpredictsimmunotherapyresponseinmetastaticurothelialcarcinoma
AT jenniferlandsberg pdl1cd274promoterhypomethylationpredictsimmunotherapyresponseinmetastaticurothelialcarcinoma
AT dimodietrich pdl1cd274promoterhypomethylationpredictsimmunotherapyresponseinmetastaticurothelialcarcinoma
AT markuseckstein pdl1cd274promoterhypomethylationpredictsimmunotherapyresponseinmetastaticurothelialcarcinoma