Programmed cell death ligand 1 (PD-L1, CD274) in cholangiocarcinoma - correlation with clinicopathological data and comparison of antibodies.


Journal

BMC cancer
ISSN: 1471-2407
Titre abrégé: BMC Cancer
Pays: England
ID NLM: 100967800

Informations de publication

Date de publication:
15 Jan 2019
Historique:
received: 13 06 2018
accepted: 26 12 2018
entrez: 17 1 2019
pubmed: 17 1 2019
medline: 30 4 2019
Statut: epublish

Résumé

Cholangiocarcinoma (CCA) may arise in the intra- or extrahepatic biliary tract and is associated with a poor prognosis. Despite recent advances, to date there is still no established targeted therapeutic approach available. Non-surgical therapeutic agents are urgently needed, as most patients are non-eligible to surgical resection. Anti-PD-L1 therapy prevents cancer cells from evading the immune system and has emerged as a new treatment option in several cancer entities. Recently, PD-L1 expression has been analyzed in comparably small CCA patient cohorts. However, a systematic validation of different PD-L1 antibodies has not been performed in CCA so far. We stained a tissue microarray consisting of 170 patients, including 72 intrahepatic cholangiocarcinomas (iCCAs), 57 perihilar cholangiocarcinomas (pCCAs) and 41 distal cholangiocarcinomas (dCCAs) by immunohistochemistry and evaluated PD-L1 positivity in tumor and stromal cells. We analyzed three different PD-L1 antibodies (clones 28-8, SP142, and SP263) that are frequently used and recommended for predictive diagnostic testing in other cancer types. For PD-L1 antibody clone SP263, 5% of iCCAs, 4% of pCCAs and 3% of dCCAs exhibited PD-L1 expression on tumor cells, thereby showing the highest frequencies of PD-L1 positivity. Accordingly, highest PD-L1 positivity rates of stromal cells with 31% in iCCA, 40% in pCCA and 61% in dCCA were detected for clone SP263. Agreement of PD-L1 positivity in tumor cells was moderate for clone 28-8 and SP263 (κ = 0.44) and poor between 28-8 and SP142 (κ = 0.13), as well as  SP142 and SP263 (κ = 0.11), respectively. Statistical analyses of PD-L1 expression (clone SP263) on tumor cells with clinicopathological data revealed a positive correlation with shortened overall survival in CCA patients. Selection of appropriate PD-L1 antibodies and careful evaluation of immunohistochemical staining patterns have a significant impact on PD-L1 testing in CCA. Clinical trials are necessary to investigate the putative beneficial effects of PD-L1 targeted immunotherapy in CCA patients.

Sections du résumé

BACKGROUND BACKGROUND
Cholangiocarcinoma (CCA) may arise in the intra- or extrahepatic biliary tract and is associated with a poor prognosis. Despite recent advances, to date there is still no established targeted therapeutic approach available. Non-surgical therapeutic agents are urgently needed, as most patients are non-eligible to surgical resection. Anti-PD-L1 therapy prevents cancer cells from evading the immune system and has emerged as a new treatment option in several cancer entities. Recently, PD-L1 expression has been analyzed in comparably small CCA patient cohorts. However, a systematic validation of different PD-L1 antibodies has not been performed in CCA so far.
METHODS METHODS
We stained a tissue microarray consisting of 170 patients, including 72 intrahepatic cholangiocarcinomas (iCCAs), 57 perihilar cholangiocarcinomas (pCCAs) and 41 distal cholangiocarcinomas (dCCAs) by immunohistochemistry and evaluated PD-L1 positivity in tumor and stromal cells. We analyzed three different PD-L1 antibodies (clones 28-8, SP142, and SP263) that are frequently used and recommended for predictive diagnostic testing in other cancer types.
RESULTS RESULTS
For PD-L1 antibody clone SP263, 5% of iCCAs, 4% of pCCAs and 3% of dCCAs exhibited PD-L1 expression on tumor cells, thereby showing the highest frequencies of PD-L1 positivity. Accordingly, highest PD-L1 positivity rates of stromal cells with 31% in iCCA, 40% in pCCA and 61% in dCCA were detected for clone SP263. Agreement of PD-L1 positivity in tumor cells was moderate for clone 28-8 and SP263 (κ = 0.44) and poor between 28-8 and SP142 (κ = 0.13), as well as  SP142 and SP263 (κ = 0.11), respectively. Statistical analyses of PD-L1 expression (clone SP263) on tumor cells with clinicopathological data revealed a positive correlation with shortened overall survival in CCA patients.
CONCLUSIONS CONCLUSIONS
Selection of appropriate PD-L1 antibodies and careful evaluation of immunohistochemical staining patterns have a significant impact on PD-L1 testing in CCA. Clinical trials are necessary to investigate the putative beneficial effects of PD-L1 targeted immunotherapy in CCA patients.

Identifiants

pubmed: 30646854
doi: 10.1186/s12885-018-5254-0
pii: 10.1186/s12885-018-5254-0
pmc: PMC6332835
doi:

Substances chimiques

Antibodies 0
B7-H1 Antigen 0
CD274 protein, human 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

72

Références

N Engl J Med. 2010 Apr 8;362(14):1273-81
pubmed: 20375404
Clin Cancer Res. 2013 Mar 1;19(5):1021-34
pubmed: 23460533
N Engl J Med. 2015 May 21;372(21):2018-28
pubmed: 25891174
N Engl J Med. 2015 Jul 2;373(1):23-34
pubmed: 26027431
Nat Genet. 2015 Sep;47(9):967-8
pubmed: 26313225
Clin Cancer Res. 2016 Jan 15;22(2):470-8
pubmed: 26373575
Lancet. 2016 Apr 9;387(10027):1540-50
pubmed: 26712084
Crit Rev Oncol Hematol. 2016 Apr;100:88-98
pubmed: 26895815
Ann Surg Oncol. 2016 Aug;23(8):2610-7
pubmed: 27012989
Nat Rev Gastroenterol Hepatol. 2016 May;13(5):261-80
pubmed: 27095655
J Hematol Oncol. 2016 May 27;9(1):47
pubmed: 27234522
Expert Rev Clin Immunol. 2017 Jan;13(1):77-84
pubmed: 27426025
J Urol. 2017 Jan;197(1):14-22
pubmed: 27460757
Int J Biol Markers. 2017 Mar 2;32(1):e68-e74
pubmed: 27470134
J Thorac Oncol. 2016 Nov;11(11):1927-1939
pubmed: 27496650
Pathologe. 2016 Nov;37(6):557-567
pubmed: 27510417
Oncotarget. 2016 Nov 8;7(45):74350-74361
pubmed: 27542277
N Engl J Med. 2016 Nov 10;375(19):1823-1833
pubmed: 27718847
Eur J Surg Oncol. 2017 Mar;43(3):604-611
pubmed: 27769635
J Clin Oncol. 2016 Dec;34(34):4102-4109
pubmed: 27863197
J Thorac Oncol. 2017 Feb;12(2):208-222
pubmed: 27913228
Pathol Int. 2017 Mar;67(3):163-170
pubmed: 28139862
Ann Pathol. 2017 Feb;37(1):39-45
pubmed: 28159404
J Hepatol. 2017 Sep;67(3):632-644
pubmed: 28389139
Histopathology. 2017 Sep;71(3):383-392
pubmed: 28419539
Oncotarget. 2017 Apr 11;8(15):24644-24651
pubmed: 28445951
Cold Spring Harb Mol Case Stud. 2017 Sep 1;3(5):null
pubmed: 28619747
Asian Pac J Cancer Prev. ;18(6):1671-1674
pubmed: 28670887
Oncol Lett. 2017 Jul;14(1):250-256
pubmed: 28693161

Auteurs

Mark Kriegsmann (M)

Institute of Pathology, University Heidelberg, Im Neuenheimer Feld 224, Heidelberg, Germany.

Stephanie Roessler (S)

Institute of Pathology, University Heidelberg, Im Neuenheimer Feld 224, Heidelberg, Germany.

Katharina Kriegsmann (K)

Department of Rheumatology, Oncology and Hematology, University of Heidelberg, Heidelberg, Germany.

Marcus Renner (M)

Institute of Pathology, University Heidelberg, Im Neuenheimer Feld 224, Heidelberg, Germany.

Rémi Longuespée (R)

Institute of Pathology, University Heidelberg, Im Neuenheimer Feld 224, Heidelberg, Germany.

Thomas Albrecht (T)

Institute of Pathology, University Heidelberg, Im Neuenheimer Feld 224, Heidelberg, Germany.

Moritz Loeffler (M)

Institute of Pathology, University Heidelberg, Im Neuenheimer Feld 224, Heidelberg, Germany.

Stephan Singer (S)

Institute of Pathology, University Heidelberg, Im Neuenheimer Feld 224, Heidelberg, Germany.

Arianeb Mehrabi (A)

Department of General Visceral and Transplantation Surgery, University Hospital Heidelberg, Im Neuenheimer Feld 110, Heidelberg, Germany.
Liver Cancer Center Heidelberg (LCCH), Heidelberg, Germany.

Monika Nadja Vogel (MN)

Diagnostic and Interventional Radiology, Thoraxklinik at University Hospital of Heidelberg, Heidelberg, Germany.

Anita Pathil (A)

Department of Internal Medicine IV, Gastroenterology and Hepatology, University Hospital Heidelberg, Im Neuenheimer Feld 410, Heidelberg, Germany.

Bruno Köhler (B)

Department of Medical Oncology, University Hospital Heidelberg, National Center for Tumor Diseases, Heidelberg, Germany.
Liver Cancer Center Heidelberg (LCCH), Heidelberg, Germany.

Christoph Springfeld (C)

Department of Medical Oncology, University Hospital Heidelberg, National Center for Tumor Diseases, Heidelberg, Germany.
Liver Cancer Center Heidelberg (LCCH), Heidelberg, Germany.

Christian Rupp (C)

Department of Internal Medicine IV, Gastroenterology and Hepatology, University Hospital Heidelberg, Im Neuenheimer Feld 410, Heidelberg, Germany.
Liver Cancer Center Heidelberg (LCCH), Heidelberg, Germany.

Karl Heinz Weiss (KH)

Department of Internal Medicine IV, Gastroenterology and Hepatology, University Hospital Heidelberg, Im Neuenheimer Feld 410, Heidelberg, Germany.
Liver Cancer Center Heidelberg (LCCH), Heidelberg, Germany.

Benjamin Goeppert (B)

Institute of Pathology, University Heidelberg, Im Neuenheimer Feld 224, Heidelberg, Germany. Benjamin.goeppert@med.uni-heidelberg.de.
Liver Cancer Center Heidelberg (LCCH), Heidelberg, Germany. Benjamin.goeppert@med.uni-heidelberg.de.

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Classifications MeSH