PD-L1 Dependent Immunogenic Landscape in Hot Lung Adenocarcinomas Identified by Transcriptome Analysis.

cold hot immune phenotype lung adenocarcinoma (LUAD) programmed cell death-ligand 1 (PD-L1) protein transcriptome

Journal

Cancers
ISSN: 2072-6694
Titre abrégé: Cancers (Basel)
Pays: Switzerland
ID NLM: 101526829

Informations de publication

Date de publication:
11 Sep 2021
Historique:
received: 08 08 2021
revised: 01 09 2021
accepted: 03 09 2021
entrez: 28 9 2021
pubmed: 29 9 2021
medline: 29 9 2021
Statut: epublish

Résumé

Lung cancer is the most frequent cause of cancer-related deaths worldwide. The clinical development of immune checkpoint blockade has dramatically changed the treatment paradigm for patients with lung cancer. Yet, an improved understanding of PD-1/PD-L1 checkpoint blockade-responsive biology is warranted. We aimed to identify the landscape of immune cell infiltration in primary lung adenocarcinoma (LUAD) in the context of tumoral PD-L1 expression and the extent of immune infiltration ("hot" vs. "cold" phenotype). The study comprises LUAD cases ( Gene set enrichment analysis defined complement, IL-JAK-STAT signaling, KRAS signaling, inflammatory response, TNF-alpha signaling, interferon-gamma response, interferon-alpha response, and allograft rejection as significantly upregulated pathways in the PD-L1-positive hot subgroup. Additionally, we demonstrated that STAT1 is upregulated in the PD-L1-positive hot subgroup and KIT in the PD-L1-negative hot subgroup. The presented study illustrates novel aspects of PD-L1 regulation, with potential biological relevance, as well as relevance for immunotherapy response stratification.

Sections du résumé

BACKGROUND BACKGROUND
Lung cancer is the most frequent cause of cancer-related deaths worldwide. The clinical development of immune checkpoint blockade has dramatically changed the treatment paradigm for patients with lung cancer. Yet, an improved understanding of PD-1/PD-L1 checkpoint blockade-responsive biology is warranted.
METHODS METHODS
We aimed to identify the landscape of immune cell infiltration in primary lung adenocarcinoma (LUAD) in the context of tumoral PD-L1 expression and the extent of immune infiltration ("hot" vs. "cold" phenotype). The study comprises LUAD cases (
RESULTS RESULTS
Gene set enrichment analysis defined complement, IL-JAK-STAT signaling, KRAS signaling, inflammatory response, TNF-alpha signaling, interferon-gamma response, interferon-alpha response, and allograft rejection as significantly upregulated pathways in the PD-L1-positive hot subgroup. Additionally, we demonstrated that STAT1 is upregulated in the PD-L1-positive hot subgroup and KIT in the PD-L1-negative hot subgroup.
CONCLUSION CONCLUSIONS
The presented study illustrates novel aspects of PD-L1 regulation, with potential biological relevance, as well as relevance for immunotherapy response stratification.

Identifiants

pubmed: 34572789
pii: cancers13184562
doi: 10.3390/cancers13184562
pmc: PMC8469831
pii:
doi:

Types de publication

Journal Article

Langues

eng

Subventions

Organisme : Bristol-Myers Squibb Foundation
ID : CA209-8C7

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Auteurs

Jutta Kirfel (J)

Institute of Pathology, University Hospital Schleswig-Holstein, Campus Luebeck, 23538 Luebeck, Germany.

Christiane Charlotte Kümpers (CC)

Institute of Pathology, University Hospital Schleswig-Holstein, Campus Luebeck, 23538 Luebeck, Germany.

Anke Fähnrich (A)

Medical Systems Biology Group, Luebeck Institute of Experimental Dermatology, University of Luebeck, 23538 Luebeck, Germany.
Institute for Cardiogenetics, University of Luebeck, 23538 Luebeck, Germany.

Carsten Heidel (C)

Institute of Pathology, University Hospital Schleswig-Holstein, Campus Luebeck, 23538 Luebeck, Germany.

Mladen Jokic (M)

Institute of Pathology, University Hospital Schleswig-Holstein, Campus Luebeck, 23538 Luebeck, Germany.

Ignacija Vlasic (I)

Institute of Pathology, University Hospital Schleswig-Holstein, Campus Luebeck, 23538 Luebeck, Germany.
Laboratory for Protein Dynamics, Division of Molecular Medicine, Ruđer Bošković Institute, 10000 Zagreb, Croatia.

Sebastian Marwitz (S)

Pathology, Research Center Borstel, Leibniz Lung Center, 23845 Borstel, Germany.
Airway Research Center North (ARCN), The German Center for Lung Research (DZL), 23845 Borstel, Germany.

Torsten Goldmann (T)

Pathology, Research Center Borstel, Leibniz Lung Center, 23845 Borstel, Germany.
Airway Research Center North (ARCN), The German Center for Lung Research (DZL), 23845 Borstel, Germany.

Helen Pasternack (H)

Institute of Pathology, University Hospital Schleswig-Holstein, Campus Luebeck, 23538 Luebeck, Germany.

Sabine Bohnet (S)

Department of Pulmonology, University Hospital Schleswig-Holstein, Campus Luebeck, Ratzeburger Allee 160, 23538 Luebeck, Germany.

Danny Jonigk (D)

Institute for Pathology, Hannover Medical School, 30625 Hannover, Germany.
Biomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), The German Center for Lung Research (DZL), 30625 Hannover, Germany.

Mark P Kühnel (MP)

Institute for Pathology, Hannover Medical School, 30625 Hannover, Germany.
Biomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), The German Center for Lung Research (DZL), 30625 Hannover, Germany.

Anne Offermann (A)

Institute of Pathology, University Hospital Schleswig-Holstein, Campus Luebeck, 23538 Luebeck, Germany.

Hauke Busch (H)

Medical Systems Biology Group, Luebeck Institute of Experimental Dermatology, University of Luebeck, 23538 Luebeck, Germany.
Institute for Cardiogenetics, University of Luebeck, 23538 Luebeck, Germany.

Sven Perner (S)

Institute of Pathology, University Hospital Schleswig-Holstein, Campus Luebeck, 23538 Luebeck, Germany.
Pathology, Research Center Borstel, Leibniz Lung Center, 23845 Borstel, Germany.

Classifications MeSH