Human leukocyte antigen variation is associated with adverse events of checkpoint inhibitors.


Journal

European journal of cancer (Oxford, England : 1990)
ISSN: 1879-0852
Titre abrégé: Eur J Cancer
Pays: England
ID NLM: 9005373

Informations de publication

Date de publication:
01 2019
Historique:
received: 22 08 2018
accepted: 01 11 2018
pubmed: 12 12 2018
medline: 6 5 2020
entrez: 12 12 2018
Statut: ppublish

Résumé

Checkpoint inhibitors (CIs) are highly effective but can induce severe immune-related adverse events (irAEs), which cannot be predicted. We investigated whether human leukocyte antigen (HLA) genes predispose to developing of irAEs during therapy and thus hold a predictive role. We established a prospective observational single-centre study and collected data from patients with either metastatic non-small cell lung cancer (NSCLC) or metastatic melanoma, who were treated with anti-PD-1 (programmed cell death receptor 1), anti-CTLA4 (cytotoxic T-lymphocyte-associated protein 4) or both CIs combined. Data include irAEs and ranges from 15th July 2016 until 10th May 2018. In addition, we performed HLA typing via next generation sequencing. We enrolled 102 patients (median [range] age, 68 [62-74] years) with metastatic cancer in our study who received CI therapy. Of these patients, 59 (58%) developed one or more irAEs, among which pruritus (n = 32 (54%)) and rash (n = 24 (41%)) had the highest rates. We did not find evidence for a single HLA gene being associated with all irAEs (all P > .05). When assessing each irAE individually, we found a significant association between HLA-DRB1*11:01 and pruritus (OR = 4.53, X The presence of two HLA alleles that are known to predispose to autoimmune diseases were associated with the development of pruritus or colitis during therapy, suggesting a genetic aetiology of irAEs. Larger genome-wide association studies should be performed to confirm our findings.

Sections du résumé

BACKGROUND
Checkpoint inhibitors (CIs) are highly effective but can induce severe immune-related adverse events (irAEs), which cannot be predicted. We investigated whether human leukocyte antigen (HLA) genes predispose to developing of irAEs during therapy and thus hold a predictive role.
METHODS
We established a prospective observational single-centre study and collected data from patients with either metastatic non-small cell lung cancer (NSCLC) or metastatic melanoma, who were treated with anti-PD-1 (programmed cell death receptor 1), anti-CTLA4 (cytotoxic T-lymphocyte-associated protein 4) or both CIs combined. Data include irAEs and ranges from 15th July 2016 until 10th May 2018. In addition, we performed HLA typing via next generation sequencing.
RESULTS
We enrolled 102 patients (median [range] age, 68 [62-74] years) with metastatic cancer in our study who received CI therapy. Of these patients, 59 (58%) developed one or more irAEs, among which pruritus (n = 32 (54%)) and rash (n = 24 (41%)) had the highest rates. We did not find evidence for a single HLA gene being associated with all irAEs (all P > .05). When assessing each irAE individually, we found a significant association between HLA-DRB1*11:01 and pruritus (OR = 4.53, X
CONCLUSIONS
The presence of two HLA alleles that are known to predispose to autoimmune diseases were associated with the development of pruritus or colitis during therapy, suggesting a genetic aetiology of irAEs. Larger genome-wide association studies should be performed to confirm our findings.

Identifiants

pubmed: 30529903
pii: S0959-8049(18)31470-9
doi: 10.1016/j.ejca.2018.11.009
pii:
doi:

Substances chimiques

Antineoplastic Agents, Immunological 0
HLA-DQ beta-Chains 0
HLA-DQB1 antigen 0

Types de publication

Clinical Trial Journal Article Observational Study Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

8-14

Informations de copyright

Copyright © 2018 The Author(s). Published by Elsevier Ltd.. All rights reserved.

Auteurs

Omar Hasan Ali (O)

Department of Dermatology, University Hospital of Zürich, CH-8091, Zürich, Switzerland; Institute of Immunobiology, Kantonsspital St.Gallen, CH-9007, St. Gallen, Switzerland.

Fiamma Berner (F)

Institute of Immunobiology, Kantonsspital St.Gallen, CH-9007, St. Gallen, Switzerland.

David Bomze (D)

Institute of Immunobiology, Kantonsspital St.Gallen, CH-9007, St. Gallen, Switzerland.

Mirjam Fässler (M)

Institute of Immunobiology, Kantonsspital St.Gallen, CH-9007, St. Gallen, Switzerland.

Stefan Diem (S)

Department of Oncology and Hematology, Kantonsspital St. Gallen, CH-9007, St. Gallen, Switzerland; Department of Oncology and Hematology, Hospital of Grabs, CH-9472, Grabs, Switzerland.

Antonio Cozzio (A)

Department of Dermatology, Kantonsspital St. Gallen, CH-9007, St. Gallen, Switzerland.

Markus Jörger (M)

Department of Oncology and Hematology, Kantonsspital St. Gallen, CH-9007, St. Gallen, Switzerland.

Martin Früh (M)

Department of Oncology and Hematology, Kantonsspital St. Gallen, CH-9007, St. Gallen, Switzerland.

Christoph Driessen (C)

Department of Oncology and Hematology, Kantonsspital St. Gallen, CH-9007, St. Gallen, Switzerland.

Tobias L Lenz (TL)

Research Group for Evolutionary Immunogenomics, Max Planck Institute for Evolutionary Biology, D-24306, Plön, Germany.

Lukas Flatz (L)

Department of Dermatology, University Hospital of Zürich, CH-8091, Zürich, Switzerland; Institute of Immunobiology, Kantonsspital St.Gallen, CH-9007, St. Gallen, Switzerland; Department of Oncology and Hematology, Kantonsspital St. Gallen, CH-9007, St. Gallen, Switzerland; Department of Dermatology, Kantonsspital St. Gallen, CH-9007, St. Gallen, Switzerland. Electronic address: lukas.flatz@kssg.ch.

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