Prognostic impact of tumour mutational burden in resected stage I and II lung adenocarcinomas from a European Thoracic Oncology Platform Lungscape cohort.


Journal

Lung cancer (Amsterdam, Netherlands)
ISSN: 1872-8332
Titre abrégé: Lung Cancer
Pays: Ireland
ID NLM: 8800805

Informations de publication

Date de publication:
12 2022
Historique:
received: 25 07 2022
revised: 20 09 2022
accepted: 28 09 2022
pubmed: 26 10 2022
medline: 15 12 2022
entrez: 25 10 2022
Statut: ppublish

Résumé

The primary objective of this study is to evaluate tumor mutational burden (TMB), its associations with selected clinicopathological and molecular characteristics as well as its clinical significance, in a retrospective cohort of surgically resected stage I-II lung adenocarcinomas, subset of the ETOP Lungscape cohort. TMB was evaluated on tumor DNA extracted from resected primary lung adenocarcinomas, based on FoundationOne®CDx (F1CDx) genomic profiling, centrally performed at the University Hospital Zurich. The F1CDx test sequences the complete exons of 324 cancer-related genes and detects substitutions, insertions and deletions (indels), copy number alterations and gene rearrangements. In addition, the genomic biomarkers TMB and microsatellite instability (MSI) are analyzed. In the Lungscape cohort, TMB was assessed in 78 surgically resected lung adenocarcinomas from two Swiss centers (62 % males, 55 %/45 % stage I/II). Median TMB was 7.6 Muts/Mb, with TMB high (≥10 Muts/Mb) in 40 % of cases (95 %CI:29 %-52 %). The most frequently mutated genes were TP53/KRAS/EGFR/MLL2 detected in 58 %/38 %/33 %/30 % of samples, respectively. TMB was significantly higher among males (TMB high: 50 % vs 23 % in females, p = 0.032), as well as among current/former smokers (TMB high: 44 % vs 8 % in never smokers, p = 0.023). Furthermore, TMB was significantly higher in TP53 mutated than in non-mutated patients (TMB high: 60 % vs 12 %, p < 0.001), while it was higher in EGFR non-mutated patients compared to EGFR mutated (TMB high: 48 % vs 23 %, p = 0.049). At a median follow-up time of 56.1 months (IQR:38.8-72.0), none of the three outcome variables (OS, RFS, TTR) differed significantly by TMB status (all p-values > 5 %). This was also true when adjusting for clinicopathological characteristics. While presence of TP53 mutations and absence of EGFR mutations are associated with high TMB, increased TMB had no significant prognostic impact in patients with resected stage I/II lung adenocarcinoma beyond T and N classification, in both unadjusted and adjusted analyses.

Sections du résumé

BACKGROUND
The primary objective of this study is to evaluate tumor mutational burden (TMB), its associations with selected clinicopathological and molecular characteristics as well as its clinical significance, in a retrospective cohort of surgically resected stage I-II lung adenocarcinomas, subset of the ETOP Lungscape cohort.
METHODS
TMB was evaluated on tumor DNA extracted from resected primary lung adenocarcinomas, based on FoundationOne®CDx (F1CDx) genomic profiling, centrally performed at the University Hospital Zurich. The F1CDx test sequences the complete exons of 324 cancer-related genes and detects substitutions, insertions and deletions (indels), copy number alterations and gene rearrangements. In addition, the genomic biomarkers TMB and microsatellite instability (MSI) are analyzed.
RESULTS
In the Lungscape cohort, TMB was assessed in 78 surgically resected lung adenocarcinomas from two Swiss centers (62 % males, 55 %/45 % stage I/II). Median TMB was 7.6 Muts/Mb, with TMB high (≥10 Muts/Mb) in 40 % of cases (95 %CI:29 %-52 %). The most frequently mutated genes were TP53/KRAS/EGFR/MLL2 detected in 58 %/38 %/33 %/30 % of samples, respectively. TMB was significantly higher among males (TMB high: 50 % vs 23 % in females, p = 0.032), as well as among current/former smokers (TMB high: 44 % vs 8 % in never smokers, p = 0.023). Furthermore, TMB was significantly higher in TP53 mutated than in non-mutated patients (TMB high: 60 % vs 12 %, p < 0.001), while it was higher in EGFR non-mutated patients compared to EGFR mutated (TMB high: 48 % vs 23 %, p = 0.049). At a median follow-up time of 56.1 months (IQR:38.8-72.0), none of the three outcome variables (OS, RFS, TTR) differed significantly by TMB status (all p-values > 5 %). This was also true when adjusting for clinicopathological characteristics.
CONCLUSIONS
While presence of TP53 mutations and absence of EGFR mutations are associated with high TMB, increased TMB had no significant prognostic impact in patients with resected stage I/II lung adenocarcinoma beyond T and N classification, in both unadjusted and adjusted analyses.

Identifiants

pubmed: 36283211
pii: S0169-5002(22)00643-2
doi: 10.1016/j.lungcan.2022.09.014
pii:
doi:

Substances chimiques

Biomarkers, Tumor 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

27-35

Informations de copyright

Copyright © 2022 Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Lukas Bubendorf (L)

Institute of Medical Genetics and Pathology, University Hospital Basel, Basel, Switzerland.

Martin Zoche (M)

Department of Pathology and Molecular Pathology, University Hospital Zurich, Zurich, Switzerland.

Urania Dafni (U)

ETOP IBCSG Partners Foundation Statistical Center, Frontier Science Foundation-Hellas & National and Kapodistrian University of Athens, Athens, Greece.

Jan Hendrik Rüschoff (JH)

Department of Pathology and Molecular Pathology, University Hospital Zurich, Zurich, Switzerland.

Spasenija Savic Prince (SS)

Institute of Medical Genetics and Pathology, University Hospital Basel, Basel, Switzerland.

Nesa Marti (N)

Translational Research Coordination, ETOP IBCSG Partners Foundation, Coordinating Center Bern, Switzerland.

Androniki Stavrou (A)

ETOP IBCSG Partners Foundation Statistical Center, Frontier Science Foundation-Hellas, Athens, Greece.

Roswitha Kammler (R)

Translational Research Coordination, ETOP IBCSG Partners Foundation, Coordinating Center Bern, Switzerland.

Stephen P Finn (SP)

Cancer Molecular Diagnostics and Histopathology, St. James's Hospital and Trinity College Dublin, Ireland.

Holger Moch (H)

Department of Pathology and Molecular Pathology, University Hospital Zurich, Zurich, Switzerland.

Solange Peters (S)

Department of Oncology, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.

Rolf A Stahel (RA)

ETOP IBCSG Partners Foundation, Coordinating Center, Bern, Switzerland. Electronic address: rolf.stahel@etop.ibcsg.org.

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Classifications MeSH