Genetic variants involved in the cGAS-STING pathway predict outcome in patients with metastatic colorectal cancer: Data from FIRE-3 and TRIBE trials.


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:
09 2022
Historique:
received: 29 03 2022
revised: 23 04 2022
accepted: 12 05 2022
pubmed: 25 6 2022
medline: 17 8 2022
entrez: 24 6 2022
Statut: ppublish

Résumé

The activation of stimulator of interferon genes (STING) was reported to enhance cetuximab-mediated natural killer cell activation and dendritic cell maturation. Polymorphisms in genes in the cyclic GMP-AMP synthase (cGAS)-STING pathway may affect innate immune response. Therefore, we hypothesised that genetic variants in the cGAS-STING pathway may predict the efficacy of cetuximab-based treatment in patients with metastatic colorectal cancer. Genomic DNA from blood samples of patients enrolled in FIRE-3 (cetuximab arm, n = 129; bevacizumab arm, n = 107) and TRIBE (bevacizumab arm, n = 215) was genotyped using the OncoArray-500K bead chip panel. Seven selected single nucleotide polymorphisms in 3 genes (cGAS, STING and interferon B1 (IFNB1)) were analysed for the association with overall survival and progression-free survival. In the cetuximab cohort, patients with STING rs1131769 any T allele showed significantly shorter overall survival (36.3 versus 56.1 months) than carriers of C/C in both univariate [hazard ratio (HR) = 2.08; 95% confidence interval (CI): 1.06-4.07; P = 0.03] and multivariate (HR = 2.98; 95% CI: 1.35-6.6; P = 0.0085) analyses; patients carrying IFNB1 rs1051922 G/A and A/A genotype showed a significantly shorter progression-free survival than carriers of G/G allele in both univariate (G/A versus G/G, 10.2 versus 14.1 months, HR = 1.84; 95% CI 1.23-2.76; A/A versus G/G, 10.7 versus 14.1 months, HR = 2.19; 95% CI 0.97-4.96; P = 0.0077) and multivariate analyses (G/A versus G/G, HR = 2; 95% CI 1.22-3.3; A/A versus G/G, HR = 2.19, 95% CI 0.92-5.26, P = 0.02). These associations were not observed in the bevacizumab arm of FIRE-3 or TRIBE. These results suggest for the first time that germline polymorphisms in STING and IFNB1 genes may predict the outcomes of cetuximab-based treatment in patients with metastatic colorectal cancer.

Sections du résumé

BACKGROUND
The activation of stimulator of interferon genes (STING) was reported to enhance cetuximab-mediated natural killer cell activation and dendritic cell maturation. Polymorphisms in genes in the cyclic GMP-AMP synthase (cGAS)-STING pathway may affect innate immune response. Therefore, we hypothesised that genetic variants in the cGAS-STING pathway may predict the efficacy of cetuximab-based treatment in patients with metastatic colorectal cancer.
METHODS
Genomic DNA from blood samples of patients enrolled in FIRE-3 (cetuximab arm, n = 129; bevacizumab arm, n = 107) and TRIBE (bevacizumab arm, n = 215) was genotyped using the OncoArray-500K bead chip panel. Seven selected single nucleotide polymorphisms in 3 genes (cGAS, STING and interferon B1 (IFNB1)) were analysed for the association with overall survival and progression-free survival.
RESULTS
In the cetuximab cohort, patients with STING rs1131769 any T allele showed significantly shorter overall survival (36.3 versus 56.1 months) than carriers of C/C in both univariate [hazard ratio (HR) = 2.08; 95% confidence interval (CI): 1.06-4.07; P = 0.03] and multivariate (HR = 2.98; 95% CI: 1.35-6.6; P = 0.0085) analyses; patients carrying IFNB1 rs1051922 G/A and A/A genotype showed a significantly shorter progression-free survival than carriers of G/G allele in both univariate (G/A versus G/G, 10.2 versus 14.1 months, HR = 1.84; 95% CI 1.23-2.76; A/A versus G/G, 10.7 versus 14.1 months, HR = 2.19; 95% CI 0.97-4.96; P = 0.0077) and multivariate analyses (G/A versus G/G, HR = 2; 95% CI 1.22-3.3; A/A versus G/G, HR = 2.19, 95% CI 0.92-5.26, P = 0.02). These associations were not observed in the bevacizumab arm of FIRE-3 or TRIBE.
CONCLUSION
These results suggest for the first time that germline polymorphisms in STING and IFNB1 genes may predict the outcomes of cetuximab-based treatment in patients with metastatic colorectal cancer.

Identifiants

pubmed: 35749909
pii: S0959-8049(22)00295-7
doi: 10.1016/j.ejca.2022.05.016
pii:
doi:

Substances chimiques

Membrane Proteins 0
STING1 protein, human 0
Bevacizumab 2S9ZZM9Q9V
Interferons 9008-11-1
Nucleotidyltransferases EC 2.7.7.-
Cetuximab PQX0D8J21J
Leucovorin Q573I9DVLP
Fluorouracil U3P01618RT
Camptothecin XT3Z54Z28A

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

22-30

Subventions

Organisme : NCI NIH HHS
ID : P30 CA014089
Pays : United States

Informations de copyright

Copyright © 2022 Elsevier Ltd. All rights reserved.

Déclaration de conflit d'intérêts

Conflict of interest statement H.-J.L. reports receiving honoraria from consultant/advisory board membership for Merck Serono, Bayer, and Genentech. S.S. reports receiving honoraria for talks and advisory board role: AMGEN, Bayer, BMS, Pierre-Fabre, Merck KGaA; MSD, Leo-Pharma, Lilly, Sanofi, Servier, Roche, Takeda, Taiho. A.F reports receiving honoraria as consultant/advisory board for Amgen, Bayer, Bristol, Daiichi Sankyo, Incyte, Lilly, Merck, MSD, Pierre-Fabre, Roche, Servier. All remaining authors have declared no conflicts of interest.

Auteurs

Jingyuan Wang (J)

Department of Medical Oncology, Zhongshan Hospital, Fudan University, Shanghai, China; Division of Medical Oncology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA; Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Gastrointestinal Oncology, Peking University Cancer Hospital and Institute, 52 Fucheng Road, Haidian District, Beijing 100142, China; Center of Evidence-based Medicine, Fudan University, Shanghai, China.

Yi Xiao (Y)

Department of Population and Public Health Sciences, Keck School of Medicine, University of Southern California, Los Angeles, USA.

Fotios Loupakis (F)

Clinical and Experimental Oncology Department, Medical Oncology Unit 1, Veneto Institute of Oncology IOV-IRCCS, Padua, Italy.

Sebastian Stintzing (S)

Department of Hematology, Oncology, and Cancer Immunology (CCM), Charité - Universitaetsmedizin Berlin, Germany.

Yan Yang (Y)

Department of Population and Public Health Sciences, Keck School of Medicine, University of Southern California, Los Angeles, USA.

Hiroyuki Arai (H)

Division of Medical Oncology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.

Francesca Battaglin (F)

Division of Medical Oncology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.

Natsuko Kawanishi (N)

Division of Medical Oncology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.

Priya Jayachandran (P)

Division of Medical Oncology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.

Shivani Soni (S)

Division of Medical Oncology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.

Wu Zhang (W)

Division of Medical Oncology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.

Christoph Mancao (C)

Oncology Biomarker Development, Genentech Inc., Basel, Switzerland.

Chiara Cremolini (C)

Department of Translational Medicine, University of Pisa, Italy.

Tianshu Liu (T)

Department of Medical Oncology, Zhongshan Hospital, Fudan University, Shanghai, China.

Volker Heinemann (V)

Department of Medicine III, University Hospital, LMU Munich, Munich, Germany.

Alfredo Falcone (A)

Department of Translational Medicine, University of Pisa, Italy.

Lin Shen (L)

Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Gastrointestinal Oncology, Peking University Cancer Hospital and Institute, 52 Fucheng Road, Haidian District, Beijing 100142, China.

Joshua Millstein (J)

Department of Population and Public Health Sciences, Keck School of Medicine, University of Southern California, Los Angeles, USA.

Heinz-Josef Lenz (HJ)

Division of Medical Oncology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA. Electronic address: lenz@usc.edu.

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Classifications MeSH