Consensus molecular subtypes in metastatic colorectal cancer treated with sequential versus combined fluoropyrimidine, bevacizumab and irinotecan (XELAVIRI trial).


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:
11 2021
Historique:
received: 05 07 2021
revised: 09 08 2021
accepted: 11 08 2021
pubmed: 11 9 2021
medline: 1 12 2021
entrez: 10 9 2021
Statut: ppublish

Résumé

The XELAVIRI trial compared sequential (fluoropyrimidine and bevacizumab; irinotecan (Iri) at progression) versus initial combination therapy (fluoropyrimidine, bevacizumab, Iri) of treatment-naïve metastatic colorectal cancer (mCRC). In the confirmatory analysis, the primary end-point (non-inferiority of sequential therapy regarding time to failure of strategy, TFS) was not met. Nevertheless, significant differences regarding treatment efficacy were observed according to RAS status. Here, we evaluate the consensus molecular subtypes (CMS) as additional biomarkers for sequential versus combination therapy. Gene expression was measured using NanoString after mRNA extraction from formalin-fixed paraffin-embedded tumour specimens. CMS were predicted using multinomial regression and correlated with updated data for TFS, overall (OS) and progression-free survival. CMS were predicted in 337 of 421 (80.0%) patients (CMS1: 18.4%; CMS2: 51.6%; CMS3: 2.7%; CMS4: 27.3%). CMS2 together with RAS/BRAF wild-type status was identified as potential predictive marker of benefit from initial combination therapy for OS (HR 0.56, 95% CI 0.33-0.96, p = 0.036) and progression-free survival (HR 0.28, 95% CI 0.29-0.79, p = 0.004) and also trending in TFS (HR 0.63, 90% CI 0.41-0.95, p = 0.066). In patients with RAS-mutated mCRC, CMS1 was associated with longer OS after initial combination therapy (HR 0.43, 95% CI 0.20-0.95, p = 0.038). Interaction testing (two-sided) of CMS and RAS/BRAF status in favour of the combination treatment strategy was significant for OS (p = 0.012) CONCLUSIONS: In patients with RAS/BRAF wild-type mCRC, CMS2 may serve as an additional biomarker of benefit from the initial combination therapy, including Iri. Trial registration ID (clinicaltrials.gov) NCT01249638.

Sections du résumé

BACKGROUND
The XELAVIRI trial compared sequential (fluoropyrimidine and bevacizumab; irinotecan (Iri) at progression) versus initial combination therapy (fluoropyrimidine, bevacizumab, Iri) of treatment-naïve metastatic colorectal cancer (mCRC). In the confirmatory analysis, the primary end-point (non-inferiority of sequential therapy regarding time to failure of strategy, TFS) was not met. Nevertheless, significant differences regarding treatment efficacy were observed according to RAS status. Here, we evaluate the consensus molecular subtypes (CMS) as additional biomarkers for sequential versus combination therapy.
MATERIAL AND METHODS
Gene expression was measured using NanoString after mRNA extraction from formalin-fixed paraffin-embedded tumour specimens. CMS were predicted using multinomial regression and correlated with updated data for TFS, overall (OS) and progression-free survival.
RESULTS
CMS were predicted in 337 of 421 (80.0%) patients (CMS1: 18.4%; CMS2: 51.6%; CMS3: 2.7%; CMS4: 27.3%). CMS2 together with RAS/BRAF wild-type status was identified as potential predictive marker of benefit from initial combination therapy for OS (HR 0.56, 95% CI 0.33-0.96, p = 0.036) and progression-free survival (HR 0.28, 95% CI 0.29-0.79, p = 0.004) and also trending in TFS (HR 0.63, 90% CI 0.41-0.95, p = 0.066). In patients with RAS-mutated mCRC, CMS1 was associated with longer OS after initial combination therapy (HR 0.43, 95% CI 0.20-0.95, p = 0.038). Interaction testing (two-sided) of CMS and RAS/BRAF status in favour of the combination treatment strategy was significant for OS (p = 0.012) CONCLUSIONS: In patients with RAS/BRAF wild-type mCRC, CMS2 may serve as an additional biomarker of benefit from the initial combination therapy, including Iri.
TRIAL REGISTRATION
Trial registration ID (clinicaltrials.gov) NCT01249638.

Identifiants

pubmed: 34507244
pii: S0959-8049(21)00535-9
doi: 10.1016/j.ejca.2021.08.017
pii:
doi:

Substances chimiques

Bevacizumab 2S9ZZM9Q9V
Irinotecan 7673326042
BRAF protein, human EC 2.7.11.1
Proto-Oncogene Proteins B-raf EC 2.7.11.1
Fluorouracil U3P01618RT

Banques de données

ClinicalTrials.gov
['NCT01249638']

Types de publication

Clinical Trial, Phase III Comparative Study Journal Article Randomized Controlled Trial Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

71-80

Informations de copyright

Copyright © 2021 Elsevier Ltd. All rights reserved.

Auteurs

Arndt Stahler (A)

Charité Universitätsmedizin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Hematology, Oncology and Tumour Immunology, Charitéplatz 1, 10117, Berlin, Germany. Electronic address: arndt.stahler@charite.de.

Volker Heinemann (V)

Department of Medicine III, University Hospital, LMU, Munich, Germany; LMU Munich, German Cancer Consortium (DKTK), Partner Site Munich, German Cancer Research Center (DKFZ), Heidelberg, Germany.

Veronika Schuster (V)

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

Kathrin Heinrich (K)

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

Annika Kurreck (A)

Charité Universitätsmedizin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Hematology, Oncology and Tumour Immunology, Charitéplatz 1, 10117, Berlin, Germany.

Clemens Gießen-Jung (C)

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

Ludwig Fischer von Weikersthal (L)

Klinikum St. Marien, Oncology, Amberg, Germany.

Florian Kaiser (F)

Onkologische Praxis, Landshut, Germany.

Thomas Decker (T)

Onkologische Praxis, Ravensburg, Germany.

Swantje Held (S)

ClinAssess GmbH, Leverkusen, Germany.

Ullrich Graeven (U)

Department of Hematology, Oncology and Gastroenterology, Kliniken Maria Hilf GmbH, Mönchengladbach, Germany.

Ingo Schwaner (I)

Onkologische Schwerpunktpraxis Kurfürstendamm, Berlin, Germany.

Claudio Denzlinger (C)

Marienhospital, Stuttgart, Germany.

Michael Schenk (M)

Krankenhaus Barmherzige Brüder Regensburg, Regensburg, Germany.

Jens Neumann (J)

Institute of Pathology, University of Munich, Germany.

Thomas Kirchner (T)

LMU Munich, German Cancer Consortium (DKTK), Partner Site Munich, German Cancer Research Center (DKFZ), Heidelberg, Germany; Institute of Pathology, University of Munich, Germany.

Andreas Jung (A)

LMU Munich, German Cancer Consortium (DKTK), Partner Site Munich, German Cancer Research Center (DKFZ), Heidelberg, Germany; Institute of Pathology, University of Munich, Germany.

Jörg Kumbrink (J)

LMU Munich, German Cancer Consortium (DKTK), Partner Site Munich, German Cancer Research Center (DKFZ), Heidelberg, Germany; Institute of Pathology, University of Munich, Germany.

Sebastian Stintzing (S)

Charité Universitätsmedizin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Hematology, Oncology and Tumour Immunology, Charitéplatz 1, 10117, Berlin, Germany; Charité - Universitätsmedizin, German Cancer Consortium (DKTK), Partner Site Berlin, German Cancer Research Center (DKFZ), Heidelberg, Germany.

Dominik P Modest (DP)

Charité Universitätsmedizin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Hematology, Oncology and Tumour Immunology, Charitéplatz 1, 10117, Berlin, Germany; Charité - Universitätsmedizin, German Cancer Consortium (DKTK), Partner Site Berlin, German Cancer Research Center (DKFZ), Heidelberg, Germany.

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