Evolution of overall survival and receipt of new therapies by subtype among 20 446 metastatic breast cancer patients in the 2008-2017 ESME cohort.


Journal

ESMO open
ISSN: 2059-7029
Titre abrégé: ESMO Open
Pays: England
ID NLM: 101690685

Informations de publication

Date de publication:
06 2021
Historique:
received: 13 12 2020
revised: 16 03 2021
accepted: 19 03 2021
pubmed: 26 4 2021
medline: 30 10 2021
entrez: 25 4 2021
Statut: ppublish

Résumé

Treatment strategies for metastatic breast cancer (MBC) have made great strides over the past 10 years. Real-world data allow us to evaluate the actual benefit of new treatments. ESME (Epidemio-Strategy-Medico-Economical)-MBC, a nationwide observational cohort (NCT03275311), gathers data of all consecutive MBC patients who initiated their treatment in 18 French Cancer Centres since 2008. We evaluated overall survival (OS) in the whole cohort (N = 20 446) and among subtypes: hormone receptor positive, human epidermal growth factor 2 negative (HR+/HER2-; N = 13 590), HER2+ (N = 3919), and triple-negative breast cancer (TNBC; N = 2937). We performed multivariable analyses including year of MBC diagnosis as one of the covariates, to assess the potential OS improvement over time, and we described exposure to newly released drugs at any time during MBC history by year of diagnosis (YOD). The median follow-up of the whole cohort was 65.5 months (95% CI 64.6-66.7). Year of metastatic diagnosis appears as a strong independent prognostic factor for OS [Year 2016 HR 0.89 (95% CI 0.82-0.97); P = 0.009, using 2008 as reference]. This effect is driven by the HER2+ subcohort, where it is dramatic [Year 2016 HR 0.52 (95% CI 0.42-0.66); P < 0.001, using 2008 as reference]. YOD had, however, no sustained impact on OS among patients with TNBC [Year 2016 HR 0.93 (95% CI 0.77-1.11); P = 0.41, using 2008 as reference] nor among those with HR+/HER2- MBC [Year 2016 HR 1.02 (95% CI 0.91-1.13); P = 0.41, using 2008 as reference]. While exposure to newly released anti-HER2 therapies appeared very high (e.g. >70% of patients received pertuzumab from 2016 onwards), use of everolimus or eribulin was recorded in less than one-third of HR+/HER2- and TNBC cohorts, respectively, whatever YOD. OS has dramatically improved among HER2+ MBC patients, probably in association with the release of several major HER2-directed therapies, whose penetrance was high. This trend was not observed in the other subtypes, but the impact of CDK4/6 inhibitors cannot yet be assessed.

Sections du résumé

BACKGROUND
Treatment strategies for metastatic breast cancer (MBC) have made great strides over the past 10 years. Real-world data allow us to evaluate the actual benefit of new treatments. ESME (Epidemio-Strategy-Medico-Economical)-MBC, a nationwide observational cohort (NCT03275311), gathers data of all consecutive MBC patients who initiated their treatment in 18 French Cancer Centres since 2008.
PATIENTS AND METHODS
We evaluated overall survival (OS) in the whole cohort (N = 20 446) and among subtypes: hormone receptor positive, human epidermal growth factor 2 negative (HR+/HER2-; N = 13 590), HER2+ (N = 3919), and triple-negative breast cancer (TNBC; N = 2937). We performed multivariable analyses including year of MBC diagnosis as one of the covariates, to assess the potential OS improvement over time, and we described exposure to newly released drugs at any time during MBC history by year of diagnosis (YOD).
RESULTS
The median follow-up of the whole cohort was 65.5 months (95% CI 64.6-66.7). Year of metastatic diagnosis appears as a strong independent prognostic factor for OS [Year 2016 HR 0.89 (95% CI 0.82-0.97); P = 0.009, using 2008 as reference]. This effect is driven by the HER2+ subcohort, where it is dramatic [Year 2016 HR 0.52 (95% CI 0.42-0.66); P < 0.001, using 2008 as reference]. YOD had, however, no sustained impact on OS among patients with TNBC [Year 2016 HR 0.93 (95% CI 0.77-1.11); P = 0.41, using 2008 as reference] nor among those with HR+/HER2- MBC [Year 2016 HR 1.02 (95% CI 0.91-1.13); P = 0.41, using 2008 as reference]. While exposure to newly released anti-HER2 therapies appeared very high (e.g. >70% of patients received pertuzumab from 2016 onwards), use of everolimus or eribulin was recorded in less than one-third of HR+/HER2- and TNBC cohorts, respectively, whatever YOD.
CONCLUSION
OS has dramatically improved among HER2+ MBC patients, probably in association with the release of several major HER2-directed therapies, whose penetrance was high. This trend was not observed in the other subtypes, but the impact of CDK4/6 inhibitors cannot yet be assessed.

Identifiants

pubmed: 33895695
pii: S2059-7029(21)00072-7
doi: 10.1016/j.esmoop.2021.100114
pmc: PMC8095121
pii:
doi:

Substances chimiques

Epidermal Growth Factor 62229-50-9
Receptor, ErbB-2 EC 2.7.10.1

Banques de données

ClinicalTrials.gov
['NCT03275311']

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

100114

Informations de copyright

Copyright © 2021 The Authors. Published by Elsevier Ltd.. All rights reserved.

Déclaration de conflit d'intérêts

Disclosure AG reports nonfinancial support from AstraZeneca, Roche, Pfizer, and Novartis, outside the submitted work. WJ reports grants, personal fees, and nonfinancial support from Astra Zeneca; personal fees and nonfinancial support from Eisai, Novartis, Roche, Pfizer, Eli Lilly, and Chugai; personal fees from MSD and BMS, outside the submitted work. P-HC reports grants and nonfinancial support from Roche and Pfizer, outside the submitted work. FC reports grants and personal fees from Merck Serono and BMS; nonfinancial support from Lilly; personal fees and nonfinancial support from Roche; and grants from AstraZeneca, outside the submitted work. ED reports personal fees and nonfinancial support from Novartis and Pfizer; and nonfinancial support from Lilly, outside the submitted work. TB reports personal fees and nonfinancial support from Roche and AstraZeneca; grants, personal fees, and nonfinancial support from Novartis and Pfizer; and personal fees from Seattle Genetics, outside the submitted work. DP reports personal fees from Laboratoire Roche, Pierre Fabre, Novartis, BMS, Eli-Lilly, Ipsen, MSD; personal fees and nonfinancial support from Laboratoire AstraZeneca; grants from Laboratoire MDS Avenir outside the submitted work and Laboratoire Roche (ESME program). SD reports grants and nonfinancial support from Pfizer, AstraZeneca, and Roche Genentech; grants from Novartis, Lilly, Puma, Myriad, Orion, Amgen, Sanofi, Genomic Health, GE, Servier, MSD, BMS, and Pierre Fabre, outside the submitted work. All remaining authors have nothing to disclose.

Auteurs

T Grinda (T)

Department of Cancer Medicine, Gustave Roussy, Villejuif, France.

A Antoine (A)

Department of Biostatistics, Centre Léon Bérard, Lyon, France.

W Jacot (W)

Department of Medical Oncology, Institut du Cancer de Montpellier, Montpellier, France.

C Blaye (C)

Department of Medical Oncology, Institut Bergonié, Bordeaux, France.

P-H Cottu (PH)

Department of Medical Oncology, Institut Curie, Paris & Saint-Cloud, France.

V Diéras (V)

Department of Medical Oncology, Centre Eugène Marquis, Rennes, France.

F Dalenc (F)

Department of Medical Oncology, Institut Claudius Regaud - IUCT Oncopole, Toulouse, France.

A Gonçalves (A)

Department of Medical Oncology, Institut Paoli-Calmettes, Marseille, France.

M Debled (M)

Department of Medical Oncology, Institut du Cancer de Montpellier, Montpellier, France.

A Patsouris (A)

Department of Medical Oncology, Institut de Cancérologie de l'Ouest Pays de Loire, Angers, France.

M-A Mouret-Reynier (MA)

Department of Medical Oncology, Centre Jean Perrin, Clermont Ferrand, France.

A Mailliez (A)

Medical Oncology Department, Centre Oscar Lambret, Lille, France.

F Clatot (F)

Department of Medical Oncology, Centre Henri Becquerel, Rouen, France.

C Levy (C)

Department of Medical Oncology, Centre François Baclesse, Caen, France.

J-M Ferrero (JM)

Department of Medical Oncology, Centre Antoine Lacassagne, Nice, France.

I Desmoulins (I)

Department of Medical Oncology, Institut de Cancérologie de Bourgogne, Dijon, France.

L Uwer (L)

Medical Oncology Department, Institut de Cancérologie de Lorraine, Vandoeuvre-lès-Nancy, Vandœuvre-lès-Nancy, France.

T Petit (T)

Department of Medical Oncology, Centre Paul Strauss, Strasbourg, France.

C Jouannaud (C)

Department of Medical Oncology, Institut de Cancérologie Jean-Godinot, Reims, France.

M Lacroix-Triki (M)

Department of BioPathology, Gustave Roussy, Villejuif.

E Deluche (E)

Department of Medical Oncology, CHU de Limoges, France.

M Robain (M)

Department of Research and Development, R&D Unicancer, Paris, France.

C Courtinard (C)

Department of Research and Development, R&D Unicancer, Paris, France; Université de Bordeaux, Inserm, Bordeaux Population Health Research Center, Bordeaux, France; Université de Bordeaux, Inserm, Bordeaux Population Health Research Center, Epicene Team, UMR 1219, Bordeaux, France.

T Bachelot (T)

Department of Medical Oncology, Centre Léon Bérard, Lyon, France.

E Brain (E)

Department of Medical Oncology, Institut Curie, Paris & Saint-Cloud, France.

D Pérol (D)

Department of Biostatistics, Centre Léon Bérard, Lyon, France.

S Delaloge (S)

Department of Cancer Medicine, Gustave Roussy, Villejuif, France. Electronic address: suzette.delaloge@gustaveroussy.fr.

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