Everolimus plus Exemestane for Hormone Receptor-Positive Advanced Breast Cancer: A PAM50 Intrinsic Subtype Analysis of BOLERO-2.


Journal

The oncologist
ISSN: 1549-490X
Titre abrégé: Oncologist
Pays: England
ID NLM: 9607837

Informations de publication

Date de publication:
07 2019
Historique:
received: 11 07 2018
accepted: 21 12 2018
pubmed: 27 1 2019
medline: 10 7 2020
entrez: 26 1 2019
Statut: ppublish

Résumé

The prognostic and predictive value of the two nonluminal (human epidermal growth factor receptor 2 [HER2]-enriched and basal-like) subtypes within advanced hormone receptor-positive (HR+) breast cancer is currently unknown. This study retrospectively analyzed 261 tumors (80.7% primary; 19.3% metastatic) from the BOLERO-2 study; BOLERO-2 randomized 724 patients with advanced HR+/HER2-negative breast cancer to everolimus plus exemestane or placebo plus exemestane. Tumors were classified using a PAM50 subtype predictor. Multivariable Cox regression analyses tested the independent prognostic significance of PAM50, and associations between PAM50 subtypes and treatment upon progression-free survival (PFS) were evaluated. Subtype distribution was 46.7% luminal A ( The HER2-enriched subtype was identified in a substantial proportion of advanced HR+/HER2-negative breast tumors, and was a consistent biomarker of poor prognosis. Tailored therapies are therefore needed for HER2-enriched tumors in the advanced HR+/HER2-negative breast cancer setting. Using 261 tumor samples from the BOLERO-2 phase III clinical trial, this study shows that a substantial proportion (20%-30%) of hormone receptor-positive (HR+)/human epidermal growth factor receptor 2 (HER2)-negative advanced breast cancers do not have a luminal A or B gene expression profile. This group of patients with nonluminal disease has a poor survival outcome regardless of the addition of everolimus to exemestane. This is the second study that confirms the prognostic value of this biomarker. Overall, these findings indicate a necessity to design novel clinical trials targeting nonluminal disease within HR+/HER2-negative breast cancer.

Sections du résumé

BACKGROUND
The prognostic and predictive value of the two nonluminal (human epidermal growth factor receptor 2 [HER2]-enriched and basal-like) subtypes within advanced hormone receptor-positive (HR+) breast cancer is currently unknown.
MATERIALS AND METHODS
This study retrospectively analyzed 261 tumors (80.7% primary; 19.3% metastatic) from the BOLERO-2 study; BOLERO-2 randomized 724 patients with advanced HR+/HER2-negative breast cancer to everolimus plus exemestane or placebo plus exemestane. Tumors were classified using a PAM50 subtype predictor. Multivariable Cox regression analyses tested the independent prognostic significance of PAM50, and associations between PAM50 subtypes and treatment upon progression-free survival (PFS) were evaluated.
RESULTS
Subtype distribution was 46.7% luminal A (
CONCLUSION
The HER2-enriched subtype was identified in a substantial proportion of advanced HR+/HER2-negative breast tumors, and was a consistent biomarker of poor prognosis. Tailored therapies are therefore needed for HER2-enriched tumors in the advanced HR+/HER2-negative breast cancer setting.
IMPLICATIONS FOR PRACTICE
Using 261 tumor samples from the BOLERO-2 phase III clinical trial, this study shows that a substantial proportion (20%-30%) of hormone receptor-positive (HR+)/human epidermal growth factor receptor 2 (HER2)-negative advanced breast cancers do not have a luminal A or B gene expression profile. This group of patients with nonluminal disease has a poor survival outcome regardless of the addition of everolimus to exemestane. This is the second study that confirms the prognostic value of this biomarker. Overall, these findings indicate a necessity to design novel clinical trials targeting nonluminal disease within HR+/HER2-negative breast cancer.

Identifiants

pubmed: 30679318
pii: theoncologist.2018-0407
doi: 10.1634/theoncologist.2018-0407
pmc: PMC6656445
doi:

Substances chimiques

Androstadienes 0
Biomarkers, Tumor 0
Receptors, Estrogen 0
Receptors, Progesterone 0
Everolimus 9HW64Q8G6G
ERBB2 protein, human EC 2.7.10.1
Receptor, ErbB-2 EC 2.7.10.1
exemestane NY22HMQ4BX

Types de publication

Journal Article Multicenter Study Randomized Controlled Trial Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

893-900

Subventions

Organisme : NCI NIH HHS
ID : P30 CA008748
Pays : United States

Informations de copyright

© AlphaMed Press 2019.

Déclaration de conflit d'intérêts

Disclosures of potential conflicts of interest may be found at the end of this article.

Références

J Clin Oncol. 2009 Mar 10;27(8):1160-7
pubmed: 19204204
J Clin Oncol. 2009 Jun 1;27(16):2630-7
pubmed: 19380449
J Clin Oncol. 2009 Sep 20;27(27):4536-41
pubmed: 19687332
Mol Oncol. 2011 Feb;5(1):5-23
pubmed: 21147047
Steroids. 2011 Jul;76(8):736-40
pubmed: 21447351
J Clin Oncol. 2011 Jun 10;29(17):2342-9
pubmed: 21555689
N Engl J Med. 2012 Feb 9;366(6):520-9
pubmed: 22149876
Ann Oncol. 2012 Nov;23(11):2866-73
pubmed: 22532584
J Clin Oncol. 2012 Aug 1;30(22):2718-24
pubmed: 22565002
Adv Ther. 2013 Oct;30(10):870-84
pubmed: 24158787
J Natl Cancer Inst. 2014 Aug 19;106(8):null
pubmed: 25139534
Mol Oncol. 2015 Jun;9(6):1081-90
pubmed: 25687451
Breast. 2015 Nov;24 Suppl 2:S26-35
pubmed: 26253814
J Clin Oncol. 2016 Feb 10;34(5):419-26
pubmed: 26503204
BMC Med. 2015 Dec 18;13:303
pubmed: 26684470
J Clin Oncol. 2016 Sep 1;34(25):3069-103
pubmed: 27217461
JAMA Oncol. 2016 Oct 1;2(10):1287-1294
pubmed: 27281556
JAMA Oncol. 2016 Oct 1;2(10):1310-1315
pubmed: 27532364
Breast. 2017 Feb;31:244-259
pubmed: 27927580
Cancer Res. 2017 May 1;77(9):2213-2221
pubmed: 28249905
Cancer Treat Rev. 2018 Jun;67:63-70
pubmed: 29763779

Auteurs

Aleix Prat (A)

Hospital Clínic de Barcelona, Barcelona, Spain alprat@clinic.ub.es.
Translational Genomics and Targeted Therapeutics in Solid Tumors Group, IDIBAPS, Barcelona, Spain.

Jan Christoph Brase (JC)

Novartis Pharma AG, Basel, Switzerland.

Yuan Cheng (Y)

Novartis Pharma AG, Basel, Switzerland.

Paolo Nuciforo (P)

Vall d'Hebron Institute of Oncology, Barcelona, Spain.

Laia Paré (L)

Hospital Clínic de Barcelona, Barcelona, Spain.
Translational Genomics and Targeted Therapeutics in Solid Tumors Group, IDIBAPS, Barcelona, Spain.

Tomás Pascual (T)

Hospital Clínic de Barcelona, Barcelona, Spain.
Translational Genomics and Targeted Therapeutics in Solid Tumors Group, IDIBAPS, Barcelona, Spain.

Débora Martínez (D)

Hospital Clínic de Barcelona, Barcelona, Spain.
Translational Genomics and Targeted Therapeutics in Solid Tumors Group, IDIBAPS, Barcelona, Spain.

Patricia Galván (P)

Hospital Clínic de Barcelona, Barcelona, Spain.
Translational Genomics and Targeted Therapeutics in Solid Tumors Group, IDIBAPS, Barcelona, Spain.

Maria Vidal (M)

Hospital Clínic de Barcelona, Barcelona, Spain.
Translational Genomics and Targeted Therapeutics in Solid Tumors Group, IDIBAPS, Barcelona, Spain.

Barbara Adamo (B)

Hospital Clínic de Barcelona, Barcelona, Spain.
Translational Genomics and Targeted Therapeutics in Solid Tumors Group, IDIBAPS, Barcelona, Spain.

Gabriel N Hortobagyi (GN)

The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

José Baselga (J)

Memorial Sloan Kettering Cancer Center, New York New York, USA.

Eva Ciruelos (E)

University Hospital 12 de Octubre, Madrid, Spain.

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Classifications MeSH