Use of Everolimus and Trastuzumab in Addition to Endocrine Therapy in Hormone-Refractory Metastatic Breast Cancer.


Journal

Clinical breast cancer
ISSN: 1938-0666
Titre abrégé: Clin Breast Cancer
Pays: United States
ID NLM: 100898731

Informations de publication

Date de publication:
06 2019
Historique:
received: 09 09 2018
revised: 17 12 2018
accepted: 26 12 2018
pubmed: 13 2 2019
medline: 20 6 2020
entrez: 13 2 2019
Statut: ppublish

Résumé

Increased signaling through growth factor receptor pathways, including HER2, plays a role in resistance to endocrine therapy (ET) in patients with hormone receptor (HR)-positive metastatic breast cancer (MBC). Inhibition of mechanistic target of rapamycin improves outcomes when used in addition to ET in patients with HR-positive MBC, who previously received ET. We hypothesized that the additional use of trastuzumab (T) or everolimus (E) could restore sensitivity to ET in patients with endocrine-resistant, HR-positive, HER2-negative MBC. Patients with endocrine-resistant HR-positive, HER2-negative MBC continued the ET during which they had experienced disease progression, and were randomized to receive T or E. At disease progression, patients could continue the therapy they were receiving and have E or T used in addition. Fifty-four patients were randomized to the additional use of E (n = 30) or T (n = 24) with existing ET. Progression-free survival (PFS) was 5.7 months, and 2.2 months, respectively, and clinical benefit rate at 24 weeks was 48% and 11% for patients receiving E or T, respectively. PFS was 4.5 months and 3.1 months for patients in whom E (n = 16) or T (n = 12) was used post progression, respectively. There were no new safety signals apart from 2 patients who had a decreased ejection fraction while receiving E with ET. These results suggest that E, but not T, can potentially reverse resistance to ET in patients with endocrine-resistant HR-positive, HER2-negative MBC. Further, the additional use of E with an ET to which the cancer has already been exposed might offer the possibility of delaying time to use of chemotherapy.

Sections du résumé

BACKGROUND
Increased signaling through growth factor receptor pathways, including HER2, plays a role in resistance to endocrine therapy (ET) in patients with hormone receptor (HR)-positive metastatic breast cancer (MBC). Inhibition of mechanistic target of rapamycin improves outcomes when used in addition to ET in patients with HR-positive MBC, who previously received ET. We hypothesized that the additional use of trastuzumab (T) or everolimus (E) could restore sensitivity to ET in patients with endocrine-resistant, HR-positive, HER2-negative MBC.
PATIENTS AND METHODS
Patients with endocrine-resistant HR-positive, HER2-negative MBC continued the ET during which they had experienced disease progression, and were randomized to receive T or E. At disease progression, patients could continue the therapy they were receiving and have E or T used in addition.
RESULTS
Fifty-four patients were randomized to the additional use of E (n = 30) or T (n = 24) with existing ET. Progression-free survival (PFS) was 5.7 months, and 2.2 months, respectively, and clinical benefit rate at 24 weeks was 48% and 11% for patients receiving E or T, respectively. PFS was 4.5 months and 3.1 months for patients in whom E (n = 16) or T (n = 12) was used post progression, respectively. There were no new safety signals apart from 2 patients who had a decreased ejection fraction while receiving E with ET.
CONCLUSION
These results suggest that E, but not T, can potentially reverse resistance to ET in patients with endocrine-resistant HR-positive, HER2-negative MBC. Further, the additional use of E with an ET to which the cancer has already been exposed might offer the possibility of delaying time to use of chemotherapy.

Identifiants

pubmed: 30745109
pii: S1526-8209(18)30637-2
doi: 10.1016/j.clbc.2018.12.017
pii:
doi:

Substances chimiques

Antineoplastic Agents, Hormonal 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
Trastuzumab P188ANX8CK

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

188-196

Subventions

Organisme : NCATS NIH HHS
ID : UL1 TR002378
Pays : United States

Informations de copyright

Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.

Auteurs

Elisavet Paplomata (E)

Department of Hematology and Medical Oncology, Winship Cancer Institute of Emory University, Atlanta, GA.

Amelia Zelnak (A)

Atlanta Cancer Care, Atlanta, GA.

Cesar A Santa-Maria (CA)

Department of Oncology, Sidney Kimmel Comprehensive Cancer Center of Johns Hopkins University, Baltimore, MD.

Yuan Liu (Y)

Department of Hematology and Medical Oncology, Winship Cancer Institute of Emory University, Atlanta, GA; Department of Bioinformatics and Biostatistics Shared Resource, Winship Cancer Institute of Emory University, Atlanta, GA.

Keerthi Gogineni (K)

Department of Hematology and Medical Oncology, Winship Cancer Institute of Emory University, Atlanta, GA.

Xiaoxian Li (X)

Department of Pathology and Laboratory Medicine, Emory University, Atlanta, GA.

Carlos S Moreno (CS)

Department of Hematology and Medical Oncology, Winship Cancer Institute of Emory University, Atlanta, GA; Department of Oncology, Sidney Kimmel Comprehensive Cancer Center of Johns Hopkins University, Baltimore, MD.

Zhengjia Chen (Z)

Department of Hematology and Medical Oncology, Winship Cancer Institute of Emory University, Atlanta, GA; Department of Bioinformatics and Biostatistics Shared Resource, Winship Cancer Institute of Emory University, Atlanta, GA.

Virginia Kaklamani (V)

Division of Hematology/Oncology, University of Texas Health Sciences Center, San Antonio, TX.

Ruth M O'Regan (RM)

Department of Medicine and Carbone Cancer Center, University of Wisconsin, Madison, WI. Electronic address: roregan@medicine.wisc.edu.

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Classifications MeSH