Outcome of Everolimus-Based Therapy in Hormone-Receptor-Positive Metastatic Breast Cancer Patients After Progression on Palbociclib.
Metastatic breast cancer
estrogen receptor-positive breast cancer
everolimus
palbociclib
Journal
Breast cancer : basic and clinical research
ISSN: 1178-2234
Titre abrégé: Breast Cancer (Auckl)
Pays: United States
ID NLM: 101474356
Informations de publication
Date de publication:
2020
2020
Historique:
received:
08
04
2020
accepted:
02
07
2020
entrez:
6
8
2020
pubmed:
6
8
2020
medline:
6
8
2020
Statut:
epublish
Résumé
Despite the approval of mTOR inhibitor everolimus and CDK4/6 inhibitors in the management of hormone-receptor-positive HER2 non-amplified metastatic breast cancer (HR+ HER2-MBC), the optimal sequence of therapy is unclear. There are no clinical data on efficacy of everolimus in HR+ HER2-MBC after cancer progresses on CDK4/6 inhibitors. The objective of this study is to find the efficacy of everolimus in HR+ HER2-MBC after they progress on a CDK4/6 inhibitor palbociclib. This is a retrospective, 2-institute review of HR+ HER2-MBC from Jan 2015 to March 2018 treated with everolimus after progression on palbociclib. Primary end point was median progression-free survival (PFS), secondary end points objective response rate (ORR), clinical benefit ratio (CBR), and overall survival (OS). Out of 41 women with median age 61 years (33, 87) enrolled, 66% had received adjuvant systemic therapy, 61% had visceral disease, and 95% had prior nonsteroidal aromatase inhibitors. About 83% women had 3 or more chemotherapy or hormonal therapies prior to everolimus. Kaplan-Meier estimates showed a median PFS of 4.2 months (95% confidence interval [CI]: 3.2-6.2). The median OS was 18.7 months (95% CI 9.5 to not reached). Objective response rate and CBR were both 17.1%. Everolimus was associated with modest PFS and ORR in HR+ HER2-MBCs postprogression on palbociclib.
Sections du résumé
BACKGROUND
BACKGROUND
Despite the approval of mTOR inhibitor everolimus and CDK4/6 inhibitors in the management of hormone-receptor-positive HER2 non-amplified metastatic breast cancer (HR+ HER2-MBC), the optimal sequence of therapy is unclear. There are no clinical data on efficacy of everolimus in HR+ HER2-MBC after cancer progresses on CDK4/6 inhibitors.
OBJECTIVE
OBJECTIVE
The objective of this study is to find the efficacy of everolimus in HR+ HER2-MBC after they progress on a CDK4/6 inhibitor palbociclib.
METHODS
METHODS
This is a retrospective, 2-institute review of HR+ HER2-MBC from Jan 2015 to March 2018 treated with everolimus after progression on palbociclib. Primary end point was median progression-free survival (PFS), secondary end points objective response rate (ORR), clinical benefit ratio (CBR), and overall survival (OS).
RESULTS
RESULTS
Out of 41 women with median age 61 years (33, 87) enrolled, 66% had received adjuvant systemic therapy, 61% had visceral disease, and 95% had prior nonsteroidal aromatase inhibitors. About 83% women had 3 or more chemotherapy or hormonal therapies prior to everolimus. Kaplan-Meier estimates showed a median PFS of 4.2 months (95% confidence interval [CI]: 3.2-6.2). The median OS was 18.7 months (95% CI 9.5 to not reached). Objective response rate and CBR were both 17.1%.
CONCLUSION
CONCLUSIONS
Everolimus was associated with modest PFS and ORR in HR+ HER2-MBCs postprogression on palbociclib.
Identifiants
pubmed: 32753876
doi: 10.1177/1178223420944864
pii: 10.1177_1178223420944864
pmc: PMC7378710
doi:
Types de publication
Journal Article
Langues
eng
Pagination
1178223420944864Subventions
Organisme : NCI NIH HHS
ID : P30 CA008748
Pays : United States
Informations de copyright
© The Author(s) 2020.
Déclaration de conflit d'intérêts
Declaration of conflicting interests:The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: E.G.L. has received royalty from UpToDate. A.B. has/had consulting or advisory role for Agendia, Bayer, bioTheranostics, Celgene, Genentech/Roche, Genomic Health, Lilly, NanoString Technologies, Novartis, Pfizer, and Puma Biotechnology. A.P.E. has received honorarium from Pfizer. M.O. has received research fund from Pfizer/NCCN and has/had consulting or advisory role for Novartis and AstraZeneca. A.D. has received honorarium from Daiichi Sankyo. All other authors declare that they have no conflict of interest.
Références
JAMA Oncol. 2018 Jul 1;4(7):977-984
pubmed: 29566104
Oncogene. 2017 Apr 20;36(16):2255-2264
pubmed: 27748766
Mol Cell. 2016 Jun 16;62(6):929-942
pubmed: 27237051
J Biol Chem. 1993 Oct 25;268(30):22825-9
pubmed: 8226793
J Biol Chem. 1998 Nov 6;273(45):29864-72
pubmed: 9792703
Cancer Res. 1999 Aug 1;59(15):3581-7
pubmed: 10446965
J Comp Eff Res. 2015 Aug;4(4):315-26
pubmed: 26274793
Curr Med Res Opin. 2015 Jun;31(6):1095-103
pubmed: 25971725
Cancer Cell. 2014 Jul 14;26(1):136-49
pubmed: 25002028
Lancet Oncol. 2016 Apr;17(4):425-439
pubmed: 26947331
N Engl J Med. 2012 Feb 9;366(6):520-9
pubmed: 22149876
J Clin Oncol. 2017 Sep 1;35(25):2875-2884
pubmed: 28580882
N Engl J Med. 2016 Nov 3;375(18):1738-1748
pubmed: 27717303
J Clin Oncol. 2017 Nov 10;35(32):3638-3646
pubmed: 28968163
Cell Rep. 2016 Feb 9;14(5):979-990
pubmed: 26804906
Ann Oncol. 2014 Dec;25(12):2357-62
pubmed: 25231953
N Engl J Med. 2016 Nov 17;375(20):1925-1936
pubmed: 27959613
Nat Rev Cancer. 2006 Sep;6(9):729-34
pubmed: 16915295
Am J Physiol Cell Physiol. 2004 Aug;287(2):C281-91
pubmed: 15028555
J Clin Oncol. 2010 Jun 1;28(16):2784-95
pubmed: 20404251
J Clin Oncol. 2018 Aug 20;36(24):2465-2472
pubmed: 29860922