Relapsed and De Novo Metastatic HER2-positive Breast Cancer Treated With Trastuzumab: Tumor Genotypes and Clinical Measures Associated With Patient Outcome.


Journal

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

Informations de publication

Date de publication:
04 2019
Historique:
received: 20 06 2018
revised: 22 08 2018
accepted: 29 10 2018
pubmed: 14 12 2018
medline: 15 4 2020
entrez: 15 12 2018
Statut: ppublish

Résumé

We examined tumor genotype characteristics of human epidermal growth factor receptor 2 (HER2)-positive relapsed (R-) and de novo (dn-) metastatic breast cancer (MBC) in trastuzumab-treated patients who were previously not exposed to this agent. We analyzed genotypes obtained upon deep sequencing from 113 HER2-positive primary tumors from 69 patients with R-MBC and 44 patients with dn-MBC. Mutations were observed in 90 (79.6%) tumors, 56 R-MBC and 34 dn-MBC (median number per tumor: 2; mean: 11.2; range: 0-150). The top mutated gene was TP53 (63.7%) followed by PIK3CA (24.8%) and others that were mostly co-mutated with TP53 (eg, 22 of 28 PIK3CA mutated tumors were co-mutated in TP53, 17 of these were R-MBC [P = .041]). dn-MBC had higher CEN17 average copies (P = .048). Tumor mutational burden inversely correlated with average HER2 copies (rho -0.32; P < .001). In all patients, PIK3CA mutations and higher proliferation rate were independent unfavorable prognosticators. In R-MBC, longer disease-free interval between initial diagnosis and relapse conferred lower risk for time-to-progression (P < .001) and death (P = .009); PIK3CA mutations conferred higher risk for death (P = .035). In dn-MBC, surgical removal of the primary tumor before any other therapy was favorable for time-to-progression (P = .002); higher tumor mutational burden was unfavorable for survival (P = .026). Except for the overall unfavorable prognostic effect of PIK3CA mutations in trastuzumab-treated MBC, our exploratory findings indicate that the outcome of patients with R-MBC is related to patient benefit from the preceding adjuvant chemotherapy and provide initial evidence that tumor mutational burden may be related to prognosis in dn-MBC, which is of potential clinical relevance and merits further investigation.

Sections du résumé

BACKGROUND
We examined tumor genotype characteristics of human epidermal growth factor receptor 2 (HER2)-positive relapsed (R-) and de novo (dn-) metastatic breast cancer (MBC) in trastuzumab-treated patients who were previously not exposed to this agent.
MATERIALS AND METHODS
We analyzed genotypes obtained upon deep sequencing from 113 HER2-positive primary tumors from 69 patients with R-MBC and 44 patients with dn-MBC.
RESULTS
Mutations were observed in 90 (79.6%) tumors, 56 R-MBC and 34 dn-MBC (median number per tumor: 2; mean: 11.2; range: 0-150). The top mutated gene was TP53 (63.7%) followed by PIK3CA (24.8%) and others that were mostly co-mutated with TP53 (eg, 22 of 28 PIK3CA mutated tumors were co-mutated in TP53, 17 of these were R-MBC [P = .041]). dn-MBC had higher CEN17 average copies (P = .048). Tumor mutational burden inversely correlated with average HER2 copies (rho -0.32; P < .001). In all patients, PIK3CA mutations and higher proliferation rate were independent unfavorable prognosticators. In R-MBC, longer disease-free interval between initial diagnosis and relapse conferred lower risk for time-to-progression (P < .001) and death (P = .009); PIK3CA mutations conferred higher risk for death (P = .035). In dn-MBC, surgical removal of the primary tumor before any other therapy was favorable for time-to-progression (P = .002); higher tumor mutational burden was unfavorable for survival (P = .026).
CONCLUSIONS
Except for the overall unfavorable prognostic effect of PIK3CA mutations in trastuzumab-treated MBC, our exploratory findings indicate that the outcome of patients with R-MBC is related to patient benefit from the preceding adjuvant chemotherapy and provide initial evidence that tumor mutational burden may be related to prognosis in dn-MBC, which is of potential clinical relevance and merits further investigation.

Identifiants

pubmed: 30545790
pii: S1526-8209(18)30424-5
doi: 10.1016/j.clbc.2018.10.014
pii:
doi:

Substances chimiques

Antineoplastic Agents, Immunological 0
Biomarkers, Tumor 0
TP53 protein, human 0
Tumor Suppressor Protein p53 0
Class I Phosphatidylinositol 3-Kinases EC 2.7.1.137
PIK3CA protein, human EC 2.7.1.137
ERBB2 protein, human EC 2.7.10.1
Receptor, ErbB-2 EC 2.7.10.1
Trastuzumab P188ANX8CK

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

113-125.e4

Informations de copyright

Copyright © 2018 Elsevier Inc. All rights reserved.

Auteurs

Vassiliki Kotoula (V)

Department of Pathology, Aristotle University of Thessaloniki, School of Health Sciences, Faculty of Medicine, Thessaloniki, Greece; Laboratory of Molecular Oncology, Hellenic Foundation for Cancer Research/Aristotle University of Thessaloniki, Thessaloniki, Greece. Electronic address: vkotoula@auth.gr.

Kalliopi Tsakiri (K)

Laboratory of Molecular Oncology, Hellenic Foundation for Cancer Research/Aristotle University of Thessaloniki, Thessaloniki, Greece.

Georgia-Angeliki Koliou (GA)

Section of Biostatistics, Hellenic Cooperative Oncology Group, Data Office, Athens, Greece.

Georgios Lazaridis (G)

Department of Medical Oncology, Papageorgiou Hospital, Aristotle University of Thessaloniki, School of Health Sciences, Faculty of Medicine, Thessaloniki, Greece.

Kyriaki Papadopoulou (K)

Laboratory of Molecular Oncology, Hellenic Foundation for Cancer Research/Aristotle University of Thessaloniki, Thessaloniki, Greece.

Eleni Giannoulatou (E)

Victor Chang Cardiac Research Institute, Darlinghurst, NSW, Australia; The University of New South Wales, Kensington, NSW, Australia.

Ioannis Tikas (I)

Laboratory of Molecular Oncology, Hellenic Foundation for Cancer Research/Aristotle University of Thessaloniki, Thessaloniki, Greece.

Christos Christodoulou (C)

Second Department of Medical Oncology, Metropolitan Hospital, Piraeus, Greece.

Kyriakos Chatzopoulos (K)

Laboratory of Molecular Oncology, Hellenic Foundation for Cancer Research/Aristotle University of Thessaloniki, Thessaloniki, Greece.

Mattheos Bobos (M)

Laboratory of Molecular Oncology, Hellenic Foundation for Cancer Research/Aristotle University of Thessaloniki, Thessaloniki, Greece.

George Pentheroudakis (G)

Department of Medical Oncology, Ioannina University Hospital, Ioannina, Greece.

Eleftheria Tsolaki (E)

Laboratory of Molecular Oncology, Hellenic Foundation for Cancer Research/Aristotle University of Thessaloniki, Thessaloniki, Greece.

Anna Batistatou (A)

Department of Pathology, Ioannina University Hospital, Ioannina, Greece.

Athanassios Kotsakis (A)

University Hospital of Heraklion, University of Crete, School of Medicine, Heraklion, Crete, Greece.

Angelos Koutras (A)

Division of Oncology, Department of Medicine, University Hospital, University of Patras Medical School, Patras, Greece.

Helena Linardou (H)

First Department of Medical Oncology, Metropolitan Hospital, Piraeus, Greece.

Evangelia Razis (E)

Third Department of Medical Oncology, Hygeia Hospital, Athens, Greece.

Eleni Res (E)

Third Department of Medical Oncology, Agii Anargiri Cancer Hospital, Athens, Greece.

Dimitrios Pectasides (D)

Oncology Section, Second Department of Internal Medicine, Hippokration Hospital, Athens, Greece.

George Fountzilas (G)

Laboratory of Molecular Oncology, Hellenic Foundation for Cancer Research/Aristotle University of Thessaloniki, Thessaloniki, Greece; Aristotle University of Thessaloniki, Thessaloniki, Greece.

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Classifications MeSH