ESR1 gene amplification and MAP3K mutations are selected during adjuvant endocrine therapies in relapsing Hormone Receptor-positive, HER2-negative breast cancer (HR+ HER2- BC).

<h4>Background</h4>Previous studies have provided a comprehensive picture of genomic alterations in primary and metastatic Hormone Receptor (HR)-positive, Human Epidermal growth factor Receptor 2 (HER2)-negative breast cancer (HR+ HER2- BC). However, the evolution of the genomic landscap...

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Main Authors: Lorenzo Ferrando, Andrea Vingiani, Anna Garuti, Claudio Vernieri, Antonino Belfiore, Luca Agnelli, Gianpaolo Dagrada, Diana Ivanoiu, Giuseppina Bonizzi, Elisabetta Munzone, Luana Lippolis, Martina Dameri, Francesco Ravera, Marco Colleoni, Giuseppe Viale, Luca Magnani, Alberto Ballestrero, Gabriele Zoppoli, Giancarlo Pruneri
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2023-01-01
Series:PLoS Genetics
Online Access:https://journals.plos.org/plosgenetics/article/file?id=10.1371/journal.pgen.1010563&type=printable
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author Lorenzo Ferrando
Andrea Vingiani
Anna Garuti
Claudio Vernieri
Antonino Belfiore
Luca Agnelli
Gianpaolo Dagrada
Diana Ivanoiu
Giuseppina Bonizzi
Elisabetta Munzone
Luana Lippolis
Martina Dameri
Francesco Ravera
Francesco Ravera
Marco Colleoni
Giuseppe Viale
Luca Magnani
Alberto Ballestrero
Gabriele Zoppoli
Giancarlo Pruneri
author_facet Lorenzo Ferrando
Andrea Vingiani
Anna Garuti
Claudio Vernieri
Antonino Belfiore
Luca Agnelli
Gianpaolo Dagrada
Diana Ivanoiu
Giuseppina Bonizzi
Elisabetta Munzone
Luana Lippolis
Martina Dameri
Francesco Ravera
Francesco Ravera
Marco Colleoni
Giuseppe Viale
Luca Magnani
Alberto Ballestrero
Gabriele Zoppoli
Giancarlo Pruneri
author_sort Lorenzo Ferrando
collection DOAJ
description <h4>Background</h4>Previous studies have provided a comprehensive picture of genomic alterations in primary and metastatic Hormone Receptor (HR)-positive, Human Epidermal growth factor Receptor 2 (HER2)-negative breast cancer (HR+ HER2- BC). However, the evolution of the genomic landscape of HR+ HER2- BC during adjuvant endocrine therapies (ETs) remains poorly investigated.<h4>Methods and findings</h4>We performed a genomic characterization of surgically resected HR+ HER2- BC patients relapsing during or at the completion of adjuvant ET. Using a customized panel, we comprehensively evaluated gene mutations and copy number variation (CNV) in paired primary and metastatic specimens. After retrieval and quality/quantity check of tumor specimens from an original cohort of 204 cases, 74 matched tumor samples were successfully evaluated for DNA mutations and CNV analysis. Along with previously reported genomic alterations, including PIK3CA, TP53, CDH1, GATA3 and ESR1 mutations/deletions, we found that ESR1 gene amplification (confirmed by FISH) and MAP3K mutations were enriched in metastatic lesions as compared to matched primary tumors. These alterations were exclusively found in patients treated with adjuvant aromatase inhibitors or LHRH analogs plus tamoxifen, but not in patients treated with tamoxifen alone. Patients with tumors bearing MAP3K mutations in metastatic lesions had significantly worse distant relapse-free survival (hazard ratio [HR] 3.4, 95% CI 1.52-7.70, p value 0.003) and worse overall survival (HR 5.2, 95% CI 2.10-12.8, p-value < 0.001) independently of other clinically relevant patient- and tumor-related variables.<h4>Conclusions</h4>ESR1 amplification and activating MAP3K mutations are potential drivers of acquired resistance to adjuvant ETs employing estrogen deprivation in HR+ HER2- BC. MAP3K mutations are associated with worse prognosis in patients with metastatic disease.
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institution Kabale University
issn 1553-7390
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publishDate 2023-01-01
publisher Public Library of Science (PLoS)
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series PLoS Genetics
spelling doaj-art-14b422e7ad2742c09e052fbd82eff0102025-08-20T03:44:45ZengPublic Library of Science (PLoS)PLoS Genetics1553-73901553-74042023-01-01191e101056310.1371/journal.pgen.1010563ESR1 gene amplification and MAP3K mutations are selected during adjuvant endocrine therapies in relapsing Hormone Receptor-positive, HER2-negative breast cancer (HR+ HER2- BC).Lorenzo FerrandoAndrea VingianiAnna GarutiClaudio VernieriAntonino BelfioreLuca AgnelliGianpaolo DagradaDiana IvanoiuGiuseppina BonizziElisabetta MunzoneLuana LippolisMartina DameriFrancesco RaveraFrancesco RaveraMarco ColleoniGiuseppe VialeLuca MagnaniAlberto BallestreroGabriele ZoppoliGiancarlo Pruneri<h4>Background</h4>Previous studies have provided a comprehensive picture of genomic alterations in primary and metastatic Hormone Receptor (HR)-positive, Human Epidermal growth factor Receptor 2 (HER2)-negative breast cancer (HR+ HER2- BC). However, the evolution of the genomic landscape of HR+ HER2- BC during adjuvant endocrine therapies (ETs) remains poorly investigated.<h4>Methods and findings</h4>We performed a genomic characterization of surgically resected HR+ HER2- BC patients relapsing during or at the completion of adjuvant ET. Using a customized panel, we comprehensively evaluated gene mutations and copy number variation (CNV) in paired primary and metastatic specimens. After retrieval and quality/quantity check of tumor specimens from an original cohort of 204 cases, 74 matched tumor samples were successfully evaluated for DNA mutations and CNV analysis. Along with previously reported genomic alterations, including PIK3CA, TP53, CDH1, GATA3 and ESR1 mutations/deletions, we found that ESR1 gene amplification (confirmed by FISH) and MAP3K mutations were enriched in metastatic lesions as compared to matched primary tumors. These alterations were exclusively found in patients treated with adjuvant aromatase inhibitors or LHRH analogs plus tamoxifen, but not in patients treated with tamoxifen alone. Patients with tumors bearing MAP3K mutations in metastatic lesions had significantly worse distant relapse-free survival (hazard ratio [HR] 3.4, 95% CI 1.52-7.70, p value 0.003) and worse overall survival (HR 5.2, 95% CI 2.10-12.8, p-value < 0.001) independently of other clinically relevant patient- and tumor-related variables.<h4>Conclusions</h4>ESR1 amplification and activating MAP3K mutations are potential drivers of acquired resistance to adjuvant ETs employing estrogen deprivation in HR+ HER2- BC. MAP3K mutations are associated with worse prognosis in patients with metastatic disease.https://journals.plos.org/plosgenetics/article/file?id=10.1371/journal.pgen.1010563&type=printable
spellingShingle Lorenzo Ferrando
Andrea Vingiani
Anna Garuti
Claudio Vernieri
Antonino Belfiore
Luca Agnelli
Gianpaolo Dagrada
Diana Ivanoiu
Giuseppina Bonizzi
Elisabetta Munzone
Luana Lippolis
Martina Dameri
Francesco Ravera
Francesco Ravera
Marco Colleoni
Giuseppe Viale
Luca Magnani
Alberto Ballestrero
Gabriele Zoppoli
Giancarlo Pruneri
ESR1 gene amplification and MAP3K mutations are selected during adjuvant endocrine therapies in relapsing Hormone Receptor-positive, HER2-negative breast cancer (HR+ HER2- BC).
PLoS Genetics
title ESR1 gene amplification and MAP3K mutations are selected during adjuvant endocrine therapies in relapsing Hormone Receptor-positive, HER2-negative breast cancer (HR+ HER2- BC).
title_full ESR1 gene amplification and MAP3K mutations are selected during adjuvant endocrine therapies in relapsing Hormone Receptor-positive, HER2-negative breast cancer (HR+ HER2- BC).
title_fullStr ESR1 gene amplification and MAP3K mutations are selected during adjuvant endocrine therapies in relapsing Hormone Receptor-positive, HER2-negative breast cancer (HR+ HER2- BC).
title_full_unstemmed ESR1 gene amplification and MAP3K mutations are selected during adjuvant endocrine therapies in relapsing Hormone Receptor-positive, HER2-negative breast cancer (HR+ HER2- BC).
title_short ESR1 gene amplification and MAP3K mutations are selected during adjuvant endocrine therapies in relapsing Hormone Receptor-positive, HER2-negative breast cancer (HR+ HER2- BC).
title_sort esr1 gene amplification and map3k mutations are selected during adjuvant endocrine therapies in relapsing hormone receptor positive her2 negative breast cancer hr her2 bc
url https://journals.plos.org/plosgenetics/article/file?id=10.1371/journal.pgen.1010563&type=printable
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