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Metastatic Breast Cancer Coexisting With HER-2 Amplification and EGFR Exon 19 Deletion Benefits From EGFR-TKI Therapy: A Case Report

Background: Patients with different molecular subtypes of breast cancers have different recurrence risks and prognoses. Clinical support and evidence to guide management are absent for patients with breast cancer coexisting with HER-2 amplification and EGFR mutations. Case presentation: We report a...

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Autores principales: Jing, Wei, Ma, Jie-Tao, Han, Cheng-Bo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7274020/
https://www.ncbi.nlm.nih.gov/pubmed/32547945
http://dx.doi.org/10.3389/fonc.2020.00771
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author Jing, Wei
Ma, Jie-Tao
Han, Cheng-Bo
author_facet Jing, Wei
Ma, Jie-Tao
Han, Cheng-Bo
author_sort Jing, Wei
collection PubMed
description Background: Patients with different molecular subtypes of breast cancers have different recurrence risks and prognoses. Clinical support and evidence to guide management are absent for patients with breast cancer coexisting with HER-2 amplification and EGFR mutations. Case presentation: We report a case of breast cancer coexisting with HER-2 amplification and EGFR exon 19 deletion (E19 del). The patient presented with solitary pulmonary nodule and enlargement of hilar and mediastinal lymph nodes 2 years after radical mastectomy. Biopsy of the subcarinal lymph node showed suspected adenocarcinoma. The specimen was too small for further immunohistochemistry, but an EGFR E19 del was discovered. Due to the primary diagnosis of EGFR-mutant lung adenocarcinoma, EGFR-TKI gefitinib was administered and resulted in 1 year of stable disease until the patient developed progression in the right pulmonary nodule with new metastatic cervical lymph nodes. According to histopathological findings of re-biopsy of the pulmonary nodule and left cervical and subcarinal lymph nodes, the patient was diagnosed with breast cancer with lung metastasis and multiple lymph node metastases. The patient received multiple anti-HER-2-targeted therapies (trastuzumab for 9.7 months, lapatinib for 9 months, and pyrotinib for 4+ months) and survived for more than 36 months after lung metastasis. Conclusions: This case suggested that breast cancer coexisting with HER-2 amplification and EGFR E19 del may be driven by both HER-2 and EGFR signaling pathways, and patients can benefit from EGFR-TKI and anti-HER-2 therapy.
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spelling pubmed-72740202020-06-15 Metastatic Breast Cancer Coexisting With HER-2 Amplification and EGFR Exon 19 Deletion Benefits From EGFR-TKI Therapy: A Case Report Jing, Wei Ma, Jie-Tao Han, Cheng-Bo Front Oncol Oncology Background: Patients with different molecular subtypes of breast cancers have different recurrence risks and prognoses. Clinical support and evidence to guide management are absent for patients with breast cancer coexisting with HER-2 amplification and EGFR mutations. Case presentation: We report a case of breast cancer coexisting with HER-2 amplification and EGFR exon 19 deletion (E19 del). The patient presented with solitary pulmonary nodule and enlargement of hilar and mediastinal lymph nodes 2 years after radical mastectomy. Biopsy of the subcarinal lymph node showed suspected adenocarcinoma. The specimen was too small for further immunohistochemistry, but an EGFR E19 del was discovered. Due to the primary diagnosis of EGFR-mutant lung adenocarcinoma, EGFR-TKI gefitinib was administered and resulted in 1 year of stable disease until the patient developed progression in the right pulmonary nodule with new metastatic cervical lymph nodes. According to histopathological findings of re-biopsy of the pulmonary nodule and left cervical and subcarinal lymph nodes, the patient was diagnosed with breast cancer with lung metastasis and multiple lymph node metastases. The patient received multiple anti-HER-2-targeted therapies (trastuzumab for 9.7 months, lapatinib for 9 months, and pyrotinib for 4+ months) and survived for more than 36 months after lung metastasis. Conclusions: This case suggested that breast cancer coexisting with HER-2 amplification and EGFR E19 del may be driven by both HER-2 and EGFR signaling pathways, and patients can benefit from EGFR-TKI and anti-HER-2 therapy. Frontiers Media S.A. 2020-05-29 /pmc/articles/PMC7274020/ /pubmed/32547945 http://dx.doi.org/10.3389/fonc.2020.00771 Text en Copyright © 2020 Jing, Ma and Han. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Oncology
Jing, Wei
Ma, Jie-Tao
Han, Cheng-Bo
Metastatic Breast Cancer Coexisting With HER-2 Amplification and EGFR Exon 19 Deletion Benefits From EGFR-TKI Therapy: A Case Report
title Metastatic Breast Cancer Coexisting With HER-2 Amplification and EGFR Exon 19 Deletion Benefits From EGFR-TKI Therapy: A Case Report
title_full Metastatic Breast Cancer Coexisting With HER-2 Amplification and EGFR Exon 19 Deletion Benefits From EGFR-TKI Therapy: A Case Report
title_fullStr Metastatic Breast Cancer Coexisting With HER-2 Amplification and EGFR Exon 19 Deletion Benefits From EGFR-TKI Therapy: A Case Report
title_full_unstemmed Metastatic Breast Cancer Coexisting With HER-2 Amplification and EGFR Exon 19 Deletion Benefits From EGFR-TKI Therapy: A Case Report
title_short Metastatic Breast Cancer Coexisting With HER-2 Amplification and EGFR Exon 19 Deletion Benefits From EGFR-TKI Therapy: A Case Report
title_sort metastatic breast cancer coexisting with her-2 amplification and egfr exon 19 deletion benefits from egfr-tki therapy: a case report
topic Oncology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7274020/
https://www.ncbi.nlm.nih.gov/pubmed/32547945
http://dx.doi.org/10.3389/fonc.2020.00771
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