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Comparison of HER2 amplification status among breast cancer subgroups offers new insights in pathways of breast cancer progression.

Authors
  • Lambein, Kathleen1, 2
  • Van Bockstal, Mieke3, 4
  • Vandemaele, Lies3
  • Van den Broecke, Rudy5
  • Cocquyt, Veronique6
  • Geenen, Sofie3
  • Denys, Hannelore6
  • Libbrecht, Louis7, 8
  • 1 Department of Pathology, AZ St Lucas Hospital, Groenebriel 1, 9000, Ghent, Belgium. , (Belgium)
  • 2 Department of Oncology, KU Leuven, Surgical Oncology, University Hospitals Leuven, Herestraat 49, 3000, Leuven, Belgium. , (Belgium)
  • 3 Department of Medical and Forensic Pathology, Ghent University, De Pintelaan 185, 9000, Ghent, Belgium. , (Belgium)
  • 4 Cancer Research Institute Ghent (CRIG), Ghent, Belgium. , (Belgium)
  • 5 Department of Gynaecology, Ghent University Hospital, De Pintelaan 185, 9000, Ghent, Belgium. , (Belgium)
  • 6 Department of Medical Oncology, Ghent University Hospital, De Pintelaan 185, 9000, Ghent, Belgium. , (Belgium)
  • 7 Department of Medical and Forensic Pathology, Ghent University, De Pintelaan 185, 9000, Ghent, Belgium. Louis.libbrech[email protected] , (Belgium)
  • 8 Department of Pathology, University Clinics St Luc, Hippokrateslaan 10, 1200, Sint-Lambrechts-Woluwe, Belgium. [email protected] , (Belgium)
Type
Published Article
Journal
Virchows Archiv : an international journal of pathology
Publication Date
Nov 01, 2017
Volume
471
Issue
5
Pages
575–587
Identifiers
DOI: 10.1007/s00428-017-2161-8
PMID: 28567637
Source
Medline
Keywords
License
Unknown

Abstract

Although the prognostic and predictive significance of human epidermal growth factor receptor 2 (HER2) in invasive breast cancer is well established, its role in ductal carcinoma in situ (DCIS) remains unclear. Reports on combined evaluation of both HER2 protein expression and HER2 amplification status in pure DCIS and DCIS adjacent to invasive ductal carcinoma (i.e., admixed DCIS) are scarce. In this study, immunohistochemistry and fluorescence in situ hybridization (FISH) were used to assess HER2 status in 72 cases of pure DCIS, 73 cases of DCIS admixed with invasive ductal carcinoma (IDC), and 60 cases of pure IDC. HER2 copy number-based amplification was present in 49% of pure DCIS, 16% of admixed DCIS, 18% of admixed IDC, and 8% of pure IDC. Amplified pure DCIS with clusters of HER2 signals showed a significantly lower HER2 copy number than amplified admixed DCIS with clusters. Whereas pure DCIS and admixed DCIS presented significant differences, the in situ and invasive component of admixed tumors showed striking similarities regarding mean HER2 and chromosome 17 centromere (CEP17) copy number, grade, and estrogen and progesterone receptor expression. The discrepant prevalence of HER2 amplification among breast cancer subgroups indirectly suggests that HER2 may not play a crucial role in the transition of in situ to invasive breast cancer. The similarities in HER2 amplification status between the in situ and invasive component of admixed tumors hint at a common biological pathway for both components. Our data support the theory that pure DCIS, pure IDC, and admixed lesions have a common progenitor, but can progress as separate lineages.

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