PMID- 28567637
OWN - NLM
STAT- MEDLINE
DCOM- 20171113
LR  - 20181113
IS  - 1432-2307 (Electronic)
IS  - 0945-6317 (Linking)
VI  - 471
IP  - 5
DP  - 2017 Nov
TI  - Comparison of HER2 amplification status among breast cancer subgroups offers new 
      insights in pathways of breast cancer progression.
PG  - 575-587
LID - 10.1007/s00428-017-2161-8 [doi]
AB  - 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.
FAU - Lambein, Kathleen
AU  - Lambein K
AD  - Department of Pathology, AZ St Lucas Hospital, Groenebriel 1, 9000, Ghent, 
      Belgium.
AD  - Department of Oncology, KU Leuven, Surgical Oncology, University Hospitals 
      Leuven, Herestraat 49, 3000, Leuven, Belgium.
FAU - Van Bockstal, Mieke
AU  - Van Bockstal M
AD  - Department of Medical and Forensic Pathology, Ghent University, De Pintelaan 185, 
      9000, Ghent, Belgium.
AD  - Cancer Research Institute Ghent (CRIG), Ghent, Belgium.
FAU - Vandemaele, Lies
AU  - Vandemaele L
AD  - Department of Medical and Forensic Pathology, Ghent University, De Pintelaan 185, 
      9000, Ghent, Belgium.
FAU - Van den Broecke, Rudy
AU  - Van den Broecke R
AD  - Department of Gynaecology, Ghent University Hospital, De Pintelaan 185, 9000, 
      Ghent, Belgium.
FAU - Cocquyt, Veronique
AU  - Cocquyt V
AD  - Department of Medical Oncology, Ghent University Hospital, De Pintelaan 185, 
      9000, Ghent, Belgium.
FAU - Geenen, Sofie
AU  - Geenen S
AD  - Department of Medical and Forensic Pathology, Ghent University, De Pintelaan 185, 
      9000, Ghent, Belgium.
FAU - Denys, Hannelore
AU  - Denys H
AD  - Department of Medical Oncology, Ghent University Hospital, De Pintelaan 185, 
      9000, Ghent, Belgium.
FAU - Libbrecht, Louis
AU  - Libbrecht L
AD  - Department of Medical and Forensic Pathology, Ghent University, De Pintelaan 185, 
      9000, Ghent, Belgium. Louis.libbrecht@uclouvain.be.
AD  - Department of Pathology, University Clinics St Luc, Hippokrateslaan 10, 1200, 
      Sint-Lambrechts-Woluwe, Belgium. Louis.libbrecht@uclouvain.be.
LA  - eng
PT  - Comparative Study
PT  - Journal Article
DEP - 20170531
PL  - Germany
TA  - Virchows Arch
JT  - Virchows Archiv : an international journal of pathology
JID - 9423843
RN  - 0 (Biomarkers, Tumor)
RN  - EC 2.7.10.1 (ERBB2 protein, human)
RN  - EC 2.7.10.1 (Receptor, ErbB-2)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Biomarkers, Tumor/analysis/*genetics
MH  - Breast Neoplasms/*genetics/pathology
MH  - Carcinoma, Ductal, Breast/*genetics/pathology
MH  - Carcinoma, Intraductal, Noninfiltrating/*genetics/pathology
MH  - Disease Progression
MH  - Female
MH  - Gene Amplification
MH  - Humans
MH  - Middle Aged
MH  - Receptor, ErbB-2/*genetics
OTO - NOTNLM
OT  - Breast cancer progression
OT  - Clusters
OT  - Ductal carcinoma in situ (DCIS)
OT  - HER2 amplification
OT  - HER2 protein overexpression
EDAT- 2017/06/02 06:00
MHDA- 2017/11/14 06:00
CRDT- 2017/06/02 06:00
PHST- 2017/03/28 00:00 [received]
PHST- 2017/05/22 00:00 [accepted]
PHST- 2017/05/09 00:00 [revised]
PHST- 2017/06/02 06:00 [pubmed]
PHST- 2017/11/14 06:00 [medline]
PHST- 2017/06/02 06:00 [entrez]
AID - 10.1007/s00428-017-2161-8 [pii]
AID - 10.1007/s00428-017-2161-8 [doi]
PST - ppublish
SO  - Virchows Arch. 2017 Nov;471(5):575-587. doi: 10.1007/s00428-017-2161-8. Epub 2017 
      May 31.