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Preferential HER-2/neu overexpression and/or amplification in aggressive histological subtypes of invasive breast cancer

Varga, Z; Zhao, J; Ohlschlegel, C; Odermatt, B; Heitz, P U (2004). Preferential HER-2/neu overexpression and/or amplification in aggressive histological subtypes of invasive breast cancer. Histopathology, 44(4):332-338.

Abstract

AIMS: To investigate whether alterations of the HER2 gene occur more frequently in histologically unfavourable subtypes of invasive breast cancer.
METHODS: The study was composed of nine invasive apocrine, six lipid-rich, 12 glycogen-rich, 11 micropapillary and 33 pleomorphic lobular breast carcinomas. Lymph node involvement was represented in all subgroups. HER2 status was confirmed in all cases by using immunohistochemistry (CB11, Herceptest) and fluorescent in-situ hybridization (FISH) analysis (Vysis).
RESULTS: Micropapillary and apocrine carcinomas showed the highest rate of protein overexpression (72% and 66%) and gene amplification (45% and 44%). Protein overexpression was common in poorly differentiated pleomorphic lobular carcinomas (56%); however, this subgroup failed to show an increased number of gene copies by FISH (31%). The incidence of HER2 overexpression (33% and 50%, respectively) and gene amplification (25% and 33%, respectively) among glycogen-rich and lipid-rich carcinomas was not higher than that observed in breast cancer generally.
CONCLUSION: Our data suggest that preferential involvement of the HER2 gene in micropapillary and apocrine breast carcinomas may contribute to their aggressive behaviour.

Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Institute of Pathology and Molecular Pathology
Dewey Decimal Classification:610 Medicine & health
Scopus Subject Areas:Health Sciences > Pathology and Forensic Medicine
Health Sciences > Histology
Language:English
Date:April 2004
Deposited On:21 Jul 2015 11:02
Last Modified:13 Mar 2025 02:37
Publisher:Wiley-Blackwell Publishing, Inc.
ISSN:0309-0167
OA Status:Closed
Publisher DOI:https://doi.org/10.1111/j.1365-2559.2004.01843.x
PubMed ID:15049898

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