Molecular Cytogenetic Comparison of Apocrine Hyperplasia and Apocrine Carcinoma of the Breast

The relationship of apocrine metaplasia to invasive breast cancer is controversial. Different authors have reported that apocrine differentiation in proliferative lesions may be a risk factor, a precursor lesion, or have no association with malignancy. The aim of this study was to compare the geneti...

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Prif Awduron: Jones, Chris, Damiani, Stefania, Wells, Dagan, Chaggar, Ranbir, Lakhani, Sunil R., Eusebi, Vincenzo
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Cyhoeddwyd: American Society for Investigative Pathology 2001
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Mynediad Ar-lein:https://ncbi.nlm.nih.gov/pmc/articles/PMC1850273/
https://ncbi.nlm.nih.gov/pubmed/11141494
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spelling pubmed-18502732007-06-15 Molecular Cytogenetic Comparison of Apocrine Hyperplasia and Apocrine Carcinoma of the Breast Jones, Chris Damiani, Stefania Wells, Dagan Chaggar, Ranbir Lakhani, Sunil R. Eusebi, Vincenzo Am J Pathol Regular Articles The relationship of apocrine metaplasia to invasive breast cancer is controversial. Different authors have reported that apocrine differentiation in proliferative lesions may be a risk factor, a precursor lesion, or have no association with malignancy. The aim of this study was to compare the genetic alterations in benign apocrine hyperplasia with apocrine ductal carcinoma in situ (DCIS) and invasive apocrine carcinomas of the breast using comparative genomic hybridization. The mean number of alterations in apocrine hyperplasia was 4.1 (n = 10) compared to 10.2 in apocrine DCIS (n = 10) and 14.8 (n = 4) in invasive carcinoma. The most common alterations in apocrine hyperplasia were gains of 2q, 13q, and 1p and losses of 1p, 17q, 22q, 2p, 10q, and 16q. Apocrine DCIS and invasive carcinomas showed gains of 1q, 2q, 1p, and losses of 1p, 22q, 17q, 12q, and 16q as their most common DNA copy number changes. Apocrine hyperplasia is considered to be a benign lesion and its relationship to invasive carcinoma remains unclear. Our data suggest that some apocrine hyperplasias may be clonal proliferations. The mean number of alterations are lower in apocrine hyperplasia, however the changes show considerable overlap with those identified in in situ and invasive apocrine carcinoma. These alterations are also commonly seen in nonapocrine breast cancer. The data are consistent with apocrine hyperplasia as a putative nonobligate precursor of apocrine carcinoma. American Society for Investigative Pathology 2001-01 /pmc/articles/PMC1850273/ /pubmed/11141494 Text en Copyright © 2001, American Society for Investigative Pathology
institution US National Library of Medicine
collection PubMed Central
language English
format Article
topic Regular Articles
spellingShingle Regular Articles
Jones, Chris
Damiani, Stefania
Wells, Dagan
Chaggar, Ranbir
Lakhani, Sunil R.
Eusebi, Vincenzo
Molecular Cytogenetic Comparison of Apocrine Hyperplasia and Apocrine Carcinoma of the Breast
description The relationship of apocrine metaplasia to invasive breast cancer is controversial. Different authors have reported that apocrine differentiation in proliferative lesions may be a risk factor, a precursor lesion, or have no association with malignancy. The aim of this study was to compare the genetic alterations in benign apocrine hyperplasia with apocrine ductal carcinoma in situ (DCIS) and invasive apocrine carcinomas of the breast using comparative genomic hybridization. The mean number of alterations in apocrine hyperplasia was 4.1 (n = 10) compared to 10.2 in apocrine DCIS (n = 10) and 14.8 (n = 4) in invasive carcinoma. The most common alterations in apocrine hyperplasia were gains of 2q, 13q, and 1p and losses of 1p, 17q, 22q, 2p, 10q, and 16q. Apocrine DCIS and invasive carcinomas showed gains of 1q, 2q, 1p, and losses of 1p, 22q, 17q, 12q, and 16q as their most common DNA copy number changes. Apocrine hyperplasia is considered to be a benign lesion and its relationship to invasive carcinoma remains unclear. Our data suggest that some apocrine hyperplasias may be clonal proliferations. The mean number of alterations are lower in apocrine hyperplasia, however the changes show considerable overlap with those identified in in situ and invasive apocrine carcinoma. These alterations are also commonly seen in nonapocrine breast cancer. The data are consistent with apocrine hyperplasia as a putative nonobligate precursor of apocrine carcinoma.
author Jones, Chris
Damiani, Stefania
Wells, Dagan
Chaggar, Ranbir
Lakhani, Sunil R.
Eusebi, Vincenzo
author_facet Jones, Chris
Damiani, Stefania
Wells, Dagan
Chaggar, Ranbir
Lakhani, Sunil R.
Eusebi, Vincenzo
author_sort Jones, Chris
title Molecular Cytogenetic Comparison of Apocrine Hyperplasia and Apocrine Carcinoma of the Breast
title_short Molecular Cytogenetic Comparison of Apocrine Hyperplasia and Apocrine Carcinoma of the Breast
title_full Molecular Cytogenetic Comparison of Apocrine Hyperplasia and Apocrine Carcinoma of the Breast
title_fullStr Molecular Cytogenetic Comparison of Apocrine Hyperplasia and Apocrine Carcinoma of the Breast
title_full_unstemmed Molecular Cytogenetic Comparison of Apocrine Hyperplasia and Apocrine Carcinoma of the Breast
title_sort molecular cytogenetic comparison of apocrine hyperplasia and apocrine carcinoma of the breast
publisher American Society for Investigative Pathology
publisher_facet American Society for Investigative Pathology
publishDate 2001
url https://ncbi.nlm.nih.gov/pmc/articles/PMC1850273/
https://ncbi.nlm.nih.gov/pubmed/11141494
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