Department of Histopathology, St. Bartholomew's Hospital, St. Bartholomew's and the Royal London School of Medicine and Dentistry, Queen Mary and Westfield College, University of London, West Smithfield, London EC1A 7BE, UK.
The Breast (Impact Factor: 2.38). 01/2003; 11(6):466-72. DOI: 10.1054/brst.2002.0474
Overexpression and/or amplification of c-myc oncogene are known to occur in human breast carcinomas, particularly those of high grade. Apocrine metaplasia (APM) is a common finding within fibrocystic change, and in some cases appears to be associated with an elevated risk of subsequent breast cancer. It has been suggested that apocrine metaplasia within sclerosing adenosis of the breast, also called apocrine adenosis (AA), has a premalignant potential. Little, however, is known about cellular level genetic alterations in either APM or AA of the breast. Because of this, c-myc expression and amplification in APM and AA were studied. Fluorescence in situ hybridisation (FISH) is a methodological approach to detecting these genetic alterations. In this study, APM and AA were studied immunohistochemically to detect c-myc oncoprotein expression, and FISH was employed using a DNA probe for the c-myc gene in archival tissue sections of cases of APM and AA of the breast. Nuclear immunostaining for c-myc was seen in all APM and AA cases studied, but amplification of the c-myc gene was not seen in any cases with APM or AA. The results of this study indicate that c-myc overexpression appears to occur early in breast oncogenesis. Amplification of the c-myc gene does not occur in APM or AA of the breast, however, suggesting that this particular genetic alteration constitutes a late event in the pathogenesis of breast carcinomas.
"It has been shown to be altered in breast carcinomas, particularly in high grade carcinomas (Selim et al., 2002; Schmitt and Reis-Filho, 2002). Interestingly, c-myc oncoprotein appears to be overexpressed in benign apocrine lesions (apocrine metaplasia and apocrine adenosis) without underlying C- MYC gene alterations (Selim et al., 2002). The status of C-MYC oncogene in apocrine carcinoma remains unknown. "
[Show abstract][Hide abstract] ABSTRACT: Apocrine carcinoma of the breast is a rare, special type of breast carcinoma showing distinct morphologic, immunohistochemical and molecular genetic features. Apocrine epithelium has a characteristic steroid receptor profile that is estrogen receptor and progesterone receptor negative and androgen receptor positive. This combination of morphologic and immunohistochemical characteristics is essential for the proper recognition of the apocrine carcinomas. Strictly defined, apocrine carcinomas express either Her-2/neu or EGFR, which along with androgen receptor positivity make patients with the apocrine carcinoma eligible for targeted therapies.
Histology and histopathology 06/2013; 28(11):1393-1409. · 2.10 Impact Factor
"Apocrine lesions are usually diagnosed based on morphological features  and their relationship with invasive disease remains controversial as different authors have described these lesions as either a precursor in malignant apocrine transformation, or as benign lesions with no correlation with malignancy [24,29,35,37,39–44]. Up to one third of the women aged 30–50 bear large apocrine cysts in their breasts  , and both their frequency and their proposed association with an increased risk of breast cancer have underpinned the importance of investigating these lesions at the molecular level in order to enlighten their putative relationship with invasive disease, in particular apocrine carcinoma    . "
[Show abstract][Hide abstract] ABSTRACT: Breast cancer is a heterogeneous disease that encompasses a wide range of histopathological types including: invasive ductal carcinoma, lobular carcinoma, medullary carcinoma, mucinous carcinoma, tubular carcinoma, and apocrine carcinoma among others. Pure apocrine carcinomas represent about 0.5% of all invasive breast cancers according to the Danish Breast Cancer Cooperative Group Registry, and despite the fact that they are morphologically distinct from other breast lesions, there are at present no standard molecular criteria available for their diagnosis. In addition, the relationship between benign apocrine changes and breast carcinoma is unclear and has been a matter of discussion for many years. Recent proteome expression profiling studies of breast apocrine macrocysts, normal breast tissue, and breast tumours have identified specific apocrine biomarkers [15-hydroxyprostaglandin dehydrogenase (15-PGDH) and hydroxymethylglutaryl coenzyme A reductase (HMG-CoA reductase)] present in early and advanced apocrine lesions. These biomarkers in combination with proteins found to be characteristically upregulated in pure apocrine carcinomas (psoriasin, S100A9, and p53) provide a protein expression signature distinctive for benign apocrine metaplasias and apocrine cystic lesions. These studies have also presented compelling evidence for a direct link, through the expression of the prostaglandin degrading enzyme 15-PGDH, between early apocrine lesions and pure apocrine carcinomas. Moreover, specific antibodies against the components of the expression signature have identified precursor lesions in the linear histological progression to apocrine carcinoma. Finally, the identification of proteins that characterize the early stages of mammary apocrine differentiation such as 15-PGDH, HMG-CoA reductase, and cyclooxygenase 2 (COX-2) has opened a window of opportunity for pharmacological intervention, not only in a therapeutic manner but also in a chemopreventive setting. Here we review published and recent results in the context of the current state of research on breast apocrine cancer.
"68 23 17 Not studied Visscher et al., 1997  33 91 a 100 b 0 Rummukainen et al., 2001  261 14.6 Not studied Not studied Selim et al., 2002  48 Not studied Not studied 0 Rummukainen et al., 2001  177 14 Not studied Not studied "
[Show abstract][Hide abstract] ABSTRACT: One hypothesis for breast cancer development suggests that breast carcinogenesis involves a progression of events leading from benign epithelium to hyperplasia (with or without atypia) to carcinoma in situ and then invasive carcinoma. The MYC gene (alias c-Myc) is a transcriptional regulator whose expression is strongly associated with cell proliferation and cell differentiation. The present study is a descriptive analysis of MYC status throughout the hypothesized stages of invasive ductal carcinoma progression. A tissue microarray (TMA) was constructed including representative selected areas (normal cells, hyperplasia, in situ carcinoma, and invasive carcinoma) from each of 15 patients. Fluorescence in situ hybridization (FISH) with the LSI c-MYC/CEN8/IgH probe was performed. Two cases displayed MYC amplification (13%), showing this amplification only in the invasive carcinoma zones selected. Five cases displayed polysomy of chromosome 8 (33%), detected only in ductal in situ and invasive zones selected. Benign lesions and normal adjacent cells were classified as normal. None of the hyperplasia specimens and normal specimens analyzed showed any alterations in MYC status or any aneusomies of chromosome 8. The presence of MYC amplification only in invasive cells suggests that the finding of MYC amplification could reflect an advanced tumor progression.
Cancer Genetics and Cytogenetics 04/2006; 165(2):151-6. DOI:10.1016/j.cancergencyto.2005.08.013 · 1.93 Impact Factor
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