Androgen metabolism and apocrine differentiation in human breast cancer

Miller, William R.; Telford, John N.; Dixon, JM; Shivas, A. A.

doi:10.1007/bf01807652

Cited by 33 publications

(17 citation statements)

References 20 publications

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“…For example, SRD5A1, the 5a-reductase which converts testosterone to dihydrotestosterone, is overexpressed in the apocrine and basal groups (Figure 1c panel 3). This is consistent with previous data showing increased 5a-reductase biochemical activity in apocrine tumours (Miller et al, 1985). The GO analysis revealed the presence of many genes involved in steroid metabolism in the apocrine group.…”

Section: Discussionsupporting

confidence: 92%

“…Although apocrine carcinoma is rare, tumour cells with apocrine features have been reported in up to 63% of cases (Miller et al, 1985). The poor survival of the patients with the molecular apocrine profile in the Sorlie and van't Veer studies (Figure 5b) is consistent with the poor prognosis expected for ER-negative, ERBB2-positive tumours.…”

Section: Discussionsupporting

confidence: 62%

“…Correlation with these reference profiles was used to assign tumours to the luminal, (Table 3 and Supplementary Table sheet 3). The number of tumours with the molecular apocrine profile in all five data sets (8-14%) is consistent with historical estimates of the number of breast tumours with marked apocrine histological features (2-15%) (Miller et al, 1985). To visualize the result, our tumours were used to train two partial least squares (PLS) models, one that separates the basal from luminal tumours, and another that separates the molecular apocrine from all other tumours.…”

Section: Identification Of Molecular Apocrine Tumours In Other Microasupporting

confidence: 69%

“…To test whether the tumours with increased androgen signalling had apocrine features, such as abundant eosinophilic cytoplasm and prominent nucleoli, tissue sections were examined histologically by a pathologist without prior knowledge of the microarray assignments. Apocrine grade was scored on a three-point scale as described by Miller et al (1985), although it must be pointed out that formal diagnosis of apocrine carcinoma is generally very difficult using frozen sections because of insufficient preservation of cell morphology. None of the biopsies contained extensive regions of benign apocrine metaplasia that could account for the gene expression data.…”

Section: The Third Group Contains Tumours With Apocrine Featuresmentioning

confidence: 99%

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Identification of molecular apocrine breast tumours by microarray analysis

et al. 2005

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 62%

Section: Identification Of Molecular Apocrine Tumours In Other Microasupporting

confidence: 69%

Section: The Third Group Contains Tumours With Apocrine Featuresmentioning

confidence: 99%

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Identification of molecular apocrine breast tumours by microarray analysis

et al. 2005

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“…Origin of apocrine tumours: relationship between benign apocrine metaplasia and apocrine carcinomas Apocrine differentiation of breast epithelial cells has attracted a great deal of attention as up to 50% of breast invasive carcinomas exhibit areas with apocrine morphology features [22][23][24][25][26][27][28], and because available data have shown that women with breast apocrine cystic disease have an increased propensity for developing breast cancer later in their lives [29][30][31][32][33].…”

Section: Introductionmentioning

confidence: 99%

Molecular pathology of breast apocrine carcinomas: A protein expression signature specific for benign apocrine metaplasia

et al. 2006

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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.

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Immunohistochemical demonstration of steroid C21 hydroxylase in normal and neoplastic human breasts

Sasano

1988

Cancer

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Steroid C21 hydroxylase was investigated immunohistochemically with the use of antibody against cytochrome P-450 specific for steroid C21 hydroxylation (P-450C21) in normal and neoplastic human breast tissues. In the histologically normal breast, P-450C21 was exclusively present in secretory tubules and ducts. In mammary dysplasia and fibroadenoma, P-450C21 was intensively stained in epithelial cells. In gynecomastia, P-450C21 was faintly observed in epithelial cells in some cases. In intraductal and invasive ductal carcinoma, P-450C21 was observed in the cells with ductal formation. P-450C21 was not observed in medullary and mucinous carcinoma. In lobular carcinoma, only two cases were positive for P-450C21 of nine cases examined. P-450C21 is considered to be closely related to the ductal differentiation in neoplastic transformation of the breast.

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Androgen metabolism and apocrine differentiation in human breast cancer

Cited by 33 publications

References 20 publications

Identification of molecular apocrine breast tumours by microarray analysis

Identification of molecular apocrine breast tumours by microarray analysis

Molecular pathology of breast apocrine carcinomas: A protein expression signature specific for benign apocrine metaplasia

Immunohistochemical demonstration of steroid C21 hydroxylase in normal and neoplastic human breasts

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