Immunohistochemical analysis of apocrine breast lesions. Consistent over-expression of androgen receptor accompanied by the loss of estrogen and progesterone receptors in apocrine metaplasia and apocrine carcinoma in situ.
Apocrine phenotype is observed in a spectrum of breast epithelial lesions spanning from benign metaplasias to apocrine carcinoma. Apocrine metaplasia is a common finding in fibrocystic change of the female breast. In situ and invasive apocrine carcinomas are rare variants of ductal carcinoma. All breast apocrine lesions were shown to be associated with increased androgen hormones metabolism. We have evaluated 10 cases of apocrine metaplasia, 3 cases of in situ apocrine carcinoma and 10 cases of invasive apocrine carcinomas using immunostaining method for steroid hormone receptors (estrogen, progesterone, androgen), p53, bcl-2 and BRST-2. Paraffin embedded tissue and avidin-biotin peroxidase complex system were used. Androgen receptor (AR) expression is consistently increased in all cases of apocrine metaplasia when compared with surrounding normal, non-apocrine breast epithelium. This androgen receptor over-expression is accompanied by the loss of immuno-detectable estrogen and progesterone receptor, and also the loss of bcl-2. An identical pattern of immuno-reactivity is seen in in situ apocrine carcinomas, but it is observed with less frequency in invasive apocrine carcinomas, which only infrequently express AR as the only steroid hormone receptor.
Gatalica
Z
Z
Department of Pathology, The University of Texas Medical Branch at Galveston, 77555-0588, USA. zgatalic@utmb.edu
D000328:Adult; D000368:Aged; D000951:Antigens, Neoplasm / Q000032:analysis; D001050:Apocrine Glands / Q000737:chemistry* / Q000473:pathology*; D014408:Biomarkers, Tumor / Q000032:analysis; D001940:Breast / Q000737:chemistry / Q000473:pathology; D001943:Breast Neoplasms / Q000737:chemistry* / Q000473:pathology; D018567:Breast Neoplasms, Male / Q000737:chemistry* / Q000473:pathology; D002278:Carcinoma in Situ / Q000737:chemistry* / Q000235:genetics / Q000473:pathology*; D018270:Carcinoma, Ductal, Breast / Q000737:chemistry / Q000145:classification / Q000473:pathology; D002467:Cell Nucleus / Q000737:chemistry; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008679:Metaplasia / Q000473:pathology; D008875:Middle Aged; D010641:Phenotype; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000032:analysis; D011944:Receptors, Androgen / Q000032:analysis / Q000096:biosynthesis; D011960:Receptors, Estrogen / Q000032:analysis / Q000378:metabolism; D011980:Receptors, Progesterone / Q000032:analysis / Q000378:metabolism; D013544:Sweat Gland Neoplasms / Q000737:chemistry* / Q000235:genetics / Q000473:pathology*; D016159:Tumor Suppressor Protein p53 / Q000032:analysis
D000951:Antigens, Neoplasm; D014408:Biomarkers, Tumor; D019253:Proto-Oncogene Proteins c-bcl-2; D011944:Receptors, Androgen; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D016159:Tumor Suppressor Protein p53