Immunocytochemical identification of cell types in benign and malignant breast diseases: variations in cell markers accompany the malignant state

We performed immunocytochemical staining of benign, in situ, and malignant breast disease to identify antigens related to the presence of the major parenchymal cell types of the normal breast. Markers for the epithelial cells, antiserum to epithelial membrane antigen, and three monoclonal antibodies...

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Veröffentlicht in:The journal of histochemistry and cytochemistry 1993-04, Vol.41 (4), p.543-553
Hauptverfasser: Rudland, PS, Leinster, SJ, Winstanley, J, Green, B, Atkinson, M, Zakhour, HD
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container_issue 4
container_start_page 543
container_title The journal of histochemistry and cytochemistry
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creator Rudland, PS
Leinster, SJ
Winstanley, J
Green, B
Atkinson, M
Zakhour, HD
description We performed immunocytochemical staining of benign, in situ, and malignant breast disease to identify antigens related to the presence of the major parenchymal cell types of the normal breast. Markers for the epithelial cells, antiserum to epithelial membrane antigen, and three monoclonal antibodies (MAb) to milk-fat globule membranes stained most of the inner cells in benign breast lesions, carcinoma in situ, and invasive carcinomas, but the peripheral cells in benign lesions, as well as in carcinoma in situ, were unstained. MAb to epithelium-specific keratin 18 stained the majority of inner cells in benign breast lesions but comparatively fewer such cells in carcinoma in situ and invasive carcinoma. Markers for the myoepithelial cells, antisera, and MAb to smooth muscle actin and vimentin stained most of the peripheral cells in benign breast lesions and in carcinoma in situ but failed to stain virtually any neoplastic cells in invasive carcinomas. Markers for the basement membrane adjacent to the myoepithelial cells, antiserum, and MAb to laminin and Type IV collagen delineated an intact basement membrane around benign lesions and carcinoma in situ, and fragmented structures in 5-10% of invasive carcinomas; the remaining carcinomas were largely unstained. Markers for both myoepithelial and epithelial cells, keratin MAb PKK2 and LP34, stained most of the inner cells in benign lesions but usually only relatively few malignant cells in carcinoma in situ and invasive carcinomas. Markers for the secretory alveolar cell, MAb to beta- and kappa-casein, stained a few isolated cells in benign lesions, many more inner cells in two such lesions in pregnant females, and none in invasive carcinomas. In conclusion, the myoepithelial cell and, under suitable hormonal conditions, the secretory alveolar cell, are retained in most benign lesions, but they are largely lost in invasive carcinomas.
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Markers for the epithelial cells, antiserum to epithelial membrane antigen, and three monoclonal antibodies (MAb) to milk-fat globule membranes stained most of the inner cells in benign breast lesions, carcinoma in situ, and invasive carcinomas, but the peripheral cells in benign lesions, as well as in carcinoma in situ, were unstained. MAb to epithelium-specific keratin 18 stained the majority of inner cells in benign breast lesions but comparatively fewer such cells in carcinoma in situ and invasive carcinoma. Markers for the myoepithelial cells, antisera, and MAb to smooth muscle actin and vimentin stained most of the peripheral cells in benign breast lesions and in carcinoma in situ but failed to stain virtually any neoplastic cells in invasive carcinomas. Markers for the basement membrane adjacent to the myoepithelial cells, antiserum, and MAb to laminin and Type IV collagen delineated an intact basement membrane around benign lesions and carcinoma in situ, and fragmented structures in 5-10% of invasive carcinomas; the remaining carcinomas were largely unstained. Markers for both myoepithelial and epithelial cells, keratin MAb PKK2 and LP34, stained most of the inner cells in benign lesions but usually only relatively few malignant cells in carcinoma in situ and invasive carcinomas. Markers for the secretory alveolar cell, MAb to beta- and kappa-casein, stained a few isolated cells in benign lesions, many more inner cells in two such lesions in pregnant females, and none in invasive carcinomas. 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Markers for the epithelial cells, antiserum to epithelial membrane antigen, and three monoclonal antibodies (MAb) to milk-fat globule membranes stained most of the inner cells in benign breast lesions, carcinoma in situ, and invasive carcinomas, but the peripheral cells in benign lesions, as well as in carcinoma in situ, were unstained. MAb to epithelium-specific keratin 18 stained the majority of inner cells in benign breast lesions but comparatively fewer such cells in carcinoma in situ and invasive carcinoma. Markers for the myoepithelial cells, antisera, and MAb to smooth muscle actin and vimentin stained most of the peripheral cells in benign breast lesions and in carcinoma in situ but failed to stain virtually any neoplastic cells in invasive carcinomas. Markers for the basement membrane adjacent to the myoepithelial cells, antiserum, and MAb to laminin and Type IV collagen delineated an intact basement membrane around benign lesions and carcinoma in situ, and fragmented structures in 5-10% of invasive carcinomas; the remaining carcinomas were largely unstained. Markers for both myoepithelial and epithelial cells, keratin MAb PKK2 and LP34, stained most of the inner cells in benign lesions but usually only relatively few malignant cells in carcinoma in situ and invasive carcinomas. Markers for the secretory alveolar cell, MAb to beta- and kappa-casein, stained a few isolated cells in benign lesions, many more inner cells in two such lesions in pregnant females, and none in invasive carcinomas. In conclusion, the myoepithelial cell and, under suitable hormonal conditions, the secretory alveolar cell, are retained in most benign lesions, but they are largely lost in invasive carcinomas.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Antibodies, Monoclonal</subject><subject>Biological and medical sciences</subject><subject>Biomarkers - analysis</subject><subject>Biomarkers, Tumor - analysis</subject><subject>Breast - chemistry</subject><subject>Breast - pathology</subject><subject>Breast Diseases - metabolism</subject><subject>Breast Diseases - pathology</subject><subject>Breast Neoplasms - chemistry</subject><subject>Breast Neoplasms - pathology</subject><subject>Carbohydrate Sequence</subject><subject>Carcinoma in Situ - chemistry</subject><subject>Carcinoma in Situ - pathology</subject><subject>Cytoskeletal Proteins - analysis</subject><subject>Epithelium - chemistry</subject><subject>Epithelium - pathology</subject><subject>Extracellular Matrix Proteins - analysis</subject><subject>Female</subject><subject>Gynecology. 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Markers for the epithelial cells, antiserum to epithelial membrane antigen, and three monoclonal antibodies (MAb) to milk-fat globule membranes stained most of the inner cells in benign breast lesions, carcinoma in situ, and invasive carcinomas, but the peripheral cells in benign lesions, as well as in carcinoma in situ, were unstained. MAb to epithelium-specific keratin 18 stained the majority of inner cells in benign breast lesions but comparatively fewer such cells in carcinoma in situ and invasive carcinoma. Markers for the myoepithelial cells, antisera, and MAb to smooth muscle actin and vimentin stained most of the peripheral cells in benign breast lesions and in carcinoma in situ but failed to stain virtually any neoplastic cells in invasive carcinomas. Markers for the basement membrane adjacent to the myoepithelial cells, antiserum, and MAb to laminin and Type IV collagen delineated an intact basement membrane around benign lesions and carcinoma in situ, and fragmented structures in 5-10% of invasive carcinomas; the remaining carcinomas were largely unstained. Markers for both myoepithelial and epithelial cells, keratin MAb PKK2 and LP34, stained most of the inner cells in benign lesions but usually only relatively few malignant cells in carcinoma in situ and invasive carcinomas. Markers for the secretory alveolar cell, MAb to beta- and kappa-casein, stained a few isolated cells in benign lesions, many more inner cells in two such lesions in pregnant females, and none in invasive carcinomas. In conclusion, the myoepithelial cell and, under suitable hormonal conditions, the secretory alveolar cell, are retained in most benign lesions, but they are largely lost in invasive carcinomas.</abstract><cop>Los Angeles, CA</cop><pub>Histochemical Soc</pub><pmid>8450194</pmid><doi>10.1177/41.4.8450194</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record>
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subjects Adolescent
Adult
Aged
Aged, 80 and over
Antibodies, Monoclonal
Biological and medical sciences
Biomarkers - analysis
Biomarkers, Tumor - analysis
Breast - chemistry
Breast - pathology
Breast Diseases - metabolism
Breast Diseases - pathology
Breast Neoplasms - chemistry
Breast Neoplasms - pathology
Carbohydrate Sequence
Carcinoma in Situ - chemistry
Carcinoma in Situ - pathology
Cytoskeletal Proteins - analysis
Epithelium - chemistry
Epithelium - pathology
Extracellular Matrix Proteins - analysis
Female
Gynecology. Andrology. Obstetrics
Humans
Immunohistochemistry
Mammary gland diseases
Medical sciences
Membrane Glycoproteins - analysis
Middle Aged
Molecular Sequence Data
Mucin-1
Pregnancy
Tumors
title Immunocytochemical identification of cell types in benign and malignant breast diseases: variations in cell markers accompany the malignant state
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