Analysis of Expression of Human Mammary Epithelial Antigens in Normal and Malignant Breast Cells at the Single Cell Level by Flow Cytofluorimetry

Peterson, Jerry A.; Bartholomew, James C.; Stampfer, Martha R.; Ceriani, Roberto L.

doi:10.1159/000163773

Cited by 10 publications

(7 citation statements)

References 11 publications

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“…Their mammary origin was verified by the presence of antigens specific for human mammary epithelial cells [8,29,30]. On the basis of the fibronectin pattern, the second and third passage epithelial cell populations used in these experiments were 98% pure, the remaining cells present had the morphological appearance of myoepithelial cells [8,9].…”

Section: Hem Ica I Smentioning

confidence: 99%

Metabolism of Benzo(a)pyrene by Human Epithelial and Fibroblastic Cells: Metabolite Patterns and DNA Adduct Formation

Bartley¹,

Bartholomew²,

Stampfer³

1982

J of Cellular Biochemistry

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We demonstrate in cell culture that mammary epithelial cells from normal human breast specimens metabolize benzo(a)pyrene (BaP) and form adducts with the bases of their DNA more readily and at lower concentrations of BaP than do fibroblasts from the same specimens. BaP metabolism and adduct formation was determined in the same incubations with epithelial cells grown out in early passage from each of three specimens and with fibroblasts from one of these specimens. The metabolite pattern of the epithelial cells was indicative of preferential formation of 7, 8-dihydrodiol-9, 10-dihydroepoxybenzo(a)pyrene the ultimate carcinogen. In contrast, fibroblasts formed mainly mono- and dihydroxide derivatives of BaP. The metabolite pattern from epithelial cells was compatible with the ease in which adducts between DNA and the diolepoxide of benzo(a)pyrene were formed. These results provide evidence that chemical carcinogens should be considered as possible factors in the induction of breast cancer in women.

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Section: Hem Ica I Smentioning

confidence: 99%

Metabolism of Benzo(a)pyrene by Human Epithelial and Fibroblastic Cells: Metabolite Patterns and DNA Adduct Formation

Bartley¹,

Bartholomew²,

Stampfer³

1982

J of Cellular Biochemistry

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“…Heterogeneity of cellular properties is not an exclusive characteristic of neoplastic cells. Although normal cells and tissues maintain relatively stable phenotypes, they also show heterogeneity in particular properties such as cell surface antigen content (9,10) and enzymatic activity (11). However, in malignant neoplasms, cellular heterogeneity may be much more pronounced endowing tumor cells with even more diverse properties and behaviors.…”

Section: Introductionmentioning

confidence: 99%

Generation of phenotypic diversity and progression in metastatic tumor cells

Nicolson

1984

Cancer Metast Rev

158

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The emergence of diversified tumor cell subpopulations in malignant neoplasms accounts for their heterogeneous cellular phenotypes and virtually ensures that some tumor cells will ultimately evolve with the most favorable properties for their enhanced abilities to survive, grow, invade and metastasize (tumor progression). The rates of cellular phenotypic diversification appear to vary greatly among different tumors and within the same tumor, and they are probably controlled, at least in part, by cellular instability due to chromosomal defects and random somatic mutational events, the rates of which are known to be higher in more malignant cells, and by epigenetic events, which may vary widely depending on the nature of the tumor cells and their microenvironments. As tumor progression proceeds, the most malignant cell subpopulations appear to lose their responsiveness to changes in tumor microenvironment while maintaining their high rates of phenotypic diversification. Tumor and normal cell-cell and cell-extracellular matrix interactions, as well as tumor cell nutrients, oxygen, hormones, growth factors, inducers and other regulatory molecules provide individual malignant cells with microenvironmental signals that could act through epigenetic cellular modifications, such as DNA methylation, and transcriptional, posttranscriptional, translational and posttranslational controls, or combinations of these. In addition, integration of viral gene sequences or viral modification of host DNA in critical regions could affect phenotypic stability. Finally, manipulation of tumor cells by antitumor therapy can also have profound effects on the rates of phenotypic diversification of the surviving tumor cells. A model for generating cellular phenotypic diversity based on the proposed mechanism for rapid generation of immunoglobulin molecular diversity in B cells may be applicable to malignant cells and to cells in general. In this model the expression and activity of gene products from multigene families are affected by a variety of genetic and epigenetic controlling mechanisms, and alterations in regulatory genes caused by recombination, methylation, mutation, or other changes could lead to differences in gene expression, resulting in widespread quantitative (and perhaps some qualitative) changes in particular gene products or their activities. As they proceed down different pathways of gene expression, each cell would be exposed to continual host selection pressures creating diverse, ever-changing malignant cell-populations.

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“…We have already proposed (7,8) that human mammary epithelial antigens (HME-Ags), cell surface components found only on the cell membranes of human mammary epithelial cells, normal or neoplastic (9)(10)(11), may be used as an alternative breast cancer marker to detect the tumor at an early stage and also to monitor tumor progression and success of therapy. HME-Ags are identified by specific antibodies, anti-HME, which are produced by immunization of rabbits with the membrane of human milk fat globule (HMFG) and subsequent extensive absorption with a series of non-breast human tissues (7).…”

Section: Introductionmentioning

confidence: 99%

Breast cancer markers: Comparison between sialyltransferase and human mammary epithelial antigens (HME-Ags) for the detection of human breast tumors grafted in nude mice

Sasaki¹,

Barber²,

Ceriani

1985

Breast Cancer Res Tr

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Sialyltransferase (CMP-sialic acid:asialofetuin sialyltransferase) and human mammary epithelial antigens (HME-Ags, cell surface antigens specific to human mammary epithelial cells) were determined in plasma of nude mice grafted with breast and non-breast human tumors to assess their possible usefulness as breast cancer markers. The plasma transferase activity was significantly higher (p less than 0.01) in tumor groups relative to the control. However, no significant difference (p less than 0.05) could be found in the transferase level between breast and non-breast tumor groups, showing the enzyme's lack of specificity for breast cancer. Furthermore, the surgical procedure performed on the control normal healthy group (no tumor), resulted in an important increase of the enzyme level, while HME-Ags remained unchanged. HME-Ags were essentially negative in control as well as non-breast tumor groups. After surgical removal of breast tumors, HME-Ags level dropped drastically to the background level (from 122 to less than 30 ng/ml plasma). These data indicate that HME-Ags are more sensitive and specific than sialyltransferase as markers for human breast tumor, and suggest that HME-Ags may be clinically useful in the early detection of breast cancer as well as in the followup of patients with metastatic breast tumor.

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Analysis of Expression of Human Mammary Epithelial Antigens in Normal and Malignant Breast Cells at the Single Cell Level by Flow Cytofluorimetry

Cited by 10 publications

References 11 publications

Metabolism of Benzo(a)pyrene by Human Epithelial and Fibroblastic Cells: Metabolite Patterns and DNA Adduct Formation

Metabolism of Benzo(a)pyrene by Human Epithelial and Fibroblastic Cells: Metabolite Patterns and DNA Adduct Formation

Generation of phenotypic diversity and progression in metastatic tumor cells

Breast cancer markers: Comparison between sialyltransferase and human mammary epithelial antigens (HME-Ags) for the detection of human breast tumors grafted in nude mice

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