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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to study the effect of estrogens and antiestrogens on the adhesive properties of human breast cancer cells, the attachment on endothelial cells (EC), on subendothelial extracellular matrix (ECM) and on ECM components (collagen I and IV, laminin, fibronectin) of estrogen-dependent (MCF-7, ZR75-1) and estrogen-independent (BT-20) breast cancer cell lines was investigated. The cells were grown under conditions of controlled exposure to estrogen [17 beta-estradiol (E2)] and/or antiestrogens [tamoxifen (Tam) or 4-hydroxytamoxifen (OH-Tam)]. Treatment by E2 enhanced the ability of ZR75-1 cells to adhere to the various substrates, which contrasts with the observed absence of effects with the BT-20 cells. Similarly, Tam or OH-Tam induced a reduction of the adhesion of ZR75-1 tumor cell, but not of BT-20 cells. This effect was reversed by competing concentrations of E2. The effects on MCF-7 cell adhesion were similar to those described for ZR75-1 cells, but could not be reproducibly observed. Adhesion assays carried out with ZR75-1 cells grown in the absence or presence of phenol red, a pH indicator which behaves as a weak estrogen, led to a similar pattern of cell attachment. Conditioned media harvested from E2- or Tam-treated ZR75-1 cells failed to induce any effect on adhesion of other ZR75-1 cells grown in E2-deprived medium, suggesting that secretory activities are not required for the control of cell adhesiveness. The results suggest that estrogens and antiestrogens can control the adhesive behavior of breast tumor cells through their hormone responsive structures possibly by regulating expression of cell adhesion proteins and/or their cell surface receptors.
Clin Exp Metastasis
PMID:Modulation of human breast cancer cell adhesion by estrogens and antiestrogens. 270 28

Platelets may promote the development of metastasis, and tumor cells that aggregate platelets are believed to be more malignant. We studied three different human mammary carcinoma cell lines, which had different interactions with human platelet-rich plasma (PRP). The MCF-7 and the T47-D cell lines induced an adenosine diphosphate (ADP)-mediated platelet aggregation. The third cell line, MDA-MB 231 did not induce any platelet aggregation. On the contrary, this cell line inhibited ADP- and arachidonic acid-induced platelet aggregation. This inhibiting activity is mainly adenosine-mediated. The mechanism by which platelets may contribute to the dissemination of cancer could be related to platelet growth factors. MCF-7 and T47-D cell lines induced a release of platelet-derived growth factor (PDGF). On the contrary, the MDA-MB 231 cell line did not induce any platelet release. The role of these platelet growth factors in tumor cell growth is discussed.
Invasion Metastasis 1986
PMID:Human platelet-tumor cell interactions vary with the tumor cell lines. 310 Apr 72

Interactions between invasive and noninvasive cells were studied via confronting cultures between mixed cell aggregates and embryonic chick heart fragments in vitro. The mixed aggregates were composed of MCF-7 and HBL-100 cells, both derived from human mammary epithelium. HBL-100 cells invade into the heart fragments when confronted as unmixed aggregates, while MCF-7 cells do not. Using mixed aggregates HBL-100 cells still invade into the heart tissue, but MCF-7 cells sort out to the periphery of the cultures and do not invade. Two mechanisms concerning the noninvasiveness of MCF-7 cells in vitro are discussed: the homotypic adhesion of the MCF-7 cell population due to the presence of numerous desmosomes, and the incapability of MCF-7 cells to migrate on extracellular laminin present in the embryonic chick heart and in the HBL-100 cell population.
Invasion Metastasis 1988
PMID:Invasiveness in vitro of mixed aggregates composed of two human mammary cell lines MCF-7 and HBL-100. 319 26

We describe a new flow cytometry procedure in which DNA analyses can be obtained selectively on pure, freshly obtained tumor cell subpopulations of human tumor specimens. This procedure is based on exclusion from analysis of the contaminating lymphohemopoietic cells mixed with tumor cells in tumor specimens. This exclusion is made possible by labeling all lymphohemopoietic cells with an antibody to HLe-1 (HLE), which is present on all lymphohemopoietic cells but on no other cells, and by gating against these labeled cells when analyzing for DNA. For the model system, a 1:1 mixture of normal human peripheral blood leukocytes and either of two human cancer cell lines, HEp-2 and MCF-7, normal leukocyte contamination can be reduced to 3.1% while retaining 94.7% of tumor cells for DNA analysis. Four examples of human tumor samples, two cases each of malignant effusions and lymph node metastases, were analyzed with this procedure. The results clearly indicate that this new method will improve ploidy analysis/aneuploidy detection and will make it possible to obtain more accurate cell-cycle analyses of tumor cells than have previously been possible. This new procedure will contribute to clinical and biological studies involving DNA of human tumors.
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PMID:Flow cytometry DNA analysis on tumor cell subpopulation of human tumor specimens by exclusion of lymphohemopoietic cells. 336 54

The phenolic lignans enterolactone and enterodiol appear periodically in women's urine, dependent upon synthesis from plant-derived lignans by the intestinal microflora. The phytoestrogen equol is also present in women's urine, and is also derived from a vegetarian diet. Antiestrogenic or antiproliferative actions of these compounds have been postulated and related to the observation that there is a reduced incidence of breast cancer associated with diet. We evaluated the estrogenic and antiestrogenic activity of these compounds using four sensitive assays in tissue culture, including the use of human breast cancer cell lines T47D and MCF-7. Unexpectedly, we found that enterolactone and enterodiol, as well as equol, are weak estrogens, and that enterolactone and equol could stimulate the growth of estrogen-dependent breast cancer cell lines. We suggest that these environmental agents can promote the growth of breast cancer, particularly hormone-dependent metastases that may be located near the gut or in the mesenteries or liver, where the concentration of these intestinally produced compounds would be highest. Treatment with an antiestrogen such as tamoxifen blocks the estrogenic activity of these compounds. In the absence of treatment with an antiestrogen such as tamoxifen, hormonal therapy to block steroidal estrogen synthesis in a patient with breast cancer could conceivably be circumvented by a vegeterian diet rich in the precursors to estrogenic compounds such as enterolactone and equol.
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PMID:Stimulation of breast cancer cells in vitro by the environmental estrogen enterolactone and the phytoestrogen equol. 342 25

There is a structural similarity between phenolphthalein and the triphenylethylenes which are known to interact with the estrogen receptor of human breast tissue. Phenolphthalein (10 microM) competed with estrogen for binding to MCF-7 human breast cancer cells in tissue culture and induced the synthesis of the progesterone receptor. The antiestrogen 4-hydroxytamoxifen blocked progesterone receptor induction both by estradiol and by phenolphthalein. Both estradiol (0.1 nM) and phenolphthalein (10 microM) stimulated cell growth as measured by DNA and protein assays. This growth stimulation was blocked by 4-hydroxytamoxifen. Phenolphthalein glucuronide, the major phenolphthalein metabolite, did not inhibit estrogen binding, induce progesterone receptor synthesis, or stimulate MCF-7 cell growth in culture. Yellow phenolphthalein, an impure phenolphthalein preparation used in nonprescription laxative preparations, had similar properties to pure phenolphthalein. Physicians should be aware of the weak estrogenic action of phenolphthalein, especially when recommending laxatives for breast cancer patients with confirmed liver and mesenteric metastases.
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PMID:Estrogenic effects of phenolphthalein on human breast cancer cells in vitro. 362 Jul 17

Seasonal variations were observed in tumor size and a number of immunologic responses among patients entered in the Breast Cancer Prognostic Study. A significantly larger number of cases were diagnosed with smaller tumors, less than 2 cm, during December through February. It was also noted that elevated inflammatory reactions were seen in breast tumors removed during November, December and January. Seasonal changes were also observed in the serum IgM and IgE concentrations at the time of the patient's mastectomy. Elevated fall-winter leukocyte migration inhibition response to MCF-7 extracts correlated with the same seasonal elevations observed with serum IgM response. Implications of seasonal variation as a reflection of immune events are considered.
Invasion Metastasis 1986
PMID:Seasonal variation in tumor size at diagnosis and immunologic responses in human breast cancer. 375 62

Certain tissues contain unique factors which are chemotactic for metastatic tumor cell lines. Extracts of bone, brain, liver, and lung were tested for their ability to promote either the migration or the chemoinvasion, i.e., their penetration through a reconstituted basement membrane barrier, of various metastatic tumor cells. Using a modified Boyden chamber assay for chemotaxis, B16-Br2 melanoma cells, which metastasize to brain, migrated most actively to brain extract. Lung-directed T241-PM2 fibrosarcoma cells migrated selectively to lung extract. Further, murine M50-76 reticulum cell sarcoma cells, which metastasize to liver and ovaries, were preferentially attracted to liver extract, and MCF-7 breast adenocarcinoma cells with high bone and brain colonization potential were found to migrate most actively to bone and brain extracts. Partial purification of tissue extracts showed that the factors in brain and liver are of different molecular weights. These data suggest that tissue-specific factors in different target tissues attract tumor cells which home to those sites.
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PMID:Migration of tumor cells to organ-derived chemoattractants. 401 33

MCF-7 cells, a human breast carcinoma line, forms tumors when injected into athymic nude mice. These tumors are able to metastasize to lungs, liver and spleen. 17 beta-estradiol treatment increases both the growth rate and frequency of metastases. Castration or diabetes prevents metastasis formation, but treatment with estrogen or insulin restores the metastasizing capacity. MCF-7 cells secrete into the culture media collagenases able to lyse types I and IV collagens. Estrogen or insulin addition to the culture enhances collagenase production. Attention is called to the coexistence of enhancement in collagenase production and metastasis formation.
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PMID:Formation of metastasis by human breast carcinoma cells (MCF-7) in nude mice. 645 Jun 36

Interactions between tumour cells and the endothelium are vital to the formation of haematogenous metastases. Binding to model endothelium of one oestrogen receptor positive breast carcinoma cell line (MCF-7) and one receptor negative line (HS578T) was examined in vitro together with endothelial retraction induced by these tumour cells. Adhesion was inhibited by monoclonal antibodies specific for the VLA integrins and by peptides containing the RGD motif which is commonly recognised as a ligand by the VLA adhesion molecules. However, binding of the two tumour cell lines was inhibited by monoclonal antibodies specific for different VLA molecules; anti-alpha 6 beta 1 inhibited MCF-7 adhesion but anti-alpha 5 beta 1 inhibited Hs578T. These results were consistent with flow cytometric quantification of the expression of these VLA integrins on the surfaces of the two tumour cell lines. Enzyme-linked immunosorbent assays (ELISA) demonstrated that laminin was present on the endothelial cell surface but collagen IV was absent. ELISA failed to detect increased exposure of the subendothelial matrix during the first hour after addition of either cancer cell type. This was supported by assays which demonstrated maintenance of the endothelial permeability barrier during this period. Slight endothelial retraction was detected within 2 hours of the addition of tumour cells. It is concluded that binding between tumour cells and confluent endothelium is inhibited by the blockade of adhesion molecules which are normally associated with interactions between the cell and the subendothelial matrix. Tumour cell to matrix interactions rather than direct tumour to endothelial cell adhesion may be the limiting step in tumour cell binding to the endothelium.
Clin Exp Metastasis 1995 May
PMID:The role of beta 1 integrins in adhesion of two breast carcinoma cell lines to a model endothelium. 753 54


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