Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0006142 (breast cancer)
 160,383 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cultured breast cancer cells express on their surface glycoproteins which are recognized by the peanut lectin (PNA). The proliferation of these cells (ZR-75.1 and 734-B) was inhibited by PNA. A mammary carcinoma cell line (BT-20) which does not react with PNA was not affected by this lectin. The combination of PNA with either retinoic acid or 4-hydroxy-tamoxifen led to an additive amplification of the antiproliferative activity. Also interferon-gamma showed in combination with PNA an improved growth-inhibitory action.
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PMID:Peanut agglutinin inhibits proliferation of cultured breast cancer cells. 244 18

The method of skin window was used in the investigation of cell reaction of healthy volunteers (25 persons) and patients with malignant melanoma (12 cases), breast cancer (18 cases), and with various malignant lymphomas (6 cases) to a local application of the lectin Concanavalin A (Con A, concentration of 10 mg/ml of saline, 0.02 ml per scarification). The obtained results were compared with cell reaction after the application of saline alone. Correlation between cell reaction and clinical state of patients was studied as well. No significant difference in the amount of lymphocytes after the application of Con A was observed between the group of healthy individuals and the group of patients with malignant tumors. On the contrary, the reaction of neutrophil granulocytes to Con A was significantly lower in cancer patients than in healthy volunteers. After the application of Con A, all preparations showed a higher absolute amount of all cells. Con A induced a significant increase in the amount of lymphocytes in patients after therapy and in poor clinical state. The persons with good clinical state reacted by a slight increase or decrease in the number of lymphocytes to the application of lectin.
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PMID:Cell reaction to concanavalin A in cancer patients. 253 20

Monoclonal antibody MA5 recognizes an epitope present on the surface and in the cytoplasm of human breast cancer cells and on the human milk fat globule membrane (MFGM). These immunoreactive determinants are found on tumor-associated glyco-proteins with apparent molecular weights of 280 and 300 kdaltons, whereas the cross-related milk fat globule membrane antigen appears larger (330 kdaltons). Comparative electrophoretic migration analyses following neuraminidase digestion, as well as differential binding to various lectins, established that these molecules are extensively sialylated, and that the tumor antigens were sialylated to a greater extent than normal antigen. Immunoaffinity purification of this class of differentiation antigens from tumor and MFGM demonstrated similar size distributions, lectin affinities and buoyant densities as their respective crude antigens.
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PMID:Related glycoproteins from normal secretory and malignant breast cells. Purification and initial comparative characterizations. 253 15

Tumor-bearing patients with breast cancer were assayed for their natural killer (NK) cell activity and for the function of activated cytotoxic T-cells, as assessed by lectin-dependent cellular cytotoxicity (LDCC). Tumor-bearing patients with breast cancer had a significant increase in NK activity and in LDCC, as compared with healthy control individuals. Although the enhanced NK cell activity and LDCC were closely associated with high levels (greater than 31 fmol/mg) of estrogen receptor (ER) content in the primary tumor, no other clinical or histologic correlation between the increase in either parameter of cytotoxic effector cell function could be found. Thus, ER levels greater than 31 fmol/mg might be associated with increased cytotoxic effector cell function in tumor-bearing patients with breast cancer.
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PMID:Association of increased lytic effector cell function with high estrogen receptor levels in tumor-bearing patients with breast cancer. 270 70

Membrane binding sites for peanut lectin or peanut agglutinin (PNA) were investigated in the established mammary carcinoma cell lines MCF-7, 734-B, ZR-75.1 and BT-20. The determination of PNA binding sites was performed in a flow cytometer after staining with fluorescein(FITC)-labeled PNA. It appeared that only the estrogen-sensitive cell lines exhibited PNA binding sites, whereas the hormone-insensitive cell line BT-20 was clearly negative. Steroid hormones, when administered singly to the cells in physiological concentrations (10(-9)-10(-8) M) had no effect on PNA binding expression. Only the combination of estradiol and progesterone together increased PNA binding sites. Pharmacological doses (10(-6) M) of medroxyprogesteroneacetate (MPA) and dexamethasone increased the number of binding sites, whereas retinoic acid decreased them. A preliminary characterization of the binding sites revealed that they have high capacity and moderate affinity for PNA (KD greater than 10(-7) M). FITC-PNA binding could be inhibited selectively by fetuin (greater than 10(-5) M) and by galactose (greater than 10(-2) M). Cytosol from MCF-7 cells and from some primary breast cancer specimens were able to decrease PNA binding to the surface of 734-B cells.
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PMID:Influence of steroids and retinoic acid on peanut-lectin binding of human breast cancer cells. 293 94

Formalin fixed, paraffin embedded tissue from 100 consecutive cases of breast carcinoma were studied for binding with Helix pomatia (HPA) and Ulex Europeus (UEA1) lectins. Serial sections were pretreated with trypsin or neuraminidase to determine the effect of these enzymes on lectin binding. The lectins were visualized by the peroxidase antiperoxidase technique and the cell staining proportion assessed in a semi-quantitative manner under the light microscope. Correlating staining with prognostic factors and patient follow-up details showed that UEA1 related to disease-free interval and survival, and HPA to lymph node stage, time to loco regional recurrence and to survival. Relationships with both lectins were abolished by pretreatment with neuraminidase. The study demonstrates that a simple assessment of lectin binding can provide prognostic information in breast cancer. This may be useful particularly when conservational surgical practice restricts the amount of nodal tissue for staging.
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PMID:Helix pomatia and Ulex europeus lectin binding in human breast carcinoma. 330 30

One hundred thirty-two patients with breast cancer were examined for exposure of cryptantigens on their erythrocytes (RBC) using a lectin panel consisting of Arachis hypogaea and Glycine soja. Eight had exposed cryptantigens; of the eight, five were classified with additional lectins as T-polyagglutination type and three as Th-polyagglutination. A control group of 300 healthy blood donors had no exposed cryptantigens on their RBC. These findings could not be correlated with the staging of the tumor, extension of metastases, or positive estrogen or progesterone receptors of malignant tumor cells. Only one study has been found that describes the incidence of agglutination of erythrocytes from cancer patients using a monoclonal antibody, which detected an epitope on the RBC from cancer patients and was considered to be distinct from the antigen bound by naturally occurring anti-T. Studies have been made describing polyagglutinable sites on breast cancer tumor cells, where there was a much higher incidence. This discrepancy can be explained either by a difference in the methods used to search for cryptantigen exposure on the various types of cells, or by the existence of a different mechanism, which causes the exposure of cryptantigens on RBC as opposed to malignant breast tumor cells.
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PMID:Exposure of cryptantigens on erythrocytes in patients with breast cancer. 336 68

Two hundred and eighty-six patients presenting with metastatic adenocarcinoma or undifferentiated carcinoma whose primary site was not identified by clinical history, physical examination and chest radiograph have been studied. Median survival from presentation was 22 weeks. Factors independently predicting improved survival were lymph node presentations, good performance status and body weight loss of less than 10 per cent. In 88 (31 per cent) patients the primary tumour site was subsequently identified, in 58 (20 per cent) during life. Lung cancer was the most frequently identified primary tumour, and in only 32 (11 per cent) of the patients was a 'treatable' primary tumour (i.e. germ cell, breast, ovarian, prostate, thyroid cancer or lymphoma) identified. Among the treatable primary tumours were those in eight out of 16 female patients presenting with axillary metastases who were subsequently shown to have primary breast cancer and four of 13 females presenting with ascites who were found to have primary ovarian cancer. Prostatic cancer was confirmed in five out of 13 men with raised serum acid phosphatase. Of 22 patients with elevated serum alphafoetoprotein (AFP) or beta-human chorionic gonadotrophin levels (beta HCG) 18 had some features of the 'atypical teratoma syndrome'. Of the total of 32 patients with treatable tumour types, 29 (90 per cent) were identified during life. Median survival for patients with treatable tumour types identified during life was 104 weeks, compared with 22 weeks for the group as a whole. Retrospective immunocytochemical staining of the original biopsy showed that prostatic specific antigen and antibodies to beta HCG and AFP were diagnostically useful, but a series of organ site non-specific markers of histogenesis or cellular differentiation (carcinoembryonic antigen, secretory component for IgA, peanut lectin binding, epithelial membrane antigen and keratin) showed no significant correlations with identified primary sites, responsiveness to empirical chemotherapy or survival. Metastatic undifferentiated carcinoma or adenocarcinoma from an unknown primary site represents 6.5 per cent of all referrals to the medical oncology unit, Royal Prince Alfred Hospital, Sydney. We offer guidelines for the rapid identification of the limited number of primary sites for which effective and specific forms of systemic treatment are available.
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PMID:Metastatic adeno or undifferentiated carcinoma from an unknown primary site--natural history and guidelines for identification of treatable subsets. 365 56

One case of the so-called "Stewart-Treves syndrome" (STS), appearing on a lymphoedematous arm complicating radical mastectomy for breast cancer, was characterized electronmicroscopically and immunohistologically, in order to elucidate its disputed (epithelial vs endothelial) histogenesis. Epithelial and endothelial differentiation markers used comprised: antibodies against keratin, vimentin, factor VIII-related antigen (F VIII-RA), HLA-DR antigens and the lectin Ulex europeaus agglutinin I (UEA I). At the ultrastructural level, neoplastic cells were found to contain typical Weibel-Palade bodies, whereas by immunohistological techniques they proved to be keratin-negative/vimentin+, F VIII-RA+, UEAI+, HLA-DR+. These results rule out a possible epithelial differentiation and strongly favour an endothelial one for STS.
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PMID:Stewart-Treves syndrome: an histogenetic (ultrastructural and immunohistological) study. 370 Jul 72

Immunologic parameters were examined preoperatively in 104 patients with breast cancer, staged according to the TNM classification and in 95 age-matched healthy women. The immunologic evaluation in the peripheral blood included lymphocyte and monocyte counts, determination of E-rosette-forming T-lymphocytes (SER+) and B-lymphocytes (MER+), T-lymphocyte subsets defined with monoclonal antibodies (Leu-1, Leu-2a, Leu-3a) and with lectin fractionation (soybean agglutinin), lymphocyte transformation test with phytohemagglutinin (PHA) and concanavalin A (ConA), and colony formation of T-lymphocytes in agar (T-lymphocyte colony-forming cells, [TL-CFC]). Two age groups (Group A: 30-50 years; Group B: 51-70 years) and the different tumor stages (Stage I-IV) were analyzed. Patients and controls did not differ in the absolute numbers of lymphocytes, T- and B-cells. In patients of Group B, the absolute number of monocytes was increased slightly in Stage II and III and significantly in Stage IV (P less than 0.05). Similarly, the lymphocyte response to PHA was significantly reduced in Stage IV Group B only (P less than 0.05). ConA-induced lymphocyte proliferation and TL-CFC capacity were not different in patients and controls. In the small number of patients and age-matched controls in whom T-lymphocyte subsets were determined, the absolute numbers of T-cells with helper or suppressor phenotype as defined with Leu-3a, Leu-2a, or lectin fractionation with soybean agglutinin were similar. This study demonstrates that in patients with early breast cancer (Stage I-III), immunocompetence as defined by either functional in vitro studies or surface marker analysis is not significantly altered at the time of diagnosis. In contrast, patients with advanced disease (Stage IV) show a significant increase in the absolute number of monocytes and a depressed PHA responsiveness of mononuclear cells.
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PMID:Unaltered immunocompetence in patients with non-disseminated breast cancer at the time of diagnosis. 387 58


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