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)

In the leukocyte adherence inhibition (LAI) assay, about 34% of adherent T-cells from patients with breast cancer exhibit nonadherence to glass when incubated with extracts of autologous cancer but not with HLA-A, -B, and -C mismatched extracts of breast cancer. To determine whether the recognition by T-cells of tumor antigen was major histocompatibility complex restricted, major histocompatibility complex antigens in the cancer extracts or on the T-cells were coated with monoclonal antibody (MAb) to nonpolymorphic determinants. Nonadherence of T-cells was antagonized by coating the target cancer extracts with MAb to a common framework determinant of Class I HLA-A, -B, and -C antigens or to the nonpolymorphic beta 2-microglobulin, which is noncovalently associated with Class I antigens. By contrast, a MAb to a monomorphic determinant on HLA-DR antigens did not change the positive T-cell response. Moreover, coating the T-cells with MAb to HLA-A, -B, and -C did not inhibit the positive T-cell response. The positive LAI response of buffy coat peripheral blood leukocytes from patients with breast cancer to extracts of allogeneic breast cancer was not affected by coating the cancer extracts with the same MAb, indicating that MAb inhibited T-cell LAI specifically and that the antibody-dependent LAI response of buffy coat peripheral blood leukocytes was not major histocompatibility complex restricted. The results indicate that HLA-A, -B, and -C antigens in extracts of autologous breast cancer restrict the LAI response to tumor antigens of T-cells from patients with breast cancer.
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PMID:Blocking of the response by human T-lymphocytes to extracts of autologous cancer by monoclonal antibody to Class-I major histocompatibility complex gene products in the leukocyte adherence inhibition assay. 660 66

The immune status of 34 breast cancer patients was investigated by measuring several parameters of peripheral blood lymphocytes--monoclonal antibodies against T cell (Leu-1) and B cell (HLA-DR) antigens, and against cytotoxic/suppressor (Leu-2a) and helper/inducer T cells (Leu-3a); E rosette formation as a T cell marker and surface Ig as a B cell marker; FcIgG receptor expression; and mitogen responsiveness of the peripheral blood lymphocytes to PHA, Con A, and PWM. Most of the patients had normal percentages of B and T cells and T cell subsets but there was a trend to lower percentages of T cells and their subsets in stage IV patients. Due to lymphopenia in stages I and IV and in patients which had received radio- or chemotherapy, the total number of B and T cells and T cell subsets was less in these groups than in the controls. The percentage of FcIgG positive cells was higher in these groups than in controls and therefore the absolute number remained unchanged. In general, a decrease in T cells seems to be indicative of a poor prognosis. Mitogen responsiveness does not have prognostic significance since a patient in stage III, in good general health, had a low mitogenic response and a terminal stage IV patient had a normal mitogenic response.
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PMID:Study of B and T lymphocyte surface markers in breast cancer patients using anti-B and anti-T cell monoclonal antibodies. 661 Aug 35

For the mobilization of CD34+ peripheral blood progenitor cells (PBPC) filgrastim (R-metHuG-CSF) can be administered either during steady-state hematopoiesis or following cytotoxic chemotherapy. We compared both mobilization modalities intra-individually in seven patients with breast cancer. The number of circulating CD34+ cells was increased after filgrastim-supported chemotherapy compared with filgrastim administration during steady-state (on average, 129 vs. 19/microliters), resulting in a sevenfold higher yield of CD34+ cells per leukapheresis (5.73 vs. 0.79 x 10(6)/kg bodyweight). CD34+ PBPC harvested post-chemotherapy comprised a smaller proportion of early progenitor cells (CD34+/HLA-DR- or CD34+/CD38-) compared with filgrastim treatment alone. However, the absolute number of these early progenitor cells harvested was fivefold higher. The filgrastim-supported rebound after chemotherapy was characterized by a greater proportion of CD34+/CD33+ cells. Correspondingly, CD34+ PBPC mobilized post-chemotherapy contained a higher proportion of CFU-GM compared with filgrastim treatment during steady-state, while the cloning efficiency of CD34+ cells for BFU-E tended to be lower. Of note, the proportion of CD34+/CD19+ lymphoid progenitor and B cells was reduced after chemotherapy. In cancer patients, filgrastim mobilizes higher numbers of CD34+ cells when administered post-chemotherapy, compensating for the smaller proportion of early hematopoietic progenitors.
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PMID:Filgrastim post-chemotherapy mobilizes more CD34+ cells with a different antigenic profile compared with use during steady-state hematopoiesis. 758 Nov 60

Peripheral blood progenitor cells (PBPC) can be mobilized using cytotoxic chemotherapy and cytokines. There is a substantial variability in the yield of hematopoietic progenitor cells between patients. We were looking for predictive parameters indicating a patient's response to a given mobilization regimen. Multiparameter flow-cytometry analysis and clonogenic assays were used to examine the hematopoietic progenitor cells in bone marrow (BM) and peripheral blood (PB) before filgrastim (R-metHuG-CSF; Amgen, Thousand Oaks, CA)-supported chemotherapy and in PB and leukapheresis products (LPs) in the recovery phase. Fifteen patients (four with high-grade non-Hodgkin's lymphoma [NHL], two with low-grade NHL, two with Hodgkin's disease, two with multiple myeloma, three with breast cancer, one with ovarian cancer, and one with germ cell tumor) were included in this study. The comparison of immunofluorescence plots showed a homogenous population of strongly CD34+ cells in steady-state and mobilized PB whereas in steady-state BM, the CD34+ cells ranged from strongly positive with continuous transition to the CD34- population. Consistent with the similarity in CD34 antigen expression, a correlation analysis showed steady-state PB CD34+ cells (r = .81, P < .001) and colony-forming cells (CFCs; r = .69, P < .01) to be a measure of a patient's mobilizable CD34+ cell pool. Individual estimates of progenitor cell yields could be calculated. With a probability of 95%, eg, 0.4 steady-state PB CD34+ cells x 10(6)/L allowed to collect in six LPs 2.5 x 10(6) CD34+ cells/kg, the reported threshold-dose of progenitor cells required for rapid and sustained engraftment after high-dose therapy. For the total steady-state BM CD34+ cell population, a weak correlation (r = .57, P < .05) with the mobilized CD34+ cells only became apparent when an outlier was removed from the analysis. Neither the CD34+ immunologic subgroups defined by the coexpression of the myeloid lineage-associated antigens CD33 or CD45-RA or the phenotypically primitive CD34+/HLA-DR- subset nor the BM CFC count had a predictive value for the mobilization outcome. This may be caused by the additional presence of maturing progenitor cells in BM, which express lower levels of the CD34 antigen and do not circulate. Our results permit us to recognize patients who are at risk to collect low numbers of progenitor cells and those who are likely to achieve sufficient or high progenitor cell yields even before mobilization chemotherapy is administered.
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PMID:Peripheral blood progenitor cell (PBPC) counts during steady-state hematopoiesis allow to estimate the yield of mobilized PBPC after filgrastim (R-metHuG-CSF)-supported cytotoxic chemotherapy. 860 80

Lymphocyte activation markers CD69 and HLA-DR were studied in metastatic breast and ovarian cancer patients who received active specific immunotherapy (ASI) using cancer vaccines containing the synthetic tumor-associated antigen sialyl-Tn or the Thomsen-Friedenreich antigen conjugated to KLH plus DETOX adjuvant. Breast cancer patients who showed prolonged survival following ASI had lower numbers of total CD69+ and CD4+CD69+ cells prior to ASI compared to patients who died. However, following ASI, the surviving patients showed an increase in CD69+ and CD4+CD69+ cells and the deceased patients showed a decrease. A greater than 50% increase in the percentage of cells bearing the activation marker CD69 is associated with an increase in survival in both ovarian and breast cancer patients. In the surviving breast cancer patients there was a significant decrease in the percentage of non-B lymphocyte HLA-DR+ (CD20-HLA-DR+) cells following cyclophosphamide treatment. A strong positive correlation was found between lymphocyte populations CD20- HLA-DR+ and CD8+CD57+, a putative suppressor cell population. Breast cancer patients who showed a greater than median decrease in CD20-HLA-DR+ lymphocytes following cyclophosphamide treatment had a survival advantage over patients who had less than the median decrease in the percent CD20-HLA-DR+ lymphocytes.
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PMID:CD69+ and HLA-DR+ activation antigens on peripheral blood lymphocyte populations in metastatic breast and ovarian cancer patients: correlations with survival following active specific immunotherapy. 753 76

This report describes the characterization of an estrogen receptor-positive breast cancer cell line, HMA-1, established from a breast cancer patient, based on the expression of tumor-associated antigens (TAAs), the HLA-DR antigen, and the c-erbB-2 proto-oncogene product. In flow cytometric and immunohistochemical analyses, HMA-1 was found to express increased levels of several TAAs including MUC1, TAG-72 (sialyl Tn), Tn, T, sialyl Le(a), Le(x), and Le(y). HMA-1 also expressed enhanced levels of the HLA-DR antigen and c-erbB-2 protein. These results indicate that HMA-1 is a unique cell line with abundant TAAs which may serve as an appropriate breast cancer cell line for application in the multidisciplinary research of breast cancer.
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PMID:Characterization of cell surface antigens expressed in the HMA-1 breast cancer cell line. 764 Apr 54

Tumor-infiltrating lymphocytes (TIL) were derived from primary breast tumors, metastatic lymph nodes and malignant pleural effusions from 34 patients with breast cancer. TIL were cultured for approximately 30 days and studied for phenotype, cytotoxicity, and the ability to secrete cytokines in response to autologous tumor stimulation. Tumor specimens were obtained from two different sites in 7 patients, resulting in 41 samples from which 38 TIL cultures were established. In addition to screening 38 bulk TIL cultures, TIL from 21 patients were separated into CD4+ and CD8+ subsets and extensively studied. Three CD4+ TIL were found specifically to secrete granulocyte macrophage-colony-stimulating factor and tumor necrosis factor alpha when stimulated by autologous tumor and not by a large panel of stimulators (24-34) consisting of autologous normal cells, allogeneic breast or melanoma tumors and EBV-B cells. This cytokine release was found to be MHC-class-II-restricted, as it was inhibited by the anti-HLA-DR antibody L243. These 3 patients' EBV-B cells, when pulsed with tumor lysates, were unable to act as antigen-presenting cells and induce cytokine secretion by their respective CD4+ TIL. These findings demonstrate that MHC-class-II-restricted CD4+ T cells recognising tumor-associated antigens can be detected in some breast cancer patients.
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PMID:CD4+ T lymphocytes infiltrating human breast cancer recognise autologous tumor in an MHC-class-II restricted fashion. 782 62

Human tumor-infiltrating lymphocytes (TIL) include a minor population of tumor-specific T cells, but the nature of the majority of TIL remains unknown. Recently, it has been suggested that T cells that recognize stressed cells may play an important role in immune surveillance. We have examined the proliferative response of anti-CD3-activated TIL cultures from human tumors against heat-stressed (hs) (42.8 degrees C, 25 min) B cell lines (TK6 (HLA-DR7+, -DRw13+, -DRw52+, and -DRw53+) and JY (HLA-DR4+ and -DRw52+)) and the mutant cell line (T2 (no HLA-DR)) by measuring [3H]thymidine incorporation. TIL lines from three of four ovarian cancers, two of four lung cancers, one of two renal cell cancers, one of two melanomas, and one of one breast cancer showed a positive proliferative response against hs-TK6 and/or hs-JY, but not against hs-T2. These TIL did not respond to autologous tumor cells. The response to hs-B cells was mediated by CD4+ TIL and inhibited by anti-HLA-DR Ab, but not by anti-HLA class I. Protein analysis revealed a significant increase of heat shock protein 70 (hsp70) expression in hs-TK6 and hs-JY. In addition, the CD4+ TIL responded to TK6 that had been pulsed with hsp70. This response could be blocked by anti-HLA-DR Ab. The CD4+ TIL produced IFN-gamma, but not IL-4, in response to hs-TK6. From these results, we conclude that hsp70-reactive CD4+ T cells exist in tumor tissues. Furthermore, these TIL recognize stressed cells and seem to play a Th1-like role that may support antitumor T cell responses at local tumor sites.
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PMID:Human tumor-infiltrating CD4+ T cells react to B cell lines expressing heat shock protein 70. 793 Jun 18

Cathepsin D, a lysosomal aspartic proteinase, is well known to be overexpressed and secreted in the form of its zymogen by many types of human breast cancer tissues. In the cell lines derived from these tissues, cathepsin D functions as an autocrine mitogen, and it was suggested that its secretion might pose some physiological functions. Recently we have identified the presence of procathepsin D in human breast milk and similar findings were reported for bovine milk which imply also some physiological function. Thus, we have tested the influence of procathepsin D and insulin-like growth factor II on the expression of CD11a, CD11b, FcRI, CD62L, and HLA-DR surface determinants on neutrophils and lymphocytes. We have used procathepsin D purified from the secretions of breast cancer cell line ZR-75-1 and commercially available IGF II. Our results showed that both studied factors significantly influence the expression of tested surface molecules.
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PMID:Activation of peripheral blood neutrophils and lymphocytes by human procathepsin D and insulin-like growth factor II. 802 52

The effect of the differentiating agent all-trans-retinoic acid on the expression of components of the milk fat globule membrane and HLA-DR by breast cancer cell lines has been examined. Effects on proliferation were also considered, to determine whether any cell surface changes were related to or independent of proliferation effects. No significant differences were observed in the expression of components detected by the milk fat globule membrane antibodies HMFG1 and HMFG2 over 8 days culture with 10(-7)-10(-9)M retinoic acid for the cell lines MCF-7, T-47 D, ZR-75, MDA-MB-231, and BT-20. In contrast , there was enhanced expression of HLA-DR by two oestrogen receptor-positive cell lines T-47 D and ZR-75 and the oestrogen receptor-negative line MDA-MB-231, with differing sensitivities. These effects were independent of inhibition of proliferation, which was only observed for oestrogen receptor-positive cell lines and for different durations of exposure. The finding of enhanced HLA-DR expression after retinoic acid treatment has not previously been reported and is of interest regarding clinical potential for the induction of tumour immunity.
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PMID:Modulation of cell surface components of human breast cancer cells by retinoic acid: enhanced HLA-DR expression. 832 57


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