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B Chorváth

Publications and source records attributed to B Chorváth.

At least 37 records · Page 2Linked to original sources
PubMed1995

Phorbol ester (TPA)-induced differential modulation of cell surface antigens in human pluripotential leukemia (K-562) cell line: effects of protein kinase inhibitors with broad- and PKC selective inhibitory activity.

Phorbol ester (TPA)-induced increase in cell surface expression of adhesion structures, i.e. intercellular adhesion molecule-1 (ICAM-1, CD54), beta 2 integrin LFA-1 (CD11a), complement-regulatory cell membrane protein-protein (CD59) and leukocyte common antigen (CD45) in human erythroid/myeloid leukemia cell line K-562 was inhibited by staurosporine, an inhibitor with broad, non-selective protein kinase inhibitory profile, but not by CGP 41,251, a benzoylated staurosporine derivative with the selective protein kinase C (PKC) inhibitory activity. Neither staurosporine nor CGP 41,251 modulated TPA-induced down-regulation of transferrin receptor (CD71). These data suggest that phorbol ester-induced cell surface antigen modulations in K-562 cells are predominantly mediated by PKC-independent signalling pathways.

Alkaloids↗
PubMed1995

[Density of adhesive proteins after oral administration of proteolytic enzymes in multiple myeloma].

The authors present information on the presence of adhesive proteins on membranes of myeloma and precursor cells isolated from bone marrow and blood from a group of 33 patients examined by fluorescent flow cytometry. They also compare the density of integrins (CD29, CD49e, CD41, CD51 and CD61) and adhesive proteins from the group of "homing" receptors (CD44) and IgG "superfamily" (LFA-1, LFA-3, ICAM-1, N-CAM) and their changes after a single oral dose of a mixture of proteolytic enzymes (Wobe Mugos, Wobenzym, MUCOS Pharma, FRG). The authors observed a significant drop of CD29, CD54 (ICAM-1), CD58 (LFA-3) after Wobe Mugos, CD49, CD51, CD58 after Wobenzyme. The insignificant decline of density of CD44 on cells, as well as of the soluble receptor of CD44 after oral administration of proteolytic enzymes in serum, incl. the mentioned changes of integrins and other adhesive proteins, indicate the importance of enzyme preparations in the supporting treatment of malignant processes.

Adjuvants, Immunologic↗
PubMed1994

Tyrosine kinase inhibitor-induced differentiation of K-562 cells: alterations of cell cycle and cell surface phenotype.

Protein tyrosine kinase (PTK) inhibitor herbimycin A inhibited proliferation, induced accumulation of cells in the G0/G1 phase of the cell cycle and a marked increae of hemoglobin-producing human leukemic K-562 cells in vitro. The isoflavonoid PTK- and topoisomerase II inhibitor genistein produced a similar effect with the accumulation of cells in the G2/M phase of cell cycle. Genistein potentiated the effect of herbimycin A on the cell cycle (i.e. decreased the proportion of S-phase cells) and induced an increased proportion of hemoglobin-producing cells. Genistein, but not herbimycin A induced a marked increase in cell surface expression of CD15 (LewisX) antigen. Both of these agents down-regulated CD45 (leukocyte common antigen) and monocyte-associated CD14 antigen on K-562 cells. Neither genistein nor herbimycin A induced increased cell surface expression of glycophorin.

Animals↗
PubMed1994

Drug-resistance associated alterations of cell surface antigen expression in a human anthracycline-resistant ovarian carcinoma cell line.

The anthracycline uptake and cell surface expression of plasma membrane antigens (HLA class I, c-erbB-2, protectin-CD59, integrin beta 1-chain-CD29, etc.) were compared on a parental anthracycline sensitive and an anthracycline-resistant subline of the human ovarian carcinoma cell line A2780. The anthracycline-resistant (A2780/ADR) subline incubated for 30 min in the presence of daunomycin displayed two subpopulations with different anthracycline cell content as determined by flow cytometry. The subpopulation with lower daunomycin cell content was absent in the parental anthracycline sensitive cell line. The most predominant antigenic changes on the resistant subline as compared with the sensitive one were as follow: Loss of HLA class I and a twofold increase in the expression of CD59 antigen and a slight decrease of integrin beta 1-chain on the cell surface of the resistant subline.

Antibiotics, Antineoplastic↗
PubMed1994

Modulation of cell surface EGF receptor and HLA expression on glioma cell lines induced with cytokines and differentiation promoters.

Alterations of cell surface expression of HLA (class I, class II DR, DP and DQ) and EGF-receptor on two malignant glioma cell lines (U-343MG and U-563MG) induced with cytokines (IFN-gamma, TNF-alpha, IL-1 alpha) and differentiation promoters (all-trans retinoic acid, phorbol ester TPA) were analyzed with the aid of flow cytometry. IFN-gamma induced a 10-15fold increase of HLA class I. TNF-alpha alone induced a two- to fivefold increase of HLA class I cell surface density and increased the IFN-gamma induced upregulation of HLA class I to approximately 20-24 times the antigen density of uninduced cells. TNF-alpha was able to increase HLA class II DR and DP cell surface expression on glioma lines, but it enhanced only the IFN-gamma-induced HLA class II DR upregulation. All-trans retinoic acid and TPA regulated in the opposite way the EGF-receptor cell surface expression on U-563MG cells.

Antigens, Surface↗
PubMed1994

Myeloid activation antigen CD66/67: immunochemical and immunocytometric characterization with the Vth workshop monoclonal antibodies.

Flow cytometric and immunochemical studies performed with the CD66/67 panel antibodies from the Vth International Workshop on Leukocyte Antigens allowed to subdivide these antibodies into five groups, according to the molecular weights of polypeptides recognized by these antibodies on pooled healthy donor granulocytes. Although some monoclonal antibodies recognized either 95-110 kDa, or 160-180 kDa polypeptides, majority of the examined antibodies reacted with epitopes shared by both 95-110 kDa and 160-180 kDa polypeptides. Differential TPA-induced modulation of recognized antigens was observed with HL-60 and U-937 leukemia/lymphoma cell lines.

Antibodies, Monoclonal↗
PubMed1993

Modulation of protectin (CD59 antigen) cell surface expression on human neoplastic cell lines.

The ability of cytokines (IFN alpha, IFN gamma, TNF alpha, IL-1 alpha, IL-6), all-trans retinoic acid, 1,25(OH)2-vitamin D3 and the tumor promoting phorbol ester TPA to regulate cell surface expression of protectin (CD59 antigen) on human hematopoietic and non-hematopoietic neoplastic cell lines was examined with the aid of immunocytofluorometric measurements. The tumor promoting phorbol ester TPA induced a marked up-regulation of protectin in all examined cell lines with the exception of promyelocytic leukemia HL-60, where TPA significantly decreased protectin cell surface expression. All-trans retinoic acid weakly down-regulated cell surface protectin on K-562, while 1,25(OH)2-vitamin D3 produced such effect on HL-60 cells. None of the examined cytokines induced a significant protectin down-regulation in the examined cell lines.

Antigens, CD↗
PubMed1993

Phorbol ester-induced modulation of cell surface antigens on U-937 cells in protein-free medium: effect of protein kinase and calmodulin inhibitors.

Phorbol ester (PMA) induced decrease in cell surface expression of CD4 antigen was potentiated on human monoblastoid cell line U-937 cultured and induced in protein-free culture medium. Down-regulation of the CD4 antigen was partially inhibited by the isoquinoline protein kinase inhibitor H7 and unaffected by the calmodulin inhibitor R24571 (calmidazolium). PMA-induced increase of the monocyte-associated CD14 antigen was dependent the presence of fetal bovine serum (FBS) in culture medium and partially abolished by calmodulin inhibitor R24571. H7 inhibitor partially abrogated this up-regulation in 4 out of 8 induction experiments. PMA-induced down-regulation of MHC class I antigen was found in both FBS-supplemented and protein-free culture media. This effect was partially inhibited by both H7 and R24571 inhibitors.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1993

Modulation of leukosialin (sialophorin, CD43 antigen) on the cell surface of human hematopoietic cell lines induced by cytokins, retinoic acid and 1,25(OH)2-vitamin D3.

Cell surface expression of leukosialin (sialophorin, CD43 antigen) on human neoplastic hematopoietic cell lines K-562, U-937, HL-60 and REH was determined with the aid of a new CD43 monoclonal antibody (Bra7G) by the immunochemical (radioimmunoprecipitation, immunoblotting) and immunocytofluorometric techniques. Interferon-gamma and TNF-alpha were utilized as the "physiological" inducers of differentiation-associated markers. The "non-physiological" inducer phorbol ester PMA induced down-regulation of leukosialin cell surface expression on immature erythroid-myeloid leukemia cell line K-562, but up-regulation of CD43 antigen on the promyelocyte leukemia cell line HL-60 and, to a lesser extent on the monocyte-like U-937 and CALLA+ ALL cell line REH. Retinoic acid down-regulated leukosialin on both U-937 monocyte-like cells and the CALLA+ ALL cell line REH. In contrast to these data, interferon-gamma, TNF-alpha, retinoic acid and 1,25(OH)2-vitamin D3 induced the up-regulation of leukosialin in a promyelocytic leukemia cell line HL-60.

Antigens, CD↗
PubMed1993

IL-1 alpha induced, TNF alpha mediated HLA class II (DR) antigen up-regulation in a human ductal breast carcinoma cell line ZR-75-1.

The IL-1 alpha induced up-regulation of HLA class I and HLA class II (DR) antigen expression on the cell surface of the human breast cancer cell line ZR-75-1 was demonstrated. This was associated with a concomitant increase in TNF alpha production. Coincubation with an anti-TNF alpha neutralizing antibody partially inhibited the IL-1 alpha induced up-regulation of HLA DR antigen but had no effect on IL-1 alpha induced HLA class I up-regulation. These data indicate that IL-1 alpha induced HLA class II (DR) antigen up-regulation in ZR-75-1 cells is partially mediated by TNF alpha and that IL-1 alpha induced HLA class I and class II (DR) antigen up-regulation in ZR-75-1 human breast cancer cells in vitro are mediated by different mechanisms.

Breast Neoplasms↗
PubMed1992

Monoclonal antibodies to two adhesive cell surface antigens (CD43 and CD59) with different distribution on hematopoietic and non-hematopoietic tumor cell lines.

Two new murine monoclonal antibodies were prepared by hybridoma technique after immunization with the immature pluripotent leukemia cell line K562. The monoclonal antibody Bra10G (IgG2b) reacted in a non-lineage pattern with all examined hematopoietic neoplastic cell lines and peripheral blood cells (granulocytes, lymphocytes, erythrocytes) of healthy donors, with the exception of monoblastoid cell line U-937 and B lymphoma cell line Daudi. This monoclonal antibody immunoprecipitated an 18-20 kDa cell surface protein expressed also on the cell surface of examined non-hematopoietic (malignant glioma, melanoma and breast carcinoma) cell lines. These properties and the efficient inhibition of Bra10G binding to the cell surface of K562 cells by the reference CD59 monoclonal antibody (MEM-43) indicated that Bra10G belongs to the CD59 cluster of monoclonal antibodies which identify the human protectin molecule. The monoclonal antibody Bra7G (IgM) reacted with a 95 kDa cell surface protein expressed on hematopoietic cells (with the exception of erythrocytes) and was absent on the examined non-hematopoietic neoplastic cell lines. These data together with a partial inhibition of Bra7G binding by the reference CD-43 monoclonal antibody suggested the CD43 (leukosialin, sialophorin) specificity of this monoclonal antibody.

Animals↗
PubMed1992

[Differentiation antigens of hematopoietic cells (CD system)].

Monoclonal antibodies allowed recognition and identification of a series of hematopoietic cell membrane antigens expressed on plasma membranes of leukemia patients and on cells of healthy subjects. Monoclonal antibodies produced in different laboratories were clustered on the basis of their reactivity with normal and malignant hematopoietic cells into CD (cluster of differentiation) groups, with defined properties of recognized antigens (glycoprotein, phosphoprotein or glycolipid nature, molecular weight, isoelectric point, amino acid or carbohydrate sequence, etc.) and with functional characteristics of the corresponding antigen and its distribution on cells of the hematopoietic system. This "CD system" of human hematopoietic cell differentiation antigens was established in a series of international laboratory workshops (1982-1989). The present state of the CD classification system, as assessed after the IVth International Workshop on Hematopoietic Cell Differentiation Antigens (1988/89), in which more than 100 laboratories analyzed over 1,000 monoclonal antibodies, is described. An overview of the data concerning properties of monoclonal antibodies produced in the authors' laboratory (monoclonal antibodies series Bra-) is presented.

Antibodies, Monoclonal↗
PubMed1992

T-lymphocyte subsets (CD4/CD8 ratio) in breast cancer patients.

T-lymphocyte subsets (CD4/CD8 antigen positive cells) were determined in peripheral lymphocytes from 48 patients with breast cancer of different stages by flow immunocytometry with the aid of anti-CD4 and CD8 monoclonal antibodies. A broad individual variability of the CD4/CD8 ratio among both healthy donors and breast cancer patients was observed. The average value of CD4/CD8 ratio decreased in groups as follows: Healthy donors and Stage I patients, Stage IIA, IIB and Stage IV breast cancer patients. These differences were generally statistically not significant. The difference between healthy donors and Stage IV breast cancer patients was statistically significant (p < 0.01), if one exceedingly elevated value of the CD4/CD8 ratio was excluded from statistical evaluation. The average CD4/CD8 value in the group of breast cancer patients with lymph node or distant metastases was lower than that of patients without metastases, but their difference was not statistically significant either.

Breast Neoplasms↗
PubMed1992

Cytokine (IFN-alpha, IFN-gamma, IL-1-alpha, TNF-alpha)-induced modulation of HLA cell surface expression in human breast cancer cell lines.

Cytokine-induced modulation of HLA expression on the cell surface of four human breast cancer cell lines was determined by continuous flow immunocytofluorometry with the aid of monoclonal antibodies directed to a non-polymorphic determinant of HLA class I and class II (DR) antigen. IFN-gamma and IFN-alpha were potent inducers of HLA class I in all examined cell lines, with decreasing inducibility as follows: BT-20, ZR-75-1, MCF-7 and MDA-MB-468 cells. HLA class II (DR) antigen was highly inducible by IFN-gamma in ZR-75-1 cells, followed by BT-20, MDA-MB-468 and MCF-7 cells. IFN-alpha increased the cell surface expression of DR antigen only in ZR-75-1 cells. IL-1-alpha induced a moderate level of HLA class I antigen in ZR-75-1, BT-20 and MDA-MB-468 cells, and HLA class II (DR) expression only in ZR-75-1 cells. This pattern of cell line inducibility by IL-1-alpha was similar to that induced by TNF-alpha. Differences in inducibility of HLA antigens on human breast cancer cell lines induced by different cytokines may reflect the differences in cytokine inducibility of the original tumor cells.

Breast Neoplasms↗
PubMed1991

Interferon alpha-induced modulation of leukocyte cell surface antigens: immunocytofluorometric study with human leukaemia/lymphoma cell lines.

Recombinant interferon alpha enhanced the MHC class I antigen density on human leukaemia/lymphoma cell lines REH, U-937 and HL-60, as measured by immunocytofluorometry using specific monoclonal antibodies. A similar effect was induced (as demonstrated in REH cells), also by human leukocyte interferon-alpha. The latter, however, caused no major alterations in the expression of leukocyte common antigen (ICA; CD45) and transferrin receptor (CD71) in the cell lines examined. In REH cells, there was no interferon-induced alteration of CD10 antigen (CALLA), which in this cell line is markedly down-regulated by 12-0-tetradecanoyl-phorbol-13-acetate (TPA). A decrease of CD4 antigen density on the cell membrane was induced by interferon-alpha in monoblastoid U-937 cells. No induction of MHC class I and II antigens by interferon-alpha was found in K-562 cell subline.

Antigens, CD↗
PubMed1991

Differential modulation of leucocyte surface antigens by various inducers on the T-cell line MOLT-4.

Pretreatment of MOLT-4 T-cell line with 12-0-tetradecanoylphorbol 13-acetate (TPA) potentiated the interferon alpha-induced cell surface expression of class I HLA. Simultaneous combined action of TPA and rIFN-alpha resulted in a synergistic effect upon the up-regulation of class I HLA. Neither TPA nor rIFN modulated the cell surface expression of HLA class II (DR and DP) antigens. Leucocyte common antigen (CD45) cell surface expression was quantitatively increased on MOLT-4 cells by TPA induction, unaltered by rIFN and up-regulated by combined action of TPA and rIFN. CD8 antigen was down-regulated by both TPA and rIFN.

Antigens, CD↗