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001-es BibID:	BIBFORM004861
035-os BibID:	(scopus)14644392200 (wos)000227768400023
Első szerző:	Diermeier, Simone
Cím:	Epidermal growth factor receptor coexpression modulates susceptibility to Herceptin in HER2/neu overexpressing breast cancer cells via specific erbB-receptor interaction and activation / Diermeier, S., Horvath, G., Knuechel-Clarke, R., Hofstaedter, F., Szollosi, J., Brockhoff, G.
Dátum:	2005
ISSN:	0014-4827
Megjegyzések:	Growth factors and Herceptin specifically and differentially modulate cell proliferation of tumor cells. However, the mechanism of action on erbB-receptor level is incompletely understood. We evaluated Herceptin's capacity to modulate erbB-receptor activation and interaction on the cell surface level and thereby potentially impair cell proliferation of HER2/neu (c-erbB2) overexpressing breast cancer cells, both in the presence and absence of relevant growth factors. METHODS: BT474 and SK-BR-3 breast cancer cell lines were treated with Epidermal Growth Factor (EGF), Heregulin, and with Herceptin in different combinations. Kinetics of cell proliferation were evaluated flow cytometrically based on BrdU-labeling. Fluorescence Resonance Energy Transfer, ELISAs and phosphorylation site specific Western Blotting was performed to investigate erbB-receptor interaction and activation. RESULTS: EGF induced EGFR/EGFR and EGFR/c-erbB2 interactions correlate with stimulation of cell proliferation in BT474 cells. Both homo- and heterodimerization are considerably less pronounced in SK-BR-3 cells and heterointeraction is additionally reduced by EGF treatment, causing inhibition of cell proliferation. Heregulin stimulates cell proliferation extensively in both cell lines. Herceptin drives BT474 cells more efficiently into quiescence than it does with SK-BR-3 cells and thereby blocks cell cycle progress. In SK-BR-3 Herceptin treatment causes c-erbB2 phosphorylation of Y877 and Y1248, EGF induces Y877 and Y1112 phosphorylation. The Y1112 phosphorylation site, activated by EGF in SK-BR-3 cell, is bypassed in BT474. In addition the inhibitory capacity of Herceptin on BT474 and SK-BR-3 cell proliferation depends on the presence and absence of growth factors to a various extent. CONCLUSION: The growth inhibitory effect of Herceptin on c-erbB2 overexpressing breast cancer cells is considerably modulated by EGFR coexpression and consequently EGFR/c-erbB2 homo- and heterointeractions, as well as the presence or absence of growth factors. C-erbB2 overexpression alone is insufficient to predict the impact of growth factors and antibodies on cell proliferation. The optimization and specification of therapeutic approaches based on erbB-receptor targeting requires to account for EGFR coexpression as well as the potential presence of erbB-receptor relevant growth factors.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Antibodies Antibodies,Monoclonal Antineoplastic Agents Breast Neoplasms Carcinoma Cell Cycle Cell Cycle Proteins Cell Line Cell Line, Tumor Cell Proliferation Cells drug effects Drug Resistance,Neoplasm Drug Synergism drug therapy Energy Transfer Epidermal Growth Factor Female Fluorescence Fluorescence Resonance Energy Transfer genetics Growth Inhibitors Humans Kinetics metabolism methods Neuregulin-1 pathology pharmacology Phosphorylation physiology Proteins Receptor, Epidermal Growth Factor Receptor, erbB-2 Receptors, Cell Surface Research Support therapeutic use
Megjelenés:	Experimental Cell Research. - 304 : 2 (2005), p. 604-619. -
További szerzők:	Horváth Gábor (1974-) (biofizikus) Knuechel-Clarke, Ruth Hofstaedter, Ferdinand Szöllősi János (1953-) (biofizikus) Brockhoff, Gero
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001-es BibID:	BIBFORM003392
Első szerző:	Soóki-Tóth Ágnes
Cím:	Cellular regulation of ADP-Ribosylation of proteins III. : selective augmentation of in vitro ADP-ribosylation of histone H3 in murine thymic cells after in vivo emetine treatment / Ágnes Soóki-Tóth, Gáspár Bánfalvi, János Szöllösi, Eva Kirsten, Maria Staub, Ferenc Antoni, Ernest Kun
Dátum:	1989
Megjegyzések:	Thymic cells were isolated at intervals of between 0 and 144 h from mice that received one intraperitoneal injection of emetine (33 mg/kg), and thymus weight, incorporation of [14C]leucine into proteins and [3H]thymidine into DNA in intact thymic cells, as well as initial rates of protein ADP-ribosylation in permeabilized cells [A. Sooki-Toth, F. Asghari, E. Kirsten, and E. Kun (1987) Exp. Cell Res. 170, 93] were simultaneously monitored. The effect of emetine as an inhibitor of protein synthesis [F. Antoni, N. G. Luat, I. Csuka, I. Olah, A. Sooki-Toth, and G. Banfalvi (1987) Int. J. Immunopharmacol. 9, 333] corresponds to the induction of sequential cellular events, such as cell exit and remigration, by other antimitotic agents [C. Penit and F. Vasseur (1988) J. Immunol. 140, 3315] and produces an activation of proliferation of cells reentering into this organ. Proliferation, as demonstrated by a large increase in DNA synthesis and entrance into S phase, was kinetically related to an apparent increase in poly(ADP-ribose) polymerase activity in thymic cells and a highly significant in vitro ADP-ribosylation of histone H3. Since no DNA fragmentation occurred in thymic cells, as tested by a fluorometric technique [C. Birnboim and J. J. Jevac (1981) Cancer Res. 41, 1889], it is probable that a selective activation of poly(ADP-ribose) polymerase may have been induced in cells that undergo differentiation and proliferation while repopulating the thymus.
Tárgyszavak:	Természettudományok Orvostudományok Biológiai tudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban murine thymic cells in vivo emetine treatment histon H3
Megjelenés:	Experimental Cell Research. - 184 : 1 (1989), p. 44-52. -
További szerzők:	Bánfalvi Gáspár (1943-) (sejtbiológus, gyógyszerész) Szöllősi János (1953-) (biofizikus) Kirsten, Eva Staub, Maria Antoni Ferenc Kun, Ernest
Internet cím:	elektronikus változat
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