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1.

001-es BibID:BIBFORM050093
Első szerző:Petrás Miklós (orvos)
Cím:Molecular interactions of ErbB1 (EGFR) and integrin-β1 in astrocytoma frozen sections predict clinical outcome and correlate with Akt-mediated in vitro radioresistance / Miklós Petrás, Tamás Lajtos, Elza Friedländer, Álmos Klekner, Éva Pintye, Burt G. Feuerstein, János Szöllősi, György Vereb
Dátum:2013
ISSN:1522-8517
Megjegyzések:INTRODUCTION: Treatment of astrocytoma is frequently hampered by radioresistance of the tumor. In addition to overexpression of ErbB1/EGFR, functional crosstalk between receptor tyrosine kinases and cell adhesion molecules may also contribute to therapy resistance. METHODS: Acceptor photobleaching FRET was implemented on frozen sections of clinical astrocytoma to check the role of ErbB1-integrin-beta1 interaction. U251 glioma subclones were obtained by introducing extra CHR7 material or the ErbB1 gene to test the relevance and mechanism of this interaction in vitro. RESULTS: Grade IV tumors showed higher ErbB1 and integrin-beta1 expression and greater ErbB1-integrin-beta1 heteroassociation than did grade II tumors. Of these, the extent of molecular association was a single determinant of tumor grade and prognosis in stepwise logistic regression. In vitro, integrin-beta1 was upregulated, and radiosensitivity was diminished by ectopic ErbB1 expression. Great excess of ErbB1 provided colony forming advantage over medium excess but did not yield better radiation resistance or faster proliferation and decreased to medium level over time, whereas integrin-beta1 levels remained elevated and defined the extent of radioresistance. Increased expression of ErbB1 and integrin-beta1 was paralleled by decreasing ErbB1 homoassociation and increasing ErbB1-integrin-beta1 heteroassociation. Microscopic two-sided FRET revealed that pixels with higher ErbB1-integrin-beta1 heteroassociation exhibited lowed ErbB1 homoassociation, indicating competition for association partners among these molecules. Boosted Akt phosphorylation response to EGF accompanied this shift toward heteroassociation, and the consequentially increased radioresistance could be reverted by inhibiting PI3K. CONCLUSION: The clinically relevant ErbB1-integrin-beta1 heteroassociation may be used as a target of both predictive diagnostics and molecular therapy
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Biophysics
Cell Adhesion
Cell Adhesion Molecules
cell biology
EGFR
ErbB1
EXPRESSION FRET
Glioma
Hungary
In Vitro
methods
molecular interaction
Phosphorylation
Photobleaching
Receptor
tyrosine kinase
Research
therapy
TUMORS
Tyrosine
Molekulatudomány
Doktori iskola
Megjelenés:Neuro-Oncology. - 15 : 8 (2013), p. 1027-1040. -
További szerzők:Lajtos Tamás Friedländer Elza (1980-) (biofizikus) Klekner Álmos (1970-) (idegsebész) Pintye Éva (1955-) (fizikus) Feuerstein, Burt G. Szöllősi János (1953-) (biofizikus) Vereb György (1965-) (biofizikus, orvos)
Pályázati támogatás:K75752
OTKA
NK101337
OTKA
F-049050
OTKA
ETT 523/2003
Egyéb
ETT 362-01/2009
Egyéb
TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
TÁMOP-4.2.2/B-10/1-2010-0024
TÁMOP
TÁMOP-4.2.2/A-11/1/KONV-2012-0025
TÁMOP
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM042489
Első szerző:Petrás Miklós (orvos)
Cím:Significance of Epidermal Growth Factor Receptor in the Radiation Resistance of Glioblastoma Tumors / Miklós Petrás, Tamás Lajtos, Éva Pintye, Burt G. Feuerstein, János Szöllősi, György Vereb
Dátum:2008
Megjegyzések:In the United States, a dramatically increased incidence and mortality of brain tumors have been observed over the past decades. Of the ~44 thousand new cases of primary malignant and benign brain tumors diagnosed per year, highgrade astrocytomas or multiform glioblastomas show particularly bad prognosis in spite of therapeutic developments. Current management of multiform glioblastoma includes the most extensive surgical resection possible, followed by adjuvant radio- and chemotherapy. However, treatment is frequently hampered by decreased radiosensitivity of the tumor. Recent studies revealed that subpopulations of glioblastoma cells show amplified checkpoint activation of the cell cycle upon ionizing radiation, which induces overactivation of DNA repair processes and leads to maintained proliferation rate as well as clinically observed radioresistance and recurrence of the tumor over time. In addition, overexpression of some transmembrane receptors has also been implicated in radioresistance. However, the role of the overexpressed proteins can only be interpreted reliably if their multi-faceted molecular interactions are properly characterized. Thus, based on recent evidence for the functional crosstalk between certain cell adhesion molecules andreceptor tyrosine kinases, we have examined the molecular interactions of the receptor tyrosine kinase EGFR and the cell adhesion molecule 1-integrin using flow cytometric and microscopic fluorescence resosnance energy transfer (FRET)measurements on two cellular model systems showing similar expression patterns to low and high grade astrocytomas. On the one hand, U251 glioblastoma clones established by introducing varying amounts of extra chromosome 7 into the cells, and on the other hand stable, high and low EGFR expressing transfenctant U251 NCI sublines were investigated. The results revealed that increased EGFR and 1-integrin expression levels correlate with stronger EGFR ? 1-integrin heteroassociation, while concurrently the EGFR homoassociation is decreased, suggesting that 1-integrins may dynamically modulate the homoassociation state of EGFR receptors. This functional relationship may play an important role in decreasing radiosensitivity and tumor progression, especially since the EGFR ? 1-integrin molecular interaction appears to promote radioresistance via the Akt pathway.
ISBN:978-0-7354-0611-7
Tárgyszavak:Orvostudományok Elméleti orvostudományok könyvfejezet
Megjelenés:Radiation Damage In Biomolecular Systems : Proceedings of the 5th International Conference (RADAM 2008) / ed. by Károly Tőkési, Béla Sulik. - p. 204-217. -
További szerzők:Lajtos Tamás Pintye Éva (1955-) (fizikus) Feuerstein, Burt G. Szöllősi János (1953-) (biofizikus) Vereb György (1965-) (biofizikus, orvos)
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM006054
Első szerző:Szöllősi János (biofizikus)
Cím:Calcium channels in PDGF-stimulated A172 cells open after intracellular calcium release and are not voltage-dependent / Szollosi, J., Feuerstein, B. G., Vereb, G., Pershadsingh, H. A., Marton, L. J.
Dátum:1991
Megjegyzések:Using laser image cytometry and Indo-1 fluorescence, we investigated the intracellular free Ca2+ concentration ([Ca2+]i) of confluent A172 human glioblastoma cells stimulated by the BB homodimer of platelet-derived growth factor (PDGF-BB). The shape of the calcium transients and the delay time between stimulation and the beginning of the transient varied considerably. The percentage of responsive cells, the peak [Ca2+]i and the duration of the response were directly related to PDGF-BB dose, while the delay time was inversely related; the maximal response occurred at a PDGF-BB concentration of 20 ng/ml. Studies with EGTA and inorganic calcium-channel blockers (Ni2+, La3+) showed that the increase of [Ca2+]i resulted from initial release of intracellular stores and subsequent calcium influx across the plasma membrane. Opening of calcium channels in the plasma membrane, monitored directly by studying Mn2+ quenching of Indo-1 fluorescence, was stimulated by PDGF-BB and blocked by La3+; the opening occurred 55 +/- 10 s after the initial increase in [Ca2+]i. Therefore, in these tumor cells, intracellular release always occurs before channel opening in the plasma membrane. Depolarization of cells with high extracellular [K+] did not generally induce calcium transients but did decrease calcium influx. L-type calcium-channel blockers (verapamil, nifedipine, and diltiazem) had little or no effect on the calcium influx induced by PDGF-BB. These results indicate that PDGF-BB induces calcium influx by a mechanism independent of voltage-sensitive calcium channels in A172 human glioblastoma cells.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Calcium
Calcium Channel Blockers
Calcium Channels
Dyes
Egtazic Acid
Electrophysiology
Fluorescence
Fluorescent Dyes
Glioblastoma
Human
Image Cytometry
Image Processing,Computer-Assisted
Indoles
Lanthanum
metabolism
pharmacology
Platelet-Derived Growth Factor
Signal Transduction
Support,Non-U.S.Gov't
Support,U.S.Gov't,P.H.S.
Tumor Cells,Cultured
Verapamil
Megjelenés:Cell Calcium. - 12 : 7 (1991), p. 477-491. -
További szerzők:Feuerstein, Burt G. Vereb György (1965-) (biofizikus, orvos) Pershadsingh, Harrihar A. Marton, Laurence J.
Internet cím:elektronikus változat
Borító:

4.

001-es BibID:BIBFORM006077
Első szerző:Vereb György (biofizikus, orvos)
Cím:Depletion of intracellular calcium stores facilitates the influx of extracellular calcium in platelet derived growth factor stimulated A172 glioblastoma cells / Vereb, G., Jr., Szollosi, J., Matyus, L., Balazs, M., Hyun, W. C., Feuerstein, B. G.
Dátum:1996
Megjegyzések:Calcium signaling in non-excitable cells is the consequence of calcium release from intracellular stores, at times followed by entry of extracellular calcium through the plasma membrane. To study whether entry of calcium depends upon the level of saturation of intracellular stores, we measured calcium channel opening in the plasma membrane of single confluent A172 glioblastoma cells stimulated with platelet derived growth factor (PDGF) and/or bradykinin (BK). We monitored the entry of extracellular calcium by measuring manganese quenching of Indo-1 fluorescence. PDGF raised intracellular calcium concentration ([Ca2+]i) after a dose-dependent delay (tdel) and then opened calcium channels after a dose-independent delay (tch). At higher doses (> 3 nM), BK increased [Ca2+]i after a tdel approximately 0 s, and tch decreased inversely with both dose and peak [Ca2+]i. Experiments with thapsigargin (TG), BK, and PDGF indicated that BK and PDGF share intracellular Ca2+ pools that are sensitive to TG. When these stores were depleted by treatment with BK and intracellular BAPTA, tdel did not change, but tch fell to almost 0 s in PDGF stimulated cells, indicating that depletion of calcium stores affects calcium channel opening in the plasma membrane. Our data support the capacitative model for calcium channel opening and the steady-state model describing quantal Ca2+ release from intracellular stores.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
antagonists and inhibitors
Biophysics
Bradykinin
Ca(2+)-Transporting ATPase
Calcium
Calcium Channel Blockers
Calcium Channels
Calcium Signaling
Dose-Response Relationship,Drug
drug effects
Fluorescence
Glioblastoma
Human
Hungary
Lanthanum
Manganese
metabolism
Neuroglia
pharmacology
Platelet-Derived Growth Factor
Signal Transduction
Support, Non-U.S. Gov't
Support, U.S.Gov't, Non-P.H.S.
Support, U.S.Gov't, P.H.S.
Terpenes
Thapsigargin
Tumor Cells,Cultured
Megjelenés:Cytometry. - 24 : 1 (1996), p. 64-73. -
További szerzők:Szöllősi János (1953-) (biofizikus) Mátyus László (1956-) (biofizikus) Balázs Margit (1952-) (sejtbiológus, molekuláris genetikus) Hyun, William C. Feuerstein, Burt G.
Internet cím:Intézményi repozitóriumban (DEA) tárolt változa
Borító:

5.

001-es BibID:BIBFORM004890
035-os BibID:(scopus)26444597596 (wos)000232299300017
Első szerző:Vereb György (biofizikus, orvos)
Cím:Biphasic calcium response of platelet-derived growth factor stimulated glioblastoma cells is a function of cell confluence / Vereb, G., Feuerstein, B. G., Hyun, W. C., Fulwyler, M. J., Balazs, M., Szollosi, J.
Dátum:2005
ISSN:1552-4922
Megjegyzések:Previous reports have linked the spiking or two-phased character of calcium transients evoked by platelet-derived growth factor (PDGF) to the position of cells in the cell cycle without regard to cell-cell contact and communication. Because cell confluence can regulate growth factor receptor expression and dephosphorylation, we investigated the effect of cell culture confluence and cell cycle on calcium responses of PDGF-BB-stimulated A172 glioblastoma cells. METHODS: Digital imaging cytometry was used to correlate the peak and duration of calcium response with bromodeoxyuridine positivity and DNA content and with culture confluence on a cell-by-cell basis. RESULTS: In serum-starved cultures, complete two-phase calcium signals and shorter, lower spikes occurred independent of cell cycle phase. However, the confluence of cell culture seemed essential for inducing a complete response because cells in sparse cultures exhibited mostly short spikes with lower peaks or no transients at all. CONCLUSION: Because cell confluence, by virtue of cell-cell contacts, is assumed to be an important regulator of proliferation, one is tempted to speculate that in transformed cells the ability to produce stronger growth signals upon reaching confluence and facing contact inhibition could provide a proliferative advantage.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
analysis
Biophysics
Bromodeoxyuridine
Calcium
Calcium Signaling
Cell Adhesion
Cell Culture
Cell Cycle
Cells
Cells,Cultured
Dna
drug effects
genetics
Glioblastoma
Hungary
metabolism
methods
pathology
pharmacology
Platelet-Derived Growth Factor
Research
Spectrometry,Fluorescence
Support
Megjelenés:Cytometry. Part A. - 67 : 2 (2005), p. 172-179. -
További szerzők:Feuerstein, Burt G. Hyun, William C. Fulwyler, Mack J. Balázs Margit (1952-) (sejtbiológus, molekuláris genetikus) Szöllősi János (1953-) (biofizikus)
Internet cím:elektronikus változat
DOI
Borító:
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