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1.

001-es BibID:BIBFORM057538
035-os BibID:(scopus)84910122146 (wos)000345023400059
Első szerző:Govers, Coen
Cím:TCRs genetically linked to CD28 and CD3[epszilon] do not mispair with endogenous TCR chains and mediate enhanced t cell persistence and anti-melanoma activity / Coen Govers, Zsolt Sebestyén, János Roszik, Mandy van Brakel, Cor Berrevoets, Árpád Szöőr, Konstantina Panoutsopoulou, Marieke Broertjes, Tan Van, György Vereb, János Szöllősi, Reno Debets
Dátum:2014
ISSN:0022-1767 1550-6606
Megjegyzések:Adoptive transfer of T cells that are gene engineered to express a defined TCR represents a feasible and promising therapy for patients with tumors. However, TCR gene therapy is hindered by the transient presence and effectiveness of transferred T cells, which are anticipated to be improved by adequate T cell costimulation. In this article, we report the identification and characterization of a novel two-chain TCR linked to CD28 and CD3[epszilon] (i.e., TCR:28[epszilon]). This modified TCR demonstrates enhanced binding of peptide-MHC and mediates enhanced T cell function following stimulation with peptide compared with wild-type TCR. Surface expression of TCR:28[epszilon] depends on the transmembrane domain of CD28, whereas T cell functions depend on the intracellular domains of both CD28 and CD3[epszilon], with IL-2 production showing dependency on CD28:LCK binding. TCR:28[epszilon], but not wild-type TCR, induces detectable immune synapses in primary human T cells, and such immune synapses show significantly enhanced accumulation of TCR transgenes and markers of early TCR signaling, such as phosphorylated LCK and ERK. Importantly, TCR:28[epszilon] does not show signs of off-target recognition, as evidenced by lack of TCR mispairing, as well as preserved specificity. Notably, when testing TCR:28[epszilon] in immune-competent mice, we observed a drastic increase in T cell survival, which was accompanied by regression of large melanomas with limited recurrence. Our data argue that TCR transgenes that contain CD28, and, thereby, may provide T cell costimulation in an immune-suppressive environment, represent candidate receptors to treat patients with tumors.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
TCR
T Cell
Megjelenés:Journal Of Immunology. - 193 : 10 (2014), p. 5315-5326. -
További szerzők:Sebestyén Zsolt Roszik János (1979-) (biofizikus) van Brakel, Mandy Berrevoets, Cor Szöőr Árpád (1984-) (orvos) Panoutsopoulou, Konstantina Broertjes, Marieke Van, Tan Vereb György (1965-) (biofizikus, orvos) Szöllősi János (1953-) (biofizikus) Debets, Reno
Pályázati támogatás: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-20120025
TÁMOP
OTKA-NK101337
OTKA
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM100193
035-os BibID:(Scopus)85123488729 (WOS)000745777900001
Első szerző:Guti Eliza (Molekuláris biológus)
Cím:The multitargeted receptor tyrosine kinase inhibitor sunitinib induces resistance of HER2 positive breast cancer cells to trastuzumab-mediated ADCC / Guti Eliza, Regdon Zsolt, Sturniolo Isotta, Kiss Alexandra, Kovács Katalin, Demény Máté, Szöőr Árpád, Vereb György, Szöllősi János, Hegedűs Csaba, Polgár Zsuzsanna, Virág László
Dátum:2022
ISSN:0340-7004
Megjegyzések:Despite recent advances in the development of novel personalized therapies, breast cancer continues to challenge physicians with resistance to various advanced therapies. The anticancer action of the anti-HER2 antibody, trastuzumab, involves antibody-dependent cell-mediated cytotoxicity (ADCC) by natural killer (NK) cells. Here, we report a repurposing screen of 774 clinically used compounds on NK-cell + trastuzumab-induced killing of JIMT-1 breast cancer cells. Using a calceinbased high-content screening (HCS) assay for the image-based quantitation of ADCC that we have developed and optimized for this purpose, we have found that the multitargeted tyrosine kinase inhibitor sunitinib inhibits ADCC in this model. The cytoprotective effect of sunitinib was also confirmed with two other assays (lactate dehydrogenase release, and electric cell substrate impedance sensing, ECIS). The drug suppressed NK cell activation as indicated by reduced granzyme B deposition on to the target cells and inhibition of interferon-? production by the NK cells. Moreover, sunitinib induced downregulation of HER2 on the target cells' surface, changed the morphology and increased adherence of the target cells. Moreover, sunitinib also triggered the autophagy pathway (speckled LC3b) as an additional potential underlying mechanism of the cytoprotective effect of the drug. Sunitinib-induced ADCC resistance has been confirmed in a 3D tumor model revealing the prevention of apoptotic cell death (Annexin V staining) in JIMT-1 spheroids co-incubated with NK cells and trastuzumab. In summary, our HCS assay may be suitable for the facile identification of ADCC boosting compounds. Our data urge caution concerning potential combinations of ADCC-based immunotherapies and sunitinib.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Sunitinib
Natural killer cell
Breast cancer
ADCC
Trastuzumab
Herceptin
Megjelenés:Cancer Immunology Immunotherapy. - 71 : 9 (2022), p. 2151-2168. -
További szerzők:Regdon Zsolt (1988-) (biokémikus, molekuláris biológus) Sturniolo, Isotta Kiss Alexandra (1991-) (klinikai laboratóriumi kutató) Kovács Katalin (1978-) (biokémikus) Demény Máté Ágoston (1976-) (molekuláris biológus) Szöőr Árpád (1984-) (orvos) Vereb György (1965-) (biofizikus, orvos) Szöllősi János (1953-) (biofizikus) Hegedűs Csaba (1980-) (biokémikus, molekuláris biológus) Polgár Zsuzsanna (1978-) (agrármérnök, biotechnológus) Virág László (1965-) (biokémikus, sejtbiológus, farmakológus)
Pályázati támogatás:GINOP-2.3.3-15-2016-00020
GINOP
GINOP-2.3.2-15-2016-00048
GINOP
K132193
OTKA
K119690
OTKA
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM096107
035-os BibID:(cikkazonosító)4301 (WoS)000695558500001 (Scopus)85113512008
Első szerző:Mezősi-Csaplár Marianna
Cím:Cytolytic Activity of CAR T Cells and Maintenance of Their CD4+ Subset Is Critical for Optimal Antitumor Activity in Preclinical Solid Tumor Models / Marianna Csaplár, János Szöllősi, Stephen Gottschalk, György Vereb, Árpád Szöőr
Dátum:2021
ISSN:2072-6694
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Cancers. - 13 : 17 (2021), p. 1-19. -
További szerzők:Szöllősi János (1953-) (biofizikus) Gottschalk, Stephen Vereb György (1965-) (biofizikus, orvos) Szöőr Árpád (1984-) (orvos)
Pályázati támogatás:Bólyai
MTA
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM020768
Első szerző:Roszik János (biofizikus)
Cím:T-cell synapse formation depends on antigen recognition but not CD3 interaction : studies with TCR : zeta, a candidate transgene for TCR gene therapy / Roszik J., Sebestyén Z., Govers C., Guri Y., Szöor A., Pályi-Krekk Z., Vereb G., Nagy P., Szöllosi J., Debets R.
Dátum:2011
Megjegyzések:T-cell receptors (TCRs) can be genetically modified to improve gene-engineered T-cell responses, a strategy considered critical for the success of clinical TCR gene therapy to treat cancers. TCR:zeta, which is a heterodimer of TCRalpha and beta chains each coupled to complete human CD3zeta, overcomes issues of mis-pairing with endogenous TCR chains, shows high surface expression and mediates antigen-specific T-cell functions in vitro. In the current study, we further characterized TCR:zeta in gene-engineered T cells and assessed whether this receptor is able to interact with surface molecules and drive correct synapse formation in Jurkat T cells. The results showed that TCR:zeta mediates the formation of synaptic areas with antigen-positive target cells, interacts closely with CD8alpha and MHC class I (MHCI), and co-localizes with CD28, CD45 and lipid rafts, similar to WT TCR. TCR:zeta did not closely associate with endogenous CD3epsilon, despite its co-presence in immune synapses, and TCR:zeta showed enhanced synaptic accumulation in T cells negative for surface-expressed TCR molecules. Notably, synaptic TCR:zeta demonstrated lowered densities when compared with TCR in dual TCR T cells, a phenomenon that was related to both extracellular and intracellular CD3zeta domains present in the TCR:zeta molecule and responsible for enlarged synapse areas
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Adoptive Transfer
Antigens
Antigens,CD28
Antigens,CD3
Antigens,CD45
Antigens,CD8
article
Biophysics
Cells
Flow Cytometry
Gene Therapy
genetics
Histocompatibility Antigens
Histocompatibility Antigens Class I
Human
Humans
Hungary
Immunity,Cellular
Immunological Synapses
immunology
In Vitro
Jurkat Cells
lipid raft
LIPID RAFTS
Membrane Microdomains
metabolism
physiology
Receptor-CD3 Complex,Antigen,T-Cell
Receptors,Antigen,T-Cell,alpha-beta
Research
Research Support
Support
Synapses
T-Lymphocytes
therapy
Transgenes
Megjelenés:European Journal of Immunology. - 41 : 5 (2011), p. 1288-1297. -
További szerzők:Sebestyén Zsolt Govers, Coen Guri, Yakir Szöőr Árpád (1984-) (orvos) Pályiné Krekk Zsuzsanna (1974-) (molekuláris biológus) Vereb György (1965-) (biofizikus, orvos) Nagy Péter (1971-) (biofizikus) Szöllősi János (1953-) (biofizikus) Debets, Reno
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
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5.

001-es BibID:BIBFORM091345
Első szerző:Szöőr Árpád (orvos)
Cím:From antibodies to living drugs : quo vadis cancer immunotherapy? / Szöőr Árpád, Szöllősi János, Vereb György
Dátum:2021
ISSN:2676-8615 2676-8607
Megjegyzések:In the last few decades, monoclonal antibodies targeting various receptors and ligands have shown signifcant advance in cancer therapy. However, still a great percentage of patients experiences tumor relapse despite persistent antigen expression. Immune cell therapy with adoptively transferred modifed T cells that express chimeric antigen receptors (CAR) is an engaging option to improve disease outcome. Designer T cells have been applied with remarkable success in the treatment for acute B cell leukemias, yielding unprecedented antitumor activity and signifcantly improved overall survival. Relying on the success of CAR T cells in leukemias, solid tumors are now emerging potential targets; however, their complexity represents a signifcant challenge. In preclinical models, CAR T cells recognized and efciently killed the wide spectrum of tumor xenografts; however, in human clinical trials, limited antitumor efcacy and serious side efects, including cytokine release syndrome, have emerged as potential limitations. The next decade will be an exciting time to further optimize this novel cellular therapeutics to improve efector functions and, at the same time, keep adverse events in check. Moreover, we need to establish whether gene-modifed T cells which are yet exclusively used for cancer patients could also be successful in the treatment for other diseases. Here, we provide a concise overview about the transition from monoclonal antibodies to the generation of chimeric antigen receptor T cells. We summarize lessons learned from preclinical models, including our own HER2-positive tumor models, as well as from clinical trials worldwide. We also discuss the challenges we are facing today and outline future prospects
taa, km
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Chimeric autoantibody receptor
Immunotherapy
Chimeric antigen receptor
Bispecifc antibody
Cell therapy
Humanized antibody
Megjelenés:Biologia Futura. - 72 : 1 (2021), p. 85-99. -
További szerzők:Szöllősi János (1953-) (biofizikus) Vereb György (1965-) (biofizikus, orvos)
Pályázati támogatás:K119690
OTKA
FK132773
OTKA
GINOP-2.3.2-15-2016-00044
GINOP
Egyéb
MTA
ÚNKP-20-5-DE-48
Egyéb
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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6.

001-es BibID:BIBFORM061401
Első szerző:Szöőr Árpád (orvos)
Cím:Cell confluence induces switching from proliferation to migratory signaling by site-selective phosphorylation of PDGF receptors on lipid raft platforms / Árpád Szöőr, László Ujlaky-Nagy, Gábor Tóth, János Szöllősi, György Vereb
Dátum:2016
ISSN:0898-6568
Megjegyzések:Platelet derived growth factor receptors (PDGFR) play an important role in tumor pathogenesis and are frequently overexpressed in glioblastoma. Earlier we have shown that only confluent glioblastoma cell cultures exhibit a biphasic calcium transient upon PDGF stimulation. Here, we examined how the change in cell density leads to differential cellular responses to the same PDGF stimulus. PDGF beta receptors and their specific phosphotyrosine residues were fluorescently colabeled on A172 and T98G glioblastoma cells. The distribution in cell membrane microdomains (lipid rafts) and the phosphorylation state of PDGFR was measured by confocal microscopy and quantitated by digital image processing. Corresponding bulk data were obtained by Western blotting. Activation of relevant downstream signaling pathways was assessed by immunofluorescence in confocal microscopy and by Western blot analysis. Functional outcomes were confirmed with bulk and single cell proliferation assays and motility measurements. In non-confluent (sparse) cultures PDGF-BB stimulation significantly increased phosphorylation of tyr716 specific for the Ras/MAPK pathway and tyr751 specific for the phosphoinositide 3-kinase/Akt pathway. As cell monolayers reached confluence, tyr771 and tyr1021 were the prominently phosphorylated residues. Tyr771 serves as adaptor for RasGAP, which inactivates the MAPK pathway, and tyr1021 feeds into the phospholipase Cgamma / PKC pathway. Coherent with this, MAPK phosphorylation, Ki67 positivity and proliferation dominated in dispersed cells, and could be abolished with inhibitors of the MAPK pathway. At the same time, RhoA activation, redistribution of cortactin to leading edges, and increased motility were the prominent output features in confluent cultures. Importantly, the stimulus-evoked confluence-specific changes in the phosphorylation of tyrosine residues occurred mainly in GM1-rich lipid microdomains (rafts). These observations suggest that the same stimulus is able to promote distinctly relevant signaling outputs through a confluence dependent, lipid raft-based regulatory mechanism. In particular, cell division and survival in sparse cultures and inhibition of proliferation and promotion of migration in confluent monolayers. In our model, the ability to switch the final output of the same stimulus as a function of cell density could be a key to the balance of proliferation and invasion in malignant glioblastoma.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
lipid rafts
site-selective phosphorylation
quantitative confocal microscopy
contact inhibition
tumor proliferation
invasive tumor growth
cell migration
glioblastoma
PDGFR
Megjelenés:Cellular Signalling. - 28 : 2 (2016), p. 81-93. -
További szerzők:Ujlaky-Nagy László (1977-) (biofizikus) Tóth Gábor (1989-) (általános orvos) Szöllősi János (1953-) (biofizikus) Vereb György (1965-) (biofizikus, orvos)
Pályázati támogatás:K75752
OTKA
NK 101337
OTKA
Baross Gabor Program
Egyéb
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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7.

001-es BibID:BIBFORM015628
Első szerző:Szöőr Árpád (orvos)
Cím:Rafts and the battleships of defense : the multifaceted microdomains for positive and negative signals in immune cells / Szoor, A., Szollosi, J., Vereb, G.
Dátum:2010
Megjegyzések:Recognition of the heterogeneity of the cell membrane was one of the most important scientific achievements in the last decades. Since coining the term "lipid rafts", continuous development of advanced microscopic and spectroscopic techniques has vastly expanded our view on these cell membrane microdomains that appear to have almost as many faces as researchers that look at them; they are variable in stability, size and composition that can change in a highly dynamic manner both by recruiting and expelling components as well as by coalescing and breaking up into smaller units. They have, however, one common feature: all eukaryotic cells present some variation of lipid rafts. Cells of the immune system are not exception to this, regardless of their lymphoid or myeloid origin their membranes show a domain structure and these domains serve to condense or reject particular transmembrane, GPI-linked and intracellularly membrane-anchored proteins as function requires. Here we provide a concise overview about the various weapons and shields that immune cells concentrate into their rafts, which have come into sight during the past years. The positive and negative regulatory roles of these microdomains are essential both in the functions of innate immunity and processes concatenated in the adaptive immune response
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
article
Biophysics
Cell Membrane
Cells
Eukaryotic Cells
Hungary
Immune System
lipid raft
Membrane Microdomains
Proteins
Research
Research Support
Support
OTKA::1
MAB::3.1
Megjelenés:Immunology Letters. - 130 : 1-2 (2010), p. 2-12. -
További szerzők:Szöllősi János (1953-) (biofizikus) Vereb György (1965-) (biofizikus, orvos)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
Borító:

8.

001-es BibID:BIBFORM083356
035-os BibID:(cikkazonosító)1039 (scopus)85079082860 (wos)000522551606025
Első szerző:Tóth Gábor (általános orvos)
Cím:A Small Number of HER2 Redirected CAR T Cells Significantly Improves Immune Response of Adoptively Transferred Mouse Lymphocytes against Human Breast Cancer Xenografts / Tóth Gábor, Szöllősi János, Abken Hinrich, Vereb György, Szöőr Árpád
Dátum:2020
ISSN:1661-6596 1422-0067
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:International Journal Of Molecular Sciences. - 21 : 3 (2020), p. 1-11. -
További szerzők:Szöllősi János (1953-) (biofizikus) Abken, Hinrich Vereb György (1965-) (biofizikus, orvos) Szöőr Árpád (1984-) (orvos)
Pályázati támogatás:K119690
OTKA
FK132773
OTKA
GINOP-2.3.2-15-2016-00050
GINOP
Deutsche Krebshilfe, Bonn, FRG
Egyéb
János Bolyai Research Scholarship of the Hungarian Academy of Sciences
MTA
UNKP-19-4-DE-167 New National Excellence Program of the Ministry for Innovation and Technology
Egyéb
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

9.

001-es BibID:BIBFORM065721
Első szerző:Tóth Gábor (általános orvos)
Cím:The combination of trastuzumab and pertuzumab administered at approved doses may delay development of trastuzumab resistance by additively enhancing antibody-dependent cell-mediated cytotoxicity / Gábor Tóth, Árpád Szöőr, László Simon, Yosef Yarden, János Szöllősi, György Vereb
Dátum:2016
ISSN:1942-0862 1942-0870
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:mAbs 8 : 7 (2016), p. 1361-1370. -
További szerzők:Szöőr Árpád (1984-) (orvos) Simon László (biofizikus) Yarden, Yosef Szöllősi János (1953-) (biofizikus) Vereb György (1965-) (biofizikus, orvos)
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DOI
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Borító:

10.

001-es BibID:BIBFORM086412
035-os BibID:(absztrakt azonosító)C3-056P
Első szerző:Ujlaky-Nagy László (biofizikus)
Cím:Cell surface pattern of PDGF receptors affects signalling in glioblastoma cells / Ujlaky-Nagy László, Szöőr Árpád, Szöllősi János, Vereb György
Dátum:2005
ISSN:1742-464X
Tárgyszavak:Orvostudományok Klinikai orvostudományok idézhető absztrakt
folyóiratcikk
Megjelenés:Febs Journal. - 272 : Suppl1 (2005), p. 230. -
További szerzők:Szöőr Árpád (1984-) (orvos) Szöllősi János (1953-) (biofizikus) Vereb György (1965-) (absztraktok, könyvfejezetek)
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DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

11.

001-es BibID:BIBFORM020773
Első szerző:Vondalova, Blanarova O.
Cím:Cisplatin and a potent platinum(IV) complex-mediated enhancement of TRAIL-induced cancer cells killing is associated with modulation of upstream events in the extrinsic apoptotic pathway / Vondalova, B. O., Jelinkova, I., Szoor, A., Skender, B., Soucek, K., Horvath, V., Vaculova, A., Andera, L., Sova, P., Szollosi, J., Hofmanova, J., Vereb, G., Kozubik, A.
Dátum:2011
Megjegyzések:TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) can selectively trigger apoptosis in various cancer cell types. However, many cancer cells are resistant to death receptor-mediated apoptosis. Combination therapy with platinum complexes may affect TRAIL-induced signaling via modulation of various steps in apoptotic pathways. Here, we show that cisplatin or a more potent platinum(IV) complex LA-12 used in 20-fold lower concentration enhanced killing effects of TRAIL in human colon and prostate cancer cell lines via stimulation of caspase activity and overall apoptosis. Both platinum complexes increased DR5 surface expression in colon cancer cells. Small interfering RNA-mediated DR5 silencing rescued cells from sensitizing effects of platinum drugs on TRAIL-induced caspase-8 activation and apoptosis, showing the functional importance of DR5 in the effects observed. In addition, both cisplatin and LA-12 triggered the relocalization of DR4 and DR5 receptors to lipid rafts and accelerated internalization of TRAIL, which may also affect TRAIL signaling. Collectively, modulations of the initial steps of the extrinsic apoptotic pathway at the level of DR5 and plasma membrane are important for sensitization of colon and prostate cancer cells to TRAIL-induced apoptosis mediated by LA-12 and cisplatin
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
ACTIVATION
Amantadine
analogs & derivatives
Apoptosis
article
Biophysics
Blotting,Western
Cell Line
Cell Line,Tumor
Cell Separation
Cells
Cisplatin
drug effects
Flow Cytometry
Fluorescent Antibody Technique
Human
Humans
ligand
lipid raft
LIPID RAFTS
metabolism
Microscopy,Confocal
Necrosis
Neoplasms
Organoplatinum Compounds
pharmacology
physiology
Protein Transport
Receptors,TNF-Related Apoptosis-Inducing Ligand
Research
Research Support
Reverse Transcriptase Polymerase Chain Reaction
RNA Interference
Signal Transduction
Support
therapy
TNF-Related Apoptosis-Inducing Ligand
Megjelenés:Carcinogenesis. - 32 : 1 (2011), p. 42-51. -
További szerzők:Jelínková, Iva Szöőr Árpád (1984-) (orvos) Skender, Belma Soucek, Karel Horváth Viktor Vaculova, Alena Andera, Ladislav Sova, Petr Szöllősi János (1953-) (biofizikus) Hofmanova, Jirin Vereb György (1965-) (biofizikus, orvos) Kozubik, Alois
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
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