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1.

001-es BibID:BIBFORM073532
Első szerző:Barok Márk (biofizikus)
Cím:Cancer-derived exosomes from HER2-positive cancer cells carry trastuzumab-emtansine into cancer cells leading to growth inhibition and caspase activation / Mark Barok, Maija Puhka, Gyorgy Vereb, Janos Szollosi, Jorma Isola, Heikki Joensuu
Dátum:2018
ISSN:1471-2407
Megjegyzések:Background: Trastuzumab emtansine (T-DM1) is an antibody-drug conjugate that carries a cytotoxic drug (DM1) toHER2-positive cancer. The target of T-DM1 (HER2) is present also on cancer-derived exosomes. We hypothesizedthat exosome-bound T-DM1 may contribute to the activity of T-DM1.Methods: Exosomes were isolated from the cell culture medium of HER2-positive SKBR-3 and EFM-192A breast cancercells, HER2-positive SNU-216 gastric cancer cells, and HER2-negative MCF-7 breast cancer cells by serial centrifugationsincluding two ultracentrifugations, and treated with T-DM1. T-DM1 not bound to exosomes was removed using HER2-coated magnetic beads. Exosome samples were analyzed by electron microscopy, flow cytometry and Westernblotting. Binding of T-DM1-containing exosomes to cancer cells and T-DM1 internalization were investigated withconfocal microscopy. Effects of T-DM1-containg exosomes on cancer cells were investigated with the AlamarBluecell proliferation assay and the Caspase-Glo 3/7 caspase activation assay.Results: T-DM1 binds to exosomes derived from HER2-positive cancer cells, but not to exosomes derived fromHER2-negative MCF-7 cells. HER2-positive SKBR-3 cells accumulated T-DM1 after being treated with T-DM1-containgexosomes, and treatment of SKBR-3 and EFM-192A cells with T-DM1-containing exosomes resulted in growth inhibitionand activation of caspases 3 and/or 7.Conclusion: T-DM1 binds to exosomes derived from HER2-positive cancer cells, and T-DM1 may be carried toother cancer cells via exosomes leading to reduced viability of the recipient cells. The results suggest a new mechanismof action for T-DM1, mediated by exosomes derived from HER2-positive cancer.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Breast cancer
Trastuzumab-emtansine
T-DM1
HER2
Exosome
Megjelenés:Bmc Cancer. - 18 : 1 (2018), p. 504-516. -
További szerzők:Puhka, Maija Vereb György (1965-) (biofizikus, orvos) Szöllősi János (1953-) (biofizikus) Isola, Jorma Joensuu, Heikki
Pályázati támogatás:GINOP-2.3.2-15-2016-00020
GINOP
GINOP-2.3.2-15-2016-00050
GINOP
Internet cím:Szerző által megadott URL
DOI
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2.

001-es BibID:BIBFORM015664
Első szerző:Barok Márk (biofizikus)
Cím:Characterization of a novel, trastuzumab resistant human breast cancer cell line / Barok Mark, Balazs Margit, Lazar Viktoria, Rakosy Zsuzsa, Toth Eniko, Treszl Andrea, Vereb Gyorgy, Colbern G. T., Park J. W., Szollosi Janos
Dátum:2010
ISSN:1945-0508
Megjegyzések:HER2-positive breast cancers represent a distinct phenotype and are intrinsically more aggressive than HER2-negative tumors. Although HER2-targeted therapies have been rationally developed, resistance to these treatments represents a process understood poorly. There are few experimental models that allow studying the molecular mechanism of resistance. Our aim was to characterize a trastuzumab resistant breast cancer cell line (B585) that was established from an invasive ductal carcinoma. B585 grows only in immunodeficient mice as a xenograft. CGH and FISH were used to define cytogenetic alterations, gene-expression analysis and immunohistochemistry were applied to detect RNA and protein expression. By array-CGH focused amplifications were identified for C-MYC, EGFR, ErbB2, CCND1 and TOP2-A oncogenes. ErbB2 was co-amplified with TOP2-A. mRNA overexpression was detected for the amplified genes. ErbB2 protein was overexpressed and showed heterogeneous distribution. In summary, molecular cytogenetic analysis and expression profiling of B585 revealed several new alterations. Based on the experiments performed in SCID mice and the genotypic/phenotypic characteristics, this new in vivo breast cancer xenograft is a valuable model to investigate molecular mechanism of trastuzumab resistance
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
analysis
Animals
Antibodies
Antibodies,Monoclonal
Antineoplastic Agents
article
Biophysics
Breast Neoplasms
Carcinoma
Carcinoma,Ductal,Breast
Cell Line
Cell Line,Tumor
Comparative Genomic Hybridization
Disease Models,Animal
Drug Resistance,Neoplasm
drug therapy
EGFR
ErbB2
Female
Gene Expression
Gene Expression Profiling
genetics
Human
Humans
Hungary
Immunohistochemistry
In Situ Hybridization,Fluorescence
metabolism
Mice
Mice,Scid
Oncogenes
Phenotype
Receptor,erbB-2
Research
Research Support
rna
Support
therapeutic use
therapy
Trastuzumab resistance
OTKA::1
MAB::3.1
Megjelenés:Frontiers In Bioscience (elite edition). - 1 : 2 (2010), p. 627-640. -
További szerzők:Balázs Margit (1952-) (sejtbiológus, molekuláris genetikus) Lázár Viktória (1981-) (molekuláris biológus) Rákosy Zsuzsa (1978-) (sejtbiológus, molekuláris biológus, genetikus) Tóth Enikő Treszl Andrea (1974-) (molekuláris biológus) Vereb György (1965-) (biofizikus, orvos) Colbern, Gail T. Park, John W. Szöllősi János (1953-) (biofizikus)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM005174
035-os BibID:(scopus)38349044364 (wos)000253278400023
Első szerző:Barok Márk (biofizikus)
Cím:Trastuzumab decreases the number of circulating and disseminated tumor cells despite trastuzumab resistance of the primary tumor / Márk Barok, Margit Balázs, Péter Nagy, Zsuzsa Rákosy, Andrea Treszl, Enikő Tóth, István Juhász, John W. Park, Jorma Isola, György Vereb, János Szöllősi
Dátum:2008
ISSN:304-3835 (Print)
Megjegyzések:We have recently shown that despite of the fact that the ErbB2-positive JIMT-1 human breast cancer cells intrinsically resistant to trastuzumab in vitro, trastuzumab inhibited the outgrowth of early phase JIMT-1 xenografts in SCID mice via antibody-dependent cellular cytotoxicity (ADCC). Here we show that trastuzumab significantly reduces the number of circulating and disseminated tumor cells (CTCs and DTCs) in this xenograft model system at a time when the primary tumor is already unresponsive to trastuzumab. This observation suggests that ErbB2 positive CTCs and DTCs might be sensitive to trastuzumab-mediated ADCC even if when the primary tumor is already non-responsive. Thus, trastuzumab treatment might also be beneficial in the case of patients with breast cancer that is already trastuzumab resistant.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
analysis
Animals
antagonists and inhibitors
Antibodies
Antibodies, Monoclonal
Antigens
Antigens, CD45
Antineoplastic Agents
article
Biophysics
blood
Bone Marrow
Breast Neoplasms
Cell Line, Tumor
Cells
Chromosomes, Human,X
drug effects
Drug Resistance, Neoplasm
drug therapy
EGFR
Epidermal Growth Factor
ErbB2
Female
genetics
Histocompatibility Antigens
Histocompatibility Antigens Class I
Human
Humans
Hungary
Immunohistochemistry
immunology
In Situ Hybridization,Fluorescence
In Vitro
metabolism
Mice
Mice, Scid
mouse
Neoplasm Circulating Cells
Neoplasm Metastasis
pathology
pharmacology
Receptor, Epidermal Growth Factor
Research
Research Support
Support
therapeutic use
Time Factors
Trastuzumab resistance
Xenograft Model Antitumor Assays
egyetemen (Magyarországon) készült közlemény
Megjelenés:Cancer Letters. - 260 : 1-2 (2008), p. 198-208. -
További szerzők:Balázs Margit (1952-) (sejtbiológus, molekuláris genetikus) Nagy Péter (1971-) (biofizikus) Rákosy Zsuzsa (1978-) (sejtbiológus, molekuláris biológus, genetikus) Treszl Andrea (1974-) (molekuláris biológus) Tóth Enikő Juhász István (1956-) (bőrgyógyász, bőrsebész, kozmetológus, klinikai onkológus) Park, John W. Isola, Jorma Vereb György (1965-) (biofizikus, orvos) Szöllősi János (1953-) (biofizikus)
Internet cím:elektronikus változat
DOI
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4.

001-es BibID:BIBFORM001053
035-os BibID:(scopus)34447298092 (wos)000248154300017
Első szerző:Barok Márk (biofizikus)
Cím:Trastuzumab causes antibody-dependent cellular cytotoxicity-mediated growth inhibition of submacroscopic JIMT-1 breast cancer xenografts despite intrinsic drug resistance / Barok M., Isola J., Pályi-Krekk Zs., Nagy P., Juhász I., Vereb Gy., Kauraniemi P., Kapanen A., Tanner M., Vereb Gy., Szöllősi J.
Dátum:2007
Megjegyzések:Trastuzumab is a recombinant antibody drug that is widely used for the treatment of breast cancer. Despite encouraging clinical results, some cancers are primarily resistant to trastuzumab, and a majority of those initially responding become resistant during prolonged treatment. The mechanisms of trastuzumab resistance have not been fully understood. We examined the role of antibody-dependent cellular cytotoxicity (ADCC) using JIMT-1 cells that are ErbB2 positive but intrinsically resistant to trastuzumab in vitro. Unexpectedly, in experiments mimicking adjuvant therapy of submacroscopic disease in vivo (JIMT-1 cells inoculated s.c. in severe combined immunodeficiency mice), trastuzumab was able to inhibit the outgrowth of macroscopically detectable xenograft tumors for up to 5-7 weeks. The effect is likely to be mediated via ADCC because trastuzumab-F(ab')(2) was ineffective in this model. Moreover, in vitro ADCC reaction of human leukocytes was equally strong against breast cancer cells intrinsically sensitive (SKBR-3) or resistant (JIMT-1) to trastuzumab or even against a subline of JIMT-1 that was established from xenograft tumors growing despite trastuzumab treatment. These results suggest that ADCC may be the predominant mechanism of trastuzumab action on submacroscopic tumor spread. Thus, measuring the ADCC activity of patient's leukocytes against the tumor cells may be a relevant predictor of clinical trastuzumab responsiveness in vivo.
Tárgyszavak:Orvostudományok Természettudományok Elméleti orvostudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
ErbB2 receptor
trastuzumab
breast cancer
antibody therapy
Megjelenés:Molecular Cancer Therapeutics. - 6 : 7 (2007), p. 2065-2072. -
További szerzők:Isola, Jorma Pályiné Krekk Zsuzsanna (1974-) (molekuláris biológus) Nagy Péter (1971-) (biofizikus) Juhász István (1956-) (bőrgyógyász, bőrsebész, kozmetológus, klinikai onkológus) Vereb György (1938-) (biokémikus, sejtbiológus) Kauraniemi, Päivikki Kapanen, Anita I. Tanner, Minna Vereb György (1965-) (biofizikus, orvos) Szöllősi János (1953-) (biofizikus)
Internet cím:elektronikus változat
DOI
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5.

001-es BibID:BIBFORM010349
035-os BibID:(scopus)59049105873 (wos)000262061700007
Első szerző:Fábián Ákos István (aneszteziológus)
Cím:Die Hard : are cancer stem cells the Bruce Willises of tumor biology? / Fabian, A., Barok, M., Vereb, G., Szollosi, J.
Dátum:2009
ISSN:1552-4922 (Print)
Megjegyzések:In recent years, an exponentially growing number of studies have focused on identifying cancer stem cells (CSC) in human malignancies. The rare CSCs could be crucial in controlling and curing cancer: through asymmetric division CSCs supposedly drive tumor growth and evade therapy with the help of traits shared with normal stem cells such as quiescence, self-renewal ability, and multidrug resistance pump activity. Here, we give a brief overview of techniques used to confirm the stem cell-like behavior of putative CSCs and discuss markers and methods for identifying, isolating, and culturing them. We touch on the limitations of each marker and why the combined use of CSC markers, in vitro and in vivo assays may still fail to identify all relevant CSC populations. Finally, the various experimental findings supporting and contradicting the CSC hypothesis are summarized. The large number of tumor types thus far with a subpopulation of uniquely tumorigenic and therapy resistant cells suggests that despite the unanswered questions and inconsistencies, the CSC hypothesis has a legitimate role to play in tumor biology. At the same time, experimental evidence supporting the established alternative theory of clonal evolution can be found as wen. Therefore, a model that describes cancer initiation and progression should combine elements of clonal evolution and CSC theory.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Cells
Human
In Vitro
methods
therapy
Megjelenés:Cytometry. Part A. - 75A : 1 (2009), p. 67-74. -
További szerzők:Barok Márk (1976-) (biofizikus) Vereb György (1965-) (biofizikus, orvos) Szöllősi János (1953-) (biofizikus)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
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6.

001-es BibID:BIBFORM005181
035-os BibID:(scopus)40149107884 (wos)000255092200005
Első szerző:Friedländer Elza (biofizikus)
Cím:ErbB-directed immunotherapy : antibodies in current practice and promising new agents / Elza Friedländer, Márk Barok, János Szöllősi, György Vereb
Dátum:2008
Megjegyzések:The ErbB family is well known for its significance in oncogenesis. As bad prognostic markers, overexpressed or mutated ErbB1 and ErbB2 have an important role in the molecular diagnosis of various cancers, but as membrane proteins, expressed often selectively in tumor tissues, they can be targeted with kinase inhibitors or therapeutic antibodies. In addition to trastuzumab, the first humanized antibody that was approved for the therapy of solid tumors by the FDA, now many humanized antibodies are in late clinical trials, or already approved. Conjugation of antibodies with radioactive isotopes, cytotoxic agents or liposomes loaded with chemotherapeutic drugs led to improved therapeutic efficiency over their parent "unarmed" antibodies. Novel, engineered antibody derivates with better pharmacodynamic properties are also available and allow the targeting of ErbB1 or ErbB2 positive cancers in a wider patient population. In this review, we discuss the biological and clinical background of ErbB targeting, and describe the most successful antibodies against ErbB1 (cetuximab, panitumumab, matuzumab, nimotuzumab, ICR62, mAb 528, ch806 and MDX-447) and ErbB2 (trastuzumab, pertuzumab, MDX-H210, 2B1, C6.5xscFv(NM3E2), ertumaxomab and FRP-5 derivates) that are in clinical trials or already approved, along with the various relevant conjugation and engineering strategies. Recent data pertinent to the prevalent problem of clinical resistance to treatment with trastuzumab are also discussed.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
agonists
analysis
Animal
Antibodies
Antibody conjugation
Antibody targeted delivery
Apoptosis
Biophysics
Brain
Carcinoma
Cell Line
Cell Proliferation
Cell Survival
Cells
Clinical trial
Cysteine
diagnosis
Dimerization
Down-Regulation
Drug Resistance
EGFR
Endocytosis
Engineered antibody
Epidermal Growth Factor
Epitopes
ErbB1
ErbB2
Fibroblasts
Glioblastoma
Glioma
Human
Humanized antibody
Hungary
In Vitro
Insulin
Membrane Proteins
Mice
Microscopy
Microspheres
Mutation
Necrosis
Paclitaxel
Phenotype
Phosphorylation
Prevalence
Progesterone
Proteins
radiotherapy
Research
Signal Transduction
therapy
toxicity
Trastuzumab resistance
Tumor Necrosis Factor
Tumor therapy/cancer therapy
Tyrosine
Up-Regulation
Megjelenés:Immunology Letters. - 116 : 2 (2008), p. 126-140. -
További szerzők:Barok Márk (1976-) (biofizikus) Szöllősi János (1953-) (biofizikus) Vereb György (1965-) (biofizikus, orvos)
Internet cím:elektronikus változat
DOI
elektronikus változat
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