@article{MTMT:32575842,
	title = {Ponatinib Exerts an Inhibitory Effect on Collagen-induced Platelet Aggregation and Generation of Coated-Platelets},
	url = {https://m2.mtmt.hu/api/publication/32575842},
	author = {Mezei, Gabriella and Batár, Péter and Kozma, Laura and Illés, Árpád and Kappelmayer, János and Bekéné Debreceni, Ildikó},
	doi = {10.21873/anticanres.15300},
	journal-iso = {ANTICANCER RES},
	journal = {ANTICANCER RESEARCH},
	volume = {41},
	unique-id = {32575842},
	issn = {0250-7005},
	abstract = {Background/Aim: BCR-ABL tyrosine kinase inhibitors (TKIs) are exceptionally effective drugs in the treatment of chronic myeloid leukemia, nevertheless, TKIs have also an effect on platelets. We aimed to investigate the effect of a third-generation TKI, ponatinib on platelet functions. Materials and Methods: Collagen-induced platelet aggregation and coated-platelet formation were examined using in vitro and in ex vivo samples of patients on ponatinib therapy. Results: In platelet rich plasma of healthy volunteers, ponatinib at a supra- therapeutic concentration (1,000 nM) significantly impaired collagen induced platelet aggregation (p <= 0.01) and reduced the formation of coated-platelets at 150 nM ponatinib concentration ( p <= 0.05). In addition, upon glycoprotein VI (GPVI) receptor activation, a significantly lower percentage of PAC1 binding platelets (p <= 0.05) was observed at 1,000 nM final concentration of ponatinib. Platelets, isolated from patients on ponatinib therapy showed impaired collagen elicited aggregation response, already in pre-dose samples compared to healthy donors. Conclusion: The therapeutic concentration of ponatinib impairs platelet activation processes elicited by GPVI receptor agonists.},
	keywords = {Platelet function; Laboratory testing; Ponatinib therapy},
	year = {2021},
	eissn = {1791-7530},
	pages = {4867-4874}
}

@article{MTMT:32285360,
	title = {A krónikus myeloid leukaemia tirozin-kináz-gátló kezelésének mellékhatásai és azok gyakorlati ellátása = Practical management of side effects of tyrosine kinase inhibitor therapy in chronic myeloid leukemia},
	url = {https://m2.mtmt.hu/api/publication/32285360},
	author = {Mezei, Gabriella and Illés, Árpád and Batár, Péter},
	doi = {10.1556/650.2021.32177},
	journal-iso = {ORV HETIL},
	journal = {ORVOSI HETILAP},
	volume = {162},
	unique-id = {32285360},
	issn = {0030-6002},
	year = {2021},
	eissn = {1788-6120},
	pages = {1198-1207}
}

@article{MTMT:31385279,
	title = {Imidazo[1,2-b]pyrazole-7-Carboxamide Derivative Induces Differentiation-Coupled Apoptosis of Immature Myeloid Cells Such as Acute Myeloid Leukemia and Myeloid-Derived Suppressor Cells},
	url = {https://m2.mtmt.hu/api/publication/31385279},
	author = {Kotogány, Edit and Balog, József Ágoston and Nagy, Lajos I. and Alföldi, Róbert and Bertagnolo, Valeria and Brugnoli, Federica and Demjén, András and Kovács, Anita Kármen and Batár, Péter and Mezei, Gabriella and Szabó, Renáta and Kanizsai, Iván and Varga, Csaba and Puskás, László and Szebeni, Gábor},
	doi = {10.3390/ijms21145135},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {21},
	unique-id = {31385279},
	issn = {1661-6596},
	year = {2020},
	eissn = {1422-0067},
	orcid-numbers = {Kovács, Anita Kármen/0000-0001-9805-1647; Varga, Csaba/0000-0002-2678-665X; Szebeni, Gábor/0000-0002-6998-5632}
}

@article{MTMT:32005205,
	title = {Dasatinib inhibits coated-platelet generation in patients with chronic myeloid leukemia},
	url = {https://m2.mtmt.hu/api/publication/32005205},
	author = {Mezei, Gabriella and Bekéné Debreceni, Ildikó and Kerenyi, Adrienne and Reményi, Gyula and Szász, Róbert and Illés, Árpád and Kappelmayer, János and Batár, Péter},
	doi = {10.1080/09537104.2018.1501470},
	journal-iso = {PLATELETS},
	journal = {PLATELETS},
	volume = {30},
	unique-id = {32005205},
	issn = {0953-7104},
	year = {2019},
	eissn = {1369-1635},
	pages = {836-843},
	orcid-numbers = {Szász, Róbert/0000-0003-1343-6017}
}

@article{MTMT:31189289,
	title = {Dasatinib Inhibits Procoagulant and Clot Retracting Activities of Human Platelets},
	url = {https://m2.mtmt.hu/api/publication/31189289},
	author = {Bekéné Debreceni, Ildikó and Mezei, Gabriella and Batár, Péter and Illés, Árpád and Kappelmayer, János},
	doi = {10.3390/ijms20215430},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {20},
	unique-id = {31189289},
	issn = {1661-6596},
	year = {2019},
	eissn = {1422-0067}
}

@article{MTMT:30319060,
	title = {Imidazo[1,2-b]pyrazole-7-carboxamides Induce Apoptosis in Human Leukemia Cells at Nanomolar Concentrations.},
	url = {https://m2.mtmt.hu/api/publication/30319060},
	author = {Szebeni, Gábor and Balog, József Ágoston and Demjén, András and Alföldi, Róbert and Végi, Vanessza L and Fehér, Z. Liliána and Mán, Imola and Kotogány, Edit and Gubán, Barbara and Batár, Péter and Hackler, László and Kanizsai, Iván and Puskás, László},
	doi = {10.3390/molecules23112845},
	journal-iso = {MOLECULES},
	journal = {MOLECULES},
	volume = {23},
	unique-id = {30319060},
	issn = {1420-3049},
	abstract = {Leukemia, the malignancy of the hematopoietic system accounts for 10% of cancer cases with poor overall survival rate in adults; therefore, there is a high unmet medical need for the development of novel therapeutics. Eight imidazo[1,2-b]pyrazole-7-carboxamides have been tested for cytotoxic activity against five leukemia cell lines: Acute promyelocytic leukemia (HL-60), acute monocytic leukemia (THP-1), acute T-lymphoblastic leukemia (MOLT-4), biphenotypic B myelomonocytic leukemia (MV-4-11), and erythroleukemia (K-562) cells in vitro. Imidazo[1,2-b]pyrazole-7-carboxamides hampered the viability of all five leukemia cell lines with different potential. Optimization through structure activity relationship resulted in the following IC50 values for the most effective lead compound DU385: 16.54 nM, 27.24 nM, and 32.25 nM on HL-60, MOLT-4, MV-4-11 cells, respectively. Human primary fibroblasts were much less sensitive in the applied concentration range. Both monolayer or spheroid cultures of murine 4T1 and human MCF7 breast cancer cells were less sensitive to treatment with 1.5⁻10.8 μM IC50 values. Flow cytometry confirmed the absence of necrosis and revealed 60% late apoptotic population for MV-4-11, and 50% early apoptotic population for HL-60. MOLT-4 cells showed only about 30% of total apoptotic population. Toxicogenomic study of DU385 on the most sensitive MV-4-11 cells revealed altered expression of sixteen genes as early (6 h), midterm (12 h), and late response (24 h) genes upon treatment. Changes in ALOX5AP, TXN, and SOD1 expression suggested that DU385 causes oxidative stress, which was confirmed by depletion of cellular glutathione and mitochondrial membrane depolarization induction. Imidazo[1,2-b]pyrazole-7-carboxamides reported herein induced apoptosis in human leukemia cells at nanomolar concentrations.},
	keywords = {APOPTOSIS; IMIDAZOLE; Acute myeloid leukemia; Toxicogenomics; pyrazole},
	year = {2018},
	eissn = {1420-3049},
	orcid-numbers = {Szebeni, Gábor/0000-0002-6998-5632}
}

@article{MTMT:3111420,
	title = {Az akut myeloid leukaemia gyógyszeres kezelése. Jelenlegi lehetőségek, jövőbeli kilátások},
	url = {https://m2.mtmt.hu/api/publication/3111420},
	author = {Telek, Béla and Rejtő, László and Batár, Péter and Miltényi, Zsófia and Reményi, Gyula and Simon, Zsófia Zsuzsanna and Ujj, Zsófia Ágnes and Mezei, Gabriella and Szász, Róbert and Kiss, Attila and Udvardy, Miklós and Illés, Árpád},
	doi = {10.1556/650.2016.30433},
	journal-iso = {ORV HETIL},
	journal = {ORVOSI HETILAP},
	volume = {157},
	unique-id = {3111420},
	issn = {0030-6002},
	keywords = {Aged; Age Factors; Middle Aged; Humans; Survival Analysis; Antineoplastic Combined Chemotherapy Protocols/*therapeutic use; Quality of Life; Drug Administration Schedule; Treatment Outcome; Cytarabine/administration & dosage; Karnofsky Performance Status; Molecular targeted therapy; Daunorubicin/administration & dosage; Leukemia, Myeloid, Acute/*drug therapy; *Induction Chemotherapy/methods},
	year = {2016},
	eissn = {1788-6120},
	pages = {843-848},
	orcid-numbers = {Szász, Róbert/0000-0003-1343-6017}
}

@article{MTMT:2580348,
	title = {Heveny myeloid leukaemiás betegeink kezelésével szerzett tapasztalataink (2007–2013)},
	url = {https://m2.mtmt.hu/api/publication/2580348},
	author = {Selmeczi, Anna and Udvardy, Miklós and Illés, Árpád and Telek, Béla and Kiss, Attila and Batár, Péter and Reményi, Gyula and Szász, Róbert and Ujj, Zsófia Ágnes and Márton, Adrienn and Ujfalusi, Anikó and Hevessy Zsuzsanna, Dóra and Pinczés, László Imre and Bedekovics, Judit and Rejtő, László},
	doi = {10.1556/OH.2014.29884},
	journal-iso = {ORV HETIL},
	journal = {ORVOSI HETILAP},
	volume = {155},
	unique-id = {2580348},
	issn = {0030-6002},
	keywords = {Aged; Age Factors; Adult; Female; Middle Aged; Male; Humans; Hungary/epidemiology; Survival Analysis; Survival Rate; Prognosis; Retrospective Studies; Aged, 80 and over; Drug Administration Schedule; Treatment Outcome; Dose-Response Relationship, Drug; Transplantation, Homologous; Disease-Free Survival; Hematopoietic Stem Cell Transplantation; Idarubicin/administration & dosage; Cytarabine/administration & dosage; Antineoplastic Combined Chemotherapy Protocols/administration &; Palliative Care/*methods; bortezomib; Granulocyte Colony-Stimulating Factor/administration & dosage; Vidarabine/administration & dosage/analogs & derivatives; Neoplasm, Residual/drug therapy; Pyrazines/administration & dosage; Mitoxantrone/administration & dosage; Boronic Acids/administration & dosage; Daunorubicin/administration & dosage; Leukemia, Myeloid, Acute/*drug therapy/mortality/surgery; *Induction Chemotherapy},
	year = {2014},
	eissn = {1788-6120},
	pages = {653-658},
	orcid-numbers = {Szász, Róbert/0000-0003-1343-6017; Pinczés, László Imre/0000-0003-0453-1709}
}

@article{MTMT:32060099,
	title = {Bortezomibkezelés hatásának vizsgálata myeloma multiplexes betegek autológ haemopoeticus őssejt-transzplantációja során},
	url = {https://m2.mtmt.hu/api/publication/32060099},
	author = {Kiss, Attila and Reményi, Gyula and Szász, Róbert and Batár, Péter and Rejtő, László and Telek, Béla and Ujfalusi, Anikó and Oláh, Éva and Radványi, Gáspár and Udvardy, Miklós},
	journal-iso = {HEMATOLÓGIA-TRANSZFUZIOLÓGIA},
	journal = {HEMATOLÓGIA-TRANSZFUZIOLÓGIA},
	volume = {46},
	unique-id = {32060099},
	issn = {1786-5913},
	year = {2013},
	pages = {23-28},
	orcid-numbers = {Szász, Róbert/0000-0003-1343-6017}
}

@article{MTMT:2736254,
	title = {Waldenstrom-macroglobulinaemia},
	url = {https://m2.mtmt.hu/api/publication/2736254},
	author = {Telek, B and Batár, Péter and Varoczy, L and Gergely, Lajos and Rejtő, László and Szász, Róbert and Miltényi, Zsófia and Simon, Z and Udvardy, Miklós and Illés, Árpád},
	doi = {10.1556/OH.2013.29776},
	journal-iso = {ORV HETIL},
	journal = {ORVOSI HETILAP},
	volume = {154},
	unique-id = {2736254},
	issn = {0030-6002},
	abstract = {Waldenstrom macroglobulinemia is a rare lymphoproliferative disease of B-cell origin.These tumorous B-cells produce monoclonal IgM type protein. Diagnosis is based on the detection of lymphoplasmacytic invasion of the bone marrow and serum electrophoresis. Clinical symptoms such as anemia, hyperviscosity and neuropathy are the commom consequences of bone marrow infiltration and serum monoclonal IgM protein. Former use of alkylating agents are replaced by purine analogues, rituximab and bortezomib. Additional clinical data have also accumulated regarding autologous and allogenous stem-cell transplantation. The authors present their own clinical experience and give a detailed review of current therapeutic approaches. Orv. Hetil., 154(50), 1970-1974.},
	year = {2013},
	eissn = {1788-6120},
	pages = {1970-1974},
	orcid-numbers = {Szász, Róbert/0000-0003-1343-6017}
}