@article{MTMT:3407826,
	title = {Green synthesis and cytotoxic activity of dibenzyl α-hydroxyphosphonates and α-hydroxyphosphonic acids},
	url = {https://m2.mtmt.hu/api/publication/3407826},
	author = {Rádai, Zita and Szeles, P and Kiss, Nóra Zsuzsa and Hegedűs, László and Windt, Tímea and Nagy, Veronika and Keglevich, György},
	doi = {10.1002/hc.21436},
	journal-iso = {HETEROATOM CHEM},
	journal = {HETEROATOM CHEMISTRY},
	volume = {29},
	unique-id = {3407826},
	issn = {1042-7163},
	abstract = {A series of dibenzyl α‐hydroxyphosphonates and the corresponding α‐hydroxyphosphonic acids, mostly new compounds, have been synthesized. The dibenzyl α‐hydroxyphosphonates have been obtained in the Pudovik reaction of substituted benzaldehydes and dibenzyl phosphite in the presence of triethylamine as the catalyst. The amount of the solvent was minimized during the reaction, and the workup involved crystallization from the reaction mixture. A new protocol was developed to transform the dibenzyl 1‐hydroxyphosphonates to the corresponding phosphonic acids by catalytic hydrogenation. The derivatives prepared were screened as potential cytotoxic agents against Mes‐Sa human uterine sarcoma cell line.},
	year = {2018},
	eissn = {1098-1071},
	orcid-numbers = {Hegedűs, László/0000-0002-7980-0443; Windt, Tímea/0000-0001-9913-3337; Nagy, Veronika/0000-0001-8310-4814}
}

@article{MTMT:3251042,
	title = {Pegylated liposomal formulation of doxorubicin overcomes drug resistance in a genetically engineered mouse model of breast cancer.},
	url = {https://m2.mtmt.hu/api/publication/3251042},
	author = {Füredi, András and Szebényi, Kornélia and Tóth, Szilárd and Cserepes, Tamás Mihály and Hámori, Lilla and Nagy, Veronika and Karai, Edina and Vajdovich, Péter and Imre, Timea and Szabó, Pál Tamás and Szüts, Dávid and Tóvári, József and Szakács, Gergely},
	doi = {10.1016/j.jconrel.2017.07.010},
	journal-iso = {J CONTROL RELEASE},
	journal = {JOURNAL OF CONTROLLED RELEASE},
	volume = {261},
	unique-id = {3251042},
	issn = {0168-3659},
	abstract = {Success of cancer treatment is often hampered by the emergence of multidrug resistance (MDR) mediated by P-glycoprotein (ABCB1/Pgp). Doxorubicin (DOX) is recognized by Pgp and therefore it can induce therapy resistance in breast cancer patients. In this study our aim was to evaluate the susceptibility of the pegylated liposomal formulation of doxorubicin (PLD/Doxil(R)/Caelyx(R)) to MDR. We show that cells selected to be resistant to DOX are cross-resistant to PLD and PLD is also ineffective in an allograft model of doxorubicin-resistant mouse B-cell leukemia. In contrast, PLD was far more efficient than DOX as reflected by a significant increase of both relapse-free and overall survival of Brca1-/-;p53-/- mammary tumor bearing mice. Increased survival could be explained by the delayed onset of drug resistance. Consistent with the higher Pgp levels needed to confer resistance, PLD administration was able to overcome doxorubicin insensitivity of the mouse mammary tumors. Our results indicate that the favorable pharmacokinetics achieved with PLD can effectively overcome Pgp-mediated resistance, suggesting that PLD therapy could be a promising strategy for the treatment of therapy-resistant breast cancer patients.},
	year = {2017},
	eissn = {1873-4995},
	pages = {287-296},
	orcid-numbers = {Füredi, András/0000-0002-7883-9901; Szebényi, Kornélia/0000-0003-1558-8372; Cserepes, Tamás Mihály/0000-0003-4816-2618; Hámori, Lilla/0000-0002-8962-0040; Nagy, Veronika/0000-0001-8310-4814; Szabó, Pál Tamás/0000-0003-2260-4641; Tóvári, József/0000-0002-5543-3204}
}

@article{MTMT:3050098,
	title = {Állatmodellek szerepe a multidrogrezisztens tumorokat célzó kemoterápia fejlesztésében},
	url = {https://m2.mtmt.hu/api/publication/3050098},
	author = {Füredi, András and Tóth, Szilárd and Hámori, Lilla and Nagy, Veronika and Tóvári, József and Szakacs, G},
	journal-iso = {MAGYAR ONKOLÓGIA},
	journal = {MAGYAR ONKOLÓGIA},
	volume = {59},
	unique-id = {3050098},
	issn = {0025-0244},
	abstract = {Anticancer compounds are typically identified in in vitro screens. Unfortunately, the in vitro drug sensitivity of cell lines does not reflect treatment efficiency in animal models, and neither show acceptable correlation to clinical results. While cell lines and laboratory animals can be readily "cured", the treatment of malignancies remains hampered by the multidrug resistance (MDR) of tumors. Genetically engineered mouse models (GEMMs) giving rise to spontaneous tumors offer a new possibility to characterize the evolution of drug resistance mechanisms and to target multidrug resistant cancer.},
	year = {2015},
	eissn = {2060-0399},
	pages = {338-345},
	orcid-numbers = {Füredi, András/0000-0002-7883-9901; Hámori, Lilla/0000-0002-8962-0040; Nagy, Veronika/0000-0001-8310-4814; Tóvári, József/0000-0002-5543-3204}
}