@inproceedings{MTMT:33138330,
	title = {Pharmacodynamics modeling based on in vitro 2D cell culture experiments},
	url = {https://m2.mtmt.hu/api/publication/33138330},
	author = {Gergics, Borbála and Gombos, Balázs and Vajda, Flóra and Füredi, András and Gergely, Szakács and Drexler, Dániel András},
	booktitle = {2022 IEEE International Conference on Systems, Man, and Cybernetics (SMC)},
	doi = {10.1109/SMC53654.2022.9945355},
	unique-id = {33138330},
	year = {2022},
	pages = {2409-2414},
	orcid-numbers = {Füredi, András/0000-0002-7883-9901}
}

@article{MTMT:31625912,
	title = {Experimental data-driven tumor modeling for chemotherapy},
	url = {https://m2.mtmt.hu/api/publication/31625912},
	author = {Drexler, Dániel András and Ferenci, Tamás and Füredi, András and Szakács, Gergely and Kovács, Levente},
	doi = {10.1016/j.ifacol.2020.12.619},
	journal-iso = {IFACOL},
	journal = {IFAC PAPERSONLINE},
	volume = {53},
	unique-id = {31625912},
	issn = {2405-8971},
	abstract = {Mathematical models of tumor growth in response to chemotherapy are crucial for therapy optimization and outcome. We create a relatively simple tumor growth model describing the antitumor effect of pegylated liposomal doxorubicin (PLD) validated with real experimental data obtained in a genetically engineered mouse model of breast cancer. We use formal reaction kinetics to describe the pathophysiological phenomena using differential equations, and carry out parametric identification based on experiments using a mixed-effect model with stochastic approximation expectation maximization. The model gives a sufficient fit to describe tumor growth and pharmacokinetic data, and a satisfactory fit for the complex case, i.e., tumor response to chemotherapy. The results showed that identification of certain subsystems is easy using experimental data even if it is not specifically designed for identification. However, the identification of the complex pathophysiological phenomena may require experiments specially designed for identification purposes. Copyright (C) 2020 The Authors.},
	year = {2020},
	eissn = {2405-8963},
	pages = {16245-16250},
	orcid-numbers = {Ferenci, Tamás/0000-0001-6791-3080; Füredi, András/0000-0002-7883-9901; Kovács, Levente/0000-0002-3188-0800}
}

@article{MTMT:31196937,
	title = {Establishment and Characterization of a Brca1−/−, p53−/− Mouse Mammary Tumor Cell Line},
	url = {https://m2.mtmt.hu/api/publication/31196937},
	author = {Hámori, Lilla and Kudlik, Gyöngyi and Szebényi, Kornélia and Kucsma, Nóra and Szeder, Bálint and Póti, Ádám and Uher, Ferenc and Várady, György and Szüts, Dávid and Tóvári, József and Füredi, András and Szakács, Gergely},
	doi = {10.3390/ijms21041185},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {21},
	unique-id = {31196937},
	issn = {1661-6596},
	abstract = {Breast cancer is the most commonly occurring cancer in women and the second most common cancer overall. By the age of 80, the estimated risk for breast cancer for women with germline BRCA1 or BRCA2 mutations is around 80%. Genetically engineered BRCA1-deficient mouse models offer a unique opportunity to study the pathogenesis and therapy of triple negative breast cancer. Here we present a newly established Brca1−/−, p53−/− mouse mammary tumor cell line, designated as CST. CST shows prominent features of BRCA1-mutated triple-negative breast cancers including increased motility, high proliferation rate, genome instability and sensitivity to platinum chemotherapy and PARP inhibitors (olaparib, veliparib, rucaparib and talazoparib). Genomic instability of CST cells was confirmed by whole genome sequencing, which also revealed the presence of COSMIC (Catalogue of Somatic Mutations in Cancer) mutation signatures 3 and 8 associated with homologous recombination (HR) deficiency. In vitro sensitivity of CST cells was tested against 11 chemotherapy agents. Tumors derived from orthotopically injected CST-mCherry cells in FVB-GFP mice showed sensitivity to cisplatin, providing a new model to study the cooperation of BRCA1-KO, mCherry-positive tumor cells and the GFP-expressing stromal compartment in therapy resistance and metastasis formation. In summary, we have established CST cells as a new model recapitulating major characteristics of BRCA1-negative breast cancers.},
	year = {2020},
	eissn = {1422-0067},
	orcid-numbers = {Hámori, Lilla/0000-0002-8962-0040; Szebényi, Kornélia/0000-0003-1558-8372; Várady, György/0000-0003-2012-9680; Tóvári, József/0000-0002-5543-3204; Füredi, András/0000-0002-7883-9901}
}

@article{MTMT:30864958,
	title = {Tumor dynamics modeling based on formal reaction kinetics},
	url = {https://m2.mtmt.hu/api/publication/30864958},
	author = {Drexler, Dániel András and Ferenci, Tamás and Lovrics, Anna and Kovács, Levente},
	doi = {10.12700/APH.16.10.2019.10.3},
	journal-iso = {ACTA POLYTECH HUNG},
	journal = {ACTA POLYTECHNICA HUNGARICA},
	volume = {16},
	unique-id = {30864958},
	issn = {1785-8860},
	year = {2019},
	eissn = {1785-8860},
	pages = {31-44},
	orcid-numbers = {Ferenci, Tamás/0000-0001-6791-3080; Kovács, Levente/0000-0002-3188-0800}
}

@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}
}