@article{MTMT:35091180,
	title = {Comprehensive investigation of the mutagenic potential of six pesticides classified by IARC as probably carcinogenic to humans},
	url = {https://m2.mtmt.hu/api/publication/35091180},
	author = {Martinek, Regina Gabriella and Lózsa, Rita Bernadett and Póti, Ádám and Németh, Eszter and Várady, György and Szabó, Pál Tamás and Szüts, Dávid},
	doi = {10.1016/j.chemosphere.2024.142700},
	journal-iso = {CHEMOSPHERE},
	journal = {CHEMOSPHERE},
	volume = {362},
	unique-id = {35091180},
	issn = {0045-6535},
	year = {2024},
	eissn = {1879-1298},
	orcid-numbers = {Martinek, Regina Gabriella/0009-0000-5502-3531; Lózsa, Rita Bernadett/0000-0001-5957-906X; Várady, György/0000-0003-2012-9680; Szabó, Pál Tamás/0000-0003-2260-4641}
}

@article{MTMT:34879245,
	title = {The mutagenic consequences of defective DNA repair},
	url = {https://m2.mtmt.hu/api/publication/34879245},
	author = {Németh, Eszter and Szüts, Dávid},
	doi = {10.1016/j.dnarep.2024.103694},
	journal-iso = {DNA REPAIR},
	journal = {DNA REPAIR},
	volume = {139},
	unique-id = {34879245},
	issn = {1568-7864},
	year = {2024},
	eissn = {1568-7856},
	pages = {103694}
}

@article{MTMT:34192915,
	title = {DNA mismatch repair protects the genome from oxygen-induced replicative mutagenesis},
	url = {https://m2.mtmt.hu/api/publication/34192915},
	author = {Lózsa, Rita Bernadett and Németh, Eszter and Gervai, Judit Zsuzsanna and Márkus, Bence Gábor and Kollarics, Sándor and Gyüre, Zsolt Tamás and Tóth, Judit and Simon, Ferenc and Szüts, Dávid},
	doi = {10.1093/nar/gkad775},
	journal-iso = {NUCLEIC ACIDS RES},
	journal = {NUCLEIC ACIDS RESEARCH},
	volume = {51},
	unique-id = {34192915},
	issn = {0305-1048},
	abstract = {DNA mismatch repair (MMR) corrects mismatched DNA bases arising from multiple sources including polymerase errors and base damage. By detecting spontaneous mutagenesis using whole genome sequencing of cultured MMR deficient human cell lines, we show that a primary role of MMR is the repair of oxygen-induced mismatches. We found an approximately twofold higher mutation rate in MSH6 deficient DLD-1 cells or MHL1 deficient HCT116 cells exposed to atmospheric conditions as opposed to mild hypoxia, which correlated with oxidant levels measured using electron paramagnetic resonance spectroscopy. The oxygen-induced mutations were dominated by T to C base substitutions and single T deletions found primarily on the lagging strand. A broad sequence context preference, dependence on replication timing and a lack of transcriptional strand bias further suggested that oxygen-induced mutations arise from polymerase errors rather than oxidative base damage. We defined separate low and high oxygen-specific MMR deficiency mutation signatures common to the two cell lines and showed that the effect of oxygen is observable in MMR deficient cancer genomes, where it best correlates with the contribution of mutation signature SBS21. Our results imply that MMR corrects oxygen-induced genomic mismatches introduced by a replicative process in proliferating cells. Graphical Abstract},
	keywords = {CELLS; NUCLEOTIDE; HYPOXIA; 8-OXOGUANINE; BYPASS; Mutational signatures; high-fidelity; Thymine glycol},
	year = {2023},
	eissn = {1362-4962},
	pages = {11040-11055},
	orcid-numbers = {Lózsa, Rita Bernadett/0000-0001-5957-906X; Márkus, Bence Gábor/0000-0003-1472-0482; Tóth, Judit/0000-0002-0965-046X}
}

@article{MTMT:34083629,
	title = {Spontaneous mutagenesis in human cells is controlled by REV1-Polymerase ζ and PRIMPOL},
	url = {https://m2.mtmt.hu/api/publication/34083629},
	author = {Gyüre, Zsolt Tamás and Póti, Ádám and Németh, Eszter and Szikriszt, Bernadett and Lózsa, Rita Bernadett and Krawczyk, Michał and Richardson, Andrea L. and Szüts, Dávid},
	doi = {10.1016/j.celrep.2023.112887},
	journal-iso = {CELL REP},
	journal = {CELL REPORTS},
	volume = {42},
	unique-id = {34083629},
	issn = {2211-1247},
	year = {2023},
	eissn = {2211-1247},
	orcid-numbers = {Lózsa, Rita Bernadett/0000-0001-5957-906X}
}

@article{MTMT:32730598,
	title = {Prospectively-defined patterns of APOBEC3A mutagenesis are prevalent in human cancers},
	url = {https://m2.mtmt.hu/api/publication/32730598},
	author = {Rachel, A. DeWeerd and Németh, Eszter and Póti, Ádám and Nataliya, Petryk and Chunlong, Chen and Olivier, Hyrien and Szüts, Dávid and Abby, Margaret Green},
	doi = {10.1016/j.celrep.2022.110555},
	journal-iso = {CELL REP},
	journal = {CELL REPORTS},
	volume = {38},
	unique-id = {32730598},
	issn = {2211-1247},
	year = {2022},
	eissn = {2211-1247}
}

@article{MTMT:32586615,
	title = {BRCA1 deficiency specific base substitution mutagenesis is dependent on translesion synthesis and regulated by 53BP1},
	url = {https://m2.mtmt.hu/api/publication/32586615},
	author = {Chen, Dan and Gervai, Judit Zsuzsanna and Póti, Ádám and Németh, Eszter and Szeltner, Zoltán and Szikriszt, Bernadett and Gyüre, Zsolt Tamás and Zámborszky, Judit and Ceccon, Marta and d’Adda di Fagagna, Fabrizio and Szállási, Zoltán and Richardson, Andrea L. and Szüts, Dávid},
	doi = {10.1038/s41467-021-27872-7},
	journal-iso = {NAT COMMUN},
	journal = {NATURE COMMUNICATIONS},
	volume = {13},
	unique-id = {32586615},
	issn = {2041-1723},
	year = {2022},
	eissn = {2041-1723},
	orcid-numbers = {d’Adda di Fagagna, Fabrizio/0000-0002-9603-5966; Szállási, Zoltán/0000-0001-5395-7509; Richardson, Andrea L./0000-0001-5221-1094}
}

@article{MTMT:31999867,
	title = {A study on the secondary structure of the metalloregulatory protein CueR: effect of pH, metal ions and DNA},
	url = {https://m2.mtmt.hu/api/publication/31999867},
	author = {Balogh, Ria Katalin and Németh, Eszter and Jones, Nykola C. and Hoffmann, Søren Vrønning and Jancsó, Attila and Gyurcsik, Béla},
	doi = {10.1007/s00249-021-01539-z},
	journal-iso = {EUR BIOPHYS J},
	journal = {EUROPEAN BIOPHYSICS JOURNAL},
	volume = {50},
	unique-id = {31999867},
	issn = {0175-7571},
	year = {2021},
	eissn = {1432-1017},
	pages = {491-500},
	orcid-numbers = {Németh, Eszter/0000-0001-9038-1772; Jones, Nykola C./0000-0002-4081-6405; Hoffmann, Søren Vrønning/0000-0002-8018-5433; Jancsó, Attila/0000-0003-2362-0758; Gyurcsik, Béla/0000-0003-1894-7414}
}

@article{MTMT:31888942,
	title = {A comparative analysis of the mutagenicity of platinum-containing chemotherapeutic agents reveals direct and indirect mutagenic mechanisms},
	url = {https://m2.mtmt.hu/api/publication/31888942},
	author = {Szikriszt, Bernadett and Póti, Ádám and Németh, Eszter and Kanu, Nnennaya and Swanton, Charles and Szüts, Dávid},
	doi = {10.1093/mutage/geab005},
	journal-iso = {MUTAGENESIS},
	journal = {MUTAGENESIS},
	volume = {36},
	unique-id = {31888942},
	issn = {0267-8357},
	year = {2021},
	eissn = {1464-3804},
	pages = {75-86},
	orcid-numbers = {Szüts, Dávid/0000-0001-7985-0136}
}

@article{MTMT:31240665,
	title = {Two main mutational processes operate in the absence of DNA mismatch repair},
	url = {https://m2.mtmt.hu/api/publication/31240665},
	author = {Németh, Eszter and Lovrics, Anna and Gervai, Judit Zsuzsanna and Seki, M. and Rospo, G. and Bardelli, A. and Szüts, Dávid},
	doi = {10.1016/j.dnarep.2020.102827},
	journal-iso = {DNA REPAIR},
	journal = {DNA REPAIR},
	volume = {89},
	unique-id = {31240665},
	issn = {1568-7864},
	abstract = {The analysis of tumour genome sequences has demonstrated high rates of base substitution mutagenesis upon the inactivation of DNA mismatch repair (MMR), and the resulting somatic mutations in MMR deficient tumours appear to significantly enhance the response to immune therapy. A handful of different algorithmically derived base substitution mutation signatures have been attributed to MMR deficiency in tumour somatic mutation datasets. In contrast, mutation data obtained from whole genome sequences of isogenic wild type and MMR deficient cell lines in this study, as well as from published sources, show a more uniform experimental mutation spectrum of MMR deficiency. In order to resolve this discrepancy, we reanalysed mutation data from MMR deficient tumour whole exome and whole genome sequences. We derived two base substitution signatures using non-negative matrix factorisation, which together adequately describe mutagenesis in all tumour and cell line samples. The two new signatures broadly resemble COSMIC signatures 6 and 20, but perform better than existing COSMIC signatures at identifying MMR deficient tumours in mutation signature deconstruction. We show that the contribution of the two identified signatures, one of which is dominated by C to T mutations at CpG sites, is biased by the different sequence composition of the exome and the whole genome. We further show that the identity of the inactivated MMR gene, the tissue type, the mutational burden or the patient's age does not influence the mutation spectrum, but that a tendency for a greater contribution by the CpG mutational process is observed in tumours as compared to cultured cells. Our analysis suggest that two separable mutational processes operate in the genomes of MMR deficient cells. © 2020 The Author(s)},
	keywords = {MUTAGENESIS; DNA MISMATCH REPAIR; Whole genome sequencing; MSH2; Mutational signatures},
	year = {2020},
	eissn = {1568-7856}
}

@article{MTMT:31240593,
	title = {Precision-engineered reporter cell lines reveal ABCG2 regulation in live lung cancer cells},
	url = {https://m2.mtmt.hu/api/publication/31240593},
	author = {Kovacsics, Daniella and Brózik, Anna and Tihanyi, Borbála and Matula, Zsolt and Borsy, Adrienn and Mészáros, Nikolett and Szabó, Edit Zsuzsanna and Németh, Eszter and Fóthi, Ábel and Zámbó, Boglárka and Szüts, Dávid and Várady, György and Orbán, Tamás I. and Apáti, Ágota and Sarkadi, Balázs},
	doi = {10.1016/j.bcp.2020.113865},
	journal-iso = {BIOCHEMIC PHARMACOL},
	journal = {BIOCHEMICAL PHARMACOLOGY},
	volume = {175},
	unique-id = {31240593},
	issn = {0006-2952},
	abstract = {Expression of the ABCG2 multidrug transporter is a marker of cancer stem cells and a predictor of recurrent malignant disease. Understanding how human ABCG2 expression is modulated by pharmacotherapy is crucial in guiding therapeutic recommendations and may aid rational drug development. Genome edited reporter cells are useful in investigating gene regulation and visualizing protein activity in live cells but require precise targeting to preserve native regulatory regions. Here, we describe a fluorescent reporter assay that allows the noninvasive assessment of ABCG2 regulation in human lung adenocarcinoma cells. Using CRISPR-Cas9 gene editing coupled with homology-directed repair, we targeted an eGFP coding sequence to the translational start site of ABCG2, generating ABCG2 knock-out and in situ tagged ABCG2 reporter cells. Using the engineered cell lines, we show that ABCG2 is upregulated by a number of anti-cancer medications, HDAC inhibitors, hypoxia-mimicking agents and glucocorticoids, supporting a model in which ABCG2 is under the control of a general stress response. To our knowledge, this is the first description of a fluorescent reporter assay system designed to follow the endogenous regulation of a human ABC transporter in live cells. The information gained may guide therapy recommendations and aid rational drug design.},
	keywords = {GLUCOCORTICOIDS; lung cancer; CRISPR-Cas9; Reporter cell lines; ABCG2 regulation},
	year = {2020},
	eissn = {1873-2968},
	orcid-numbers = {Várady, György/0000-0003-2012-9680; Orbán, Tamás I./0000-0002-3424-3428; Sarkadi, Balázs/0000-0003-0592-4539}
}