@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:32679015, title = {Characterisation of the spectrum and genetic dependence of collateral mutations induced by translesion DNA synthesis}, url = {https://m2.mtmt.hu/api/publication/32679015}, author = {Póti, Ádám and Szikriszt, Bernadett and Gervai, Judit Zsuzsanna and Chen, Dan and Szüts, Dávid}, doi = {10.1371/journal.pgen.1010051}, journal-iso = {PLOS GENET}, journal = {PLOS GENETICS}, volume = {18}, unique-id = {32679015}, issn = {1553-7390}, year = {2022}, eissn = {1553-7404} } @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: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:30923894, title = {Correlation of homologous recombination deficiency induced mutational signatures with sensitivity to PARP inhibitors and cytotoxic agents.}, url = {https://m2.mtmt.hu/api/publication/30923894}, author = {Póti, Ádám and Gyergyák, Hella and Németh, Eszter and Rusz, Orsolya and Tóth, Szilárd and Kovácsházi, Csenger and Chen, Dan and Szikriszt, Bernadett and Spisák, Sándor and Takeda, Shunichi and Szakács, Gergely and Szállási, Zoltán and Richardson, Andrea L and Szüts, Dávid}, doi = {10.1186/s13059-019-1867-0}, journal-iso = {GENOME BIOL}, journal = {GENOME BIOLOGY}, volume = {20}, unique-id = {30923894}, issn = {1474-7596}, abstract = {Homologous recombination (HR) repair deficiency arising from defects in BRCA1 or BRCA2 is associated with characteristic patterns of somatic mutations. In this genetic study, we ask whether inactivating mutations in further genes of the HR pathway or the DNA damage checkpoint also give rise to somatic mutation patterns that can be used for treatment prediction.Using whole genome sequencing of an isogenic knockout cell line panel, we find a universal HR deficiency-specific base substitution signature that is similar to COSMIC signature 3. In contrast, we detect different deletion phenotypes corresponding to specific HR mutants. The inactivation of BRCA2 or PALB2 leads to larger deletions, typically with microhomology, when compared to the disruption of BRCA1, RAD51 paralogs, or RAD54. Comparison with the deletion spectrum of Cas9 cut sites suggests that most spontaneously arising genomic deletions are not the consequence of double-strand breaks. Surprisingly, the inactivation of checkpoint kinases ATM and CHK2 has no mutagenic consequences. Analysis of tumor exomes with biallelic inactivating mutations in the investigated genes confirms the validity of the cell line models. We present a comprehensive analysis of sensitivity of the investigated mutants to 13 therapeutic agents for the purpose of correlating genomic mutagenic phenotypes with drug sensitivity.Our results suggest that no single genomic mutational class shows perfect correlation with sensitivity to common treatments, but the contribution of COSMIC signature 3 to base substitutions, or a combined measure of different features, may be reasonably good at predicting platinum and PARP inhibitor sensitivity.}, keywords = {PALB2; BRCA2; BRCA1; ATM; RAD51C; Rad52; Mutation signature; CHEK2; PARP inhibitor; Microhomology deletion}, year = {2019}, eissn = {1474-760X}, orcid-numbers = {Rusz, Orsolya/0000-0001-5726-4072; Kovácsházi, Csenger/0000-0003-0283-9486; Szállási, Zoltán/0000-0001-5395-7509} } @article{MTMT:3118171, title = {Loss of BRCA1 or BRCA2 markedly increases the rate of base substitution mutagenesis and has distinct effects on genomic deletions}, url = {https://m2.mtmt.hu/api/publication/3118171}, author = {Zámborszky, Judit and Szikriszt, Bernadett and Gervai, Judit Zsuzsanna and Pipek, Orsolya Anna and Póti, Ádám and Krzystanek, M and Ribli, Dezső and Szalai-Gindl, János Márk and Csabai, István and Szállási, Zoltán and Swanton, C and Richardson, AL and Szüts, Dávid}, doi = {10.1038/onc.2016.243}, journal-iso = {ONCOGENE}, journal = {ONCOGENE}, volume = {36}, unique-id = {3118171}, issn = {0950-9232}, abstract = {Loss-of-function mutations in the BRCA1 and BRCA2 genes increase the risk of cancer. Owing to their function in homologous recombination repair, much research has focused on the unstable genomic phenotype of BRCA1/2 mutant cells manifest mainly as large-scale rearrangements. We used whole-genome sequencing of multiple isogenic chicken DT40 cell clones to precisely determine the consequences of BRCA1/2 loss on all types of genomic mutagenesis. Spontaneous base substitution mutation rates increased sevenfold upon the disruption of either BRCA1 or BRCA2, and the arising mutation spectra showed strong and specific correlation with a mutation signature associated with BRCA1/2 mutant tumours. To model endogenous alkylating damage, we determined the mutation spectrum caused by methyl methanesulfonate (MMS), and showed that MMS also induces more base substitution mutations in BRCA1/2-deficient cells. Spontaneously arising and MMS-induced insertion/deletion mutations and large rearrangements were also more common in BRCA1/2 mutant cells compared with the wild-type control. A difference in the short deletion phenotypes of BRCA1 and BRCA2 suggested distinct roles for the two proteins in the processing of DNA lesions, as BRCA2 mutants contained more short deletions, with a wider size distribution, which frequently showed microhomology near the breakpoints resembling repair by non-homologous end joining. An increased and prolonged gamma-H2AX signal in MMS-treated BRCA1/2 cells suggested an aberrant processing of stalled replication forks as the cause of increased mutagenesis. The high rate of base substitution mutagenesis demonstrated by our experiments is likely to significantly contribute to the oncogenic effect of the inactivation of BRCA1 or BRCA2.Oncogene advance online publication, 25 July 2016; doi:10.1038/onc.2016.243. © 2016 The Author(s)}, year = {2017}, eissn = {1476-5594}, pages = {746-755}, orcid-numbers = {Pipek, Orsolya Anna/0000-0001-8109-0340; Szalai-Gindl, János Márk/0000-0002-0169-0547; Csabai, István/0000-0001-9232-9898; Szállási, Zoltán/0000-0001-5395-7509} } @article{MTMT:3052186, title = {A comprehensive survey of the mutagenic impact of common cancer cytotoxics}, url = {https://m2.mtmt.hu/api/publication/3052186}, author = {Szikriszt, Bernadett and Póti, Ádám and Pipek, Orsolya Anna and Krzystanek, M and Kanu, N and Molnár, János and Ribli, Dezső and Szeltner, Zoltán and Tusnády, Gábor and Csabai, István and Szállási, Zoltán and Swanton, C and Szüts, Dávid}, doi = {10.1186/s13059-016-0963-7}, journal-iso = {GENOME BIOL}, journal = {GENOME BIOLOGY}, volume = {17}, unique-id = {3052186}, issn = {1474-7596}, year = {2016}, eissn = {1474-760X}, orcid-numbers = {Pipek, Orsolya Anna/0000-0001-8109-0340; Csabai, István/0000-0001-9232-9898; Szállási, Zoltán/0000-0001-5395-7509} } @article{MTMT:2944718, title = {Genome Sequence Analysis of Mycoplasma sp. HU2014, Isolated from Tissue Culture.}, url = {https://m2.mtmt.hu/api/publication/2944718}, author = {Calcutt, MJ and Szikriszt, Bernadett and Póti, Ádám and Molnár, János and Gervai, Judit Zsuzsanna and Tusnády, Gábor and Foecking, MF and Szüts, Dávid}, doi = {10.1128/genomeA.01086-15}, journal-iso = {GENOME ANNOUNC}, journal = {GENOME ANNOUNCEMENTS}, volume = {3}, unique-id = {2944718}, abstract = {The draft genome sequence of a novel Mycoplasma strain, designated Mycoplasma sp. HU2014, has been determined. The genome comprises 1,084,927 nucleotides and was obtained from a mycoplasma-infected culture of chicken DT40 cells. Phylogenetic analysis places this taxon in a group comprising the closely related species Mycoplasma yeatsii and Mycoplasma cottewii.}, year = {2015}, eissn = {2169-8287} } @article{MTMT:2372489, title = {The S-genotyping of wild-growing apricots reveals only self-incompatible accessions in the Erzincan region of Turkey.}, url = {https://m2.mtmt.hu/api/publication/2372489}, author = {Halász, Júlia and Hegedűs, Attila and Szikriszt, Bernadett and Ercisli, S and Orhan, E and Ünlü, H M}, doi = {10.3906/biy-1306-27}, journal-iso = {TURK J BIOL}, journal = {TURKISH JOURNAL OF BIOLOGY}, volume = {37}, unique-id = {2372489}, issn = {1300-0152}, year = {2013}, eissn = {1303-6092}, pages = {733-740} } @misc{MTMT:2366125, title = {UKRÁN CSERESZNYEFAJTÁK FELHASZNÁLÁSÁNAK LEHETŐSÉGEI EGY FUNKCIONÁLIS NEMESÍTÉSI PROGRAMBAN}, url = {https://m2.mtmt.hu/api/publication/2366125}, author = {Taller, Dénes}, editor = {Taller, Dénes and Hegedűs, Attila and Szikriszt, Bernadett}, unique-id = {2366125}, year = {2013}, pages = {1-44} }