TY - JOUR AU - Gyüre, Zsolt Tamás AU - Póti, Ádám AU - Németh, Eszter AU - Szikriszt, Bernadett AU - Lózsa, Rita Bernadett AU - Krawczyk, Michał AU - Richardson, Andrea L. AU - Szüts, Dávid TI - Spontaneous mutagenesis in human cells is controlled by REV1-Polymerase ζ and PRIMPOL JF - CELL REPORTS J2 - CELL REP VL - 42 PY - 2023 IS - 8 PG - 18 SN - 2211-1247 DO - 10.1016/j.celrep.2023.112887 UR - https://m2.mtmt.hu/api/publication/34083629 ID - 34083629 N1 - Institute of Enzymology, Research Centre for Natural Sciences, Budapest, 1117, Hungary Doctoral School of Molecular Medicine, Semmelweis University, Budapest, 1085, Hungary Turbine Simulated Cell Technologies, Budapest, 1027, Hungary Johns Hopkins University School of Medicine, Baltimore, MD 21287, United States National Laboratory for Drug Research and Development, Budapest, 1117, Hungary Cited By :2 Export Date: 17 January 2024 Correspondence Address: Richardson, A.L.; Johns Hopkins University School of MedicineUnited States; email: aricha58@jhu.edu Correspondence Address: Szüts, D.; Institute of Enzymology, Hungary; email: szuts.david@ttk.hu LA - English DB - MTMT ER - TY - JOUR AU - Póti, Ádám AU - Szikriszt, Bernadett AU - Gervai, Judit Zsuzsanna AU - Chen, Dan AU - Szüts, Dávid TI - Characterisation of the spectrum and genetic dependence of collateral mutations induced by translesion DNA synthesis JF - PLOS GENETICS J2 - PLOS GENET VL - 18 PY - 2022 IS - 2 SN - 1553-7390 DO - 10.1371/journal.pgen.1010051 UR - https://m2.mtmt.hu/api/publication/32679015 ID - 32679015 N1 - Export Date: 30 March 2022 Correspondence Address: Szüts, D.; Institute of Enzymology, Hungary; email: szuts.david@ttk.hu Funding details: FIEK_16-1-2016-0005, K_134779, PD_121381, VEKOP-2.3.3-15-2017-00014 Funding details: Magyar Tudományos Akadémia, MTA, LP2011-015 Funding text 1: This work was supported by the Hungarian Academy of Sciences (https://mta.hu) [Momentum Grant LP2011-015 to DS] and the National Research, Technology and Innovation Fund of Hungary (https://nkfih.gov.hu) [K_124881, K_134779, FIEK_16-1-2016-0005 and VEKOP-2.3.3-15-2017-00014 to DS, PD_121381 to BS and DS]. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. LA - English DB - MTMT ER - TY - JOUR AU - Chen, Dan AU - Gervai, Judit Zsuzsanna AU - Póti, Ádám AU - Németh, Eszter AU - Szeltner, Zoltán AU - Szikriszt, Bernadett AU - Gyüre, Zsolt Tamás AU - Zámborszky, Judit AU - Ceccon, Marta AU - d’Adda di Fagagna, Fabrizio AU - Szállási, Zoltán AU - Richardson, Andrea L. AU - Szüts, Dávid TI - BRCA1 deficiency specific base substitution mutagenesis is dependent on translesion synthesis and regulated by 53BP1 JF - NATURE COMMUNICATIONS J2 - NAT COMMUN VL - 13 PY - 2022 IS - 1 PG - 13 SN - 2041-1723 DO - 10.1038/s41467-021-27872-7 UR - https://m2.mtmt.hu/api/publication/32586615 ID - 32586615 N1 - These authors contributed equally: Dan Chen, Judit Z. Gervai. LA - English DB - MTMT ER - TY - JOUR AU - Szikriszt, Bernadett AU - Póti, Ádám AU - Németh, Eszter AU - Kanu, Nnennaya AU - Swanton, Charles AU - Szüts, Dávid TI - A comparative analysis of the mutagenicity of platinum-containing chemotherapeutic agents reveals direct and indirect mutagenic mechanisms JF - MUTAGENESIS J2 - MUTAGENESIS VL - 36 PY - 2021 IS - 1 SP - 75 EP - 86 PG - 12 SN - 0267-8357 DO - 10.1093/mutage/geab005 UR - https://m2.mtmt.hu/api/publication/31888942 ID - 31888942 N1 - Institute of Enzymology, Research Centre for Natural SciencesBudapest, Hungary Cancer Evolution and Genome Instability Laboratory, Francis Crick Institute, London, United Kingdom Export Date: 8 June 2021 LA - English DB - MTMT ER - TY - JOUR AU - Póti, Ádám AU - Gyergyák, Hella AU - Németh, Eszter AU - Rusz, Orsolya AU - Tóth, Szilárd AU - Kovácsházi, Csenger AU - Chen, Dan AU - Szikriszt, Bernadett AU - Spisák, Sándor AU - Takeda, Shunichi AU - Szakács, Gergely AU - Szállási, Zoltán AU - Richardson, Andrea L AU - Szüts, Dávid TI - Correlation of homologous recombination deficiency induced mutational signatures with sensitivity to PARP inhibitors and cytotoxic agents. JF - GENOME BIOLOGY J2 - GENOME BIOL VL - 20 PY - 2019 IS - 1 PG - 13 SN - 1474-7596 DO - 10.1186/s13059-019-1867-0 UR - https://m2.mtmt.hu/api/publication/30923894 ID - 30923894 N1 - Institute of Enzymology, Research Centre for Natural Sciences, Hungarian Academy of Sciences, Magyar tudosok krt 2, Budapest, H-1117, Hungary Department of Oncotherapy, University of Szeged, Szeged, Hungary Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, United States Center for Functional Cancer Epigenetics, Dana-Farber Cancer Institute, Boston, MA 02215, United States Department of Radiation Genetics, Kyoto University Medical School, Kyoto, 606-8501, Japan Institute of Cancer Research, Medical University Vienna, Vienna, Austria Computational Health Informatics Program (CHIP), Boston Children's Hospital, Boston, MA, United States Harvard Medical School, Boston, MA, United States Danish Cancer Society Research Center, Copenhagen, Denmark SE-NAP, Brain Metastasis Research Group, 2nd Department of Pathology, Semmelweis University, Budapest, Hungary Johns Hopkins University, School of Medicine, Baltimore, MD, United States Cited By :2 Export Date: 8 April 2020 CODEN: GNBLF Correspondence Address: Szüts, D.; Institute of Enzymology, Research Centre for Natural Sciences, Hungarian Academy of Sciences, Magyar tudosok krt 2, Hungary; email: szuts.david@ttk.mta.hu Chemicals/CAS: Poly(ADP-ribose) Polymerase Inhibitors Institute of Enzymology, Research Centre for Natural Sciences, Hungarian Academy of Sciences, Magyar tudosok krt 2, Budapest, H-1117, Hungary Department of Oncotherapy, University of Szeged, Szeged, Hungary Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, United States Center for Functional Cancer Epigenetics, Dana-Farber Cancer Institute, Boston, MA 02215, United States Department of Radiation Genetics, Kyoto University Medical School, Kyoto, 606-8501, Japan Institute of Cancer Research, Medical University Vienna, Vienna, Austria Computational Health Informatics Program (CHIP), Boston Children's Hospital, Boston, MA, United States Harvard Medical School, Boston, MA, United States Danish Cancer Society Research Center, Copenhagen, Denmark SE-NAP, Brain Metastasis Research Group, 2nd Department of Pathology, Semmelweis University, Budapest, Hungary Johns Hopkins University, School of Medicine, Baltimore, MD, United States Cited By :3 Export Date: 10 June 2020 CODEN: GNBLF Correspondence Address: Szüts, D.; Institute of Enzymology, Research Centre for Natural Sciences, Hungarian Academy of Sciences, Magyar tudosok krt 2, Hungary; email: szuts.david@ttk.mta.hu Chemicals/CAS: Poly(ADP-ribose) Polymerase Inhibitors AB - 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. LA - English DB - MTMT ER - TY - JOUR AU - Zámborszky, Judit AU - Szikriszt, Bernadett AU - Gervai, Judit Zsuzsanna AU - Pipek, Orsolya Anna AU - Póti, Ádám AU - Krzystanek, M AU - Ribli, Dezső AU - Szalai-Gindl, János Márk AU - Csabai, István AU - Szállási, Zoltán AU - Swanton, C AU - Richardson, AL AU - Szüts, Dávid TI - Loss of BRCA1 or BRCA2 markedly increases the rate of base substitution mutagenesis and has distinct effects on genomic deletions JF - ONCOGENE J2 - ONCOGENE VL - 36 PY - 2017 IS - 6 SP - 746 EP - 755 PG - 10 SN - 0950-9232 DO - 10.1038/onc.2016.243 UR - https://m2.mtmt.hu/api/publication/3118171 ID - 3118171 AB - 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) LA - English DB - MTMT ER - TY - JOUR AU - Szikriszt, Bernadett AU - Póti, Ádám AU - Pipek, Orsolya Anna AU - Krzystanek, M AU - Kanu, N AU - Molnár, János AU - Ribli, Dezső AU - Szeltner, Zoltán AU - Tusnády, Gábor AU - Csabai, István AU - Szállási, Zoltán AU - Swanton, C AU - Szüts, Dávid TI - A comprehensive survey of the mutagenic impact of common cancer cytotoxics JF - GENOME BIOLOGY J2 - GENOME BIOL VL - 17 PY - 2016 IS - 1 PG - 16 SN - 1474-7596 DO - 10.1186/s13059-016-0963-7 UR - https://m2.mtmt.hu/api/publication/3052186 ID - 3052186 LA - English DB - MTMT ER - TY - JOUR AU - Calcutt, MJ AU - Szikriszt, Bernadett AU - Póti, Ádám AU - Molnár, János AU - Gervai, Judit Zsuzsanna AU - Tusnády, Gábor AU - Foecking, MF AU - Szüts, Dávid TI - Genome Sequence Analysis of Mycoplasma sp. HU2014, Isolated from Tissue Culture. JF - GENOME ANNOUNCEMENTS J2 - GENOME ANNOUNC VL - 3 PY - 2015 IS - 5 PG - 2 SN - 2169-8287 DO - 10.1128/genomeA.01086-15 UR - https://m2.mtmt.hu/api/publication/2944718 ID - 2944718 AB - 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. LA - English DB - MTMT ER - TY - JOUR AU - Halász, Júlia AU - Hegedűs, Attila AU - Szikriszt, Bernadett AU - Ercisli, S AU - Orhan, E AU - Ünlü, H M TI - The S-genotyping of wild-growing apricots reveals only self-incompatible accessions in the Erzincan region of Turkey. JF - TURKISH JOURNAL OF BIOLOGY J2 - TURK J BIOL VL - 37 PY - 2013 IS - 6 SP - 733 EP - 740 PG - 8 SN - 1300-0152 DO - 10.3906/biy-1306-27 UR - https://m2.mtmt.hu/api/publication/2372489 ID - 2372489 LA - English DB - MTMT ER - TY - GEN AU - Taller, Dénes ED - Taller, Dénes ED - Hegedűs, Attila ED - Szikriszt, Bernadett TI - UKRÁN CSERESZNYEFAJTÁK FELHASZNÁLÁSÁNAK LEHETŐSÉGEI EGY FUNKCIONÁLIS NEMESÍTÉSI PROGRAMBAN PY - 2013 SP - 1 EP - 44 PG - 44 UR - https://m2.mtmt.hu/api/publication/2366125 ID - 2366125 LA - Hungarian DB - MTMT ER -