@article{MTMT:32474433,
	title = {Comparative Assessment of Diagnostic Homologous Recombination Deficiency-Associated Mutational Signatures in Ovarian Cancer},
	url = {https://m2.mtmt.hu/api/publication/32474433},
	author = {Sztupinszki, Zsófia and Diossy, Miklos and Borcsok, Judit and Prosz, Aurel and Cornelius, Nanna and Kjeldsen, Maj K. and Mirza, Mansoor R. and Szállási, Zoltán},
	doi = {10.1158/1078-0432.CCR-21-0981},
	journal-iso = {CLIN CANCER RES},
	journal = {CLINICAL CANCER RESEARCH},
	volume = {27},
	unique-id = {32474433},
	issn = {1078-0432},
	abstract = {Purpose: Homologous recombination (HR) deficiency (HRD) is one of the key determinants of PARP inhibitor response in ovarian cancer, and its accurate detection in tumor biopsies is expected to improve the efficacy of this therapy. Because HRD induces a wide array of genomic aberrations, mutational signatures may serve as a companion diagnostic to identify PARP inhibitor-responsive cases. Experimental Design: From the The Cancer Genome Atlas (TCGA) whole-exome sequencing (WES) data, we extracted different types of mutational signature-based HRD measures, such as the HRD score, genome-wide LOH, and HRDetect trained on ovarian and breast cancer-specific sequencing data. We compared their performance to identify BRCA1/2-deficient cases in the TCGA ovarian cancer cohort and predict survival benefit in platinum-treated, BRCA1/2 wild-type ovarian cancer. Results: We found that the HRD score, which is based on large chromosomal alterations alone, performed similarly well to an ovarian cancer-specific HRDetect, which incorporates mutations on a finer scale as well (AUC = 0.823 vs. AUC = 0.837). In an independent cohort these two methods were equally accurate predicting long- term survival after platinum treatment (AUC = 0.787 vs. AUC = 0.823). We also found that HRDetect trained on ovarian cancer was more accurate than HRDetect trained on breast cancer data (AUC = 0.837 vs. AUC = 0.795; P = 0.0072). Conclusions: When WES data are available, methods that quantify only large chromosomal alterations such as the HRD score and HRDetect that captures a wider array of HRD-induced genomic aberrations are equally efficient identifying HRD ovarian cancer cases.},
	keywords = {CARCINOMA; Therapy; MAINTENANCE; REPAIR; rucaparib},
	year = {2021},
	eissn = {1557-3265},
	pages = {5681-5687},
	orcid-numbers = {Diossy, Miklos/0000-0003-0308-6615; Borcsok, Judit/0000-0002-3290-3971; Szállási, Zoltán/0000-0001-5395-7509}
}

@article{MTMT:32076418,
	title = {A subset of lung cancer cases shows robust signs of homologous recombination deficiency associated genomic mutational signatures},
	url = {https://m2.mtmt.hu/api/publication/32076418},
	author = {Diossy, Miklos and Sztupinszki, Zsófia and Borcsok, Judit and Krzystanek, Marcin and Tisza, Viktoria and Spisák, Sándor and Rusz, Orsolya and Tímár, József and Csabai, István and Fillinger, János and Moldvay, Judit and Pedersen, Anders Gorm and Szüts, Dávid and Szállási, Zoltán},
	doi = {10.1038/s41698-021-00199-8},
	journal-iso = {NPJ PRECIS ONCOL},
	journal = {NPJ PRECISION ONCOLOGY},
	volume = {5},
	unique-id = {32076418},
	year = {2021},
	eissn = {2397-768X},
	orcid-numbers = {Diossy, Miklos/0000-0003-0308-6615; Borcsok, Judit/0000-0002-3290-3971; Rusz, Orsolya/0000-0001-5726-4072; Tímár, József/0000-0001-9183-0859; Szüts, Dávid/0000-0001-7985-0136; Szállási, Zoltán/0000-0001-5395-7509}
}

@article{MTMT:32034134,
	title = {Strand Orientation Bias Detector to determine the probability of FFPE sequencing artifacts.},
	url = {https://m2.mtmt.hu/api/publication/32034134},
	author = {Diossy, Miklos and Sztupinszki, Zsófia and Krzystanek, Marcin and Borcsok, Judit and Eklund, Aron C and Csabai, István and Pedersen, Anders Gorm and Szállási, Zoltán},
	doi = {10.1093/bib/bbab186},
	journal-iso = {BRIEF BIOINFORM},
	journal = {BRIEFINGS IN BIOINFORMATICS},
	volume = {22},
	unique-id = {32034134},
	issn = {1467-5463},
	abstract = {Formalin-fixed paraffin-embedded tissue, the most common tissue specimen stored in clinical practice, presents challenges in the analysis due to formalin-induced artifacts. Here, we present Strand Orientation Bias Detector (SOBDetector), a flexible computational platform compatible with all the common somatic SNV-calling pipelines, designed to assess the probability whether a given detected mutation is an artifact. The underlying predictor mechanism is based on the posterior distribution of a Bayesian logistic regression model trained on The Cancer Genome Atlas whole exomes. SOBDetector is a freely available cross-platform program, implemented in Java 1.8.},
	keywords = {filtering FFPE artifacts; formalin fixation caused mutations; somatic variant calling on FFPE samples},
	year = {2021},
	eissn = {1477-4054},
	pages = {1-10},
	orcid-numbers = {Csabai, István/0000-0001-9232-9898; Szállási, Zoltán/0000-0001-5395-7509}
}

@article{MTMT:31781512,
	title = {Identification of a Synthetic Lethal Relationship between Nucleotide Excision Repair Deficiency and Irofulven Sensitivity in Urothelial Cancer},
	url = {https://m2.mtmt.hu/api/publication/31781512},
	author = {Börcsök, Judit and Sztupinszki, Zsófia and Bekele, Raie and Gao, Sizhi P and Diossy, Miklos and Samant, Amruta S and Dillon, Kasia M and Tisza, Viktoria and Spisák, Sándor and Rusz, Orsolya and Csabai, Istvan and Pappot, Helle and Frazier, Zoe J and Konieczkowski, David J and Liu, David and Vasani, Naresh and Rodrigues, James A and Solit, David B and Hoffman-Censits, Jean H and Plimack, Elizabeth R. and Rosenberg, Jonathan E and Lazaro, Jean-Bernard and Taplin, Mary-Ellen and Iyer, Gopa and Brunak, Søren and Lózsa, Rita Bernadett and Van Allen, Eliezer M and Szüts, Dávid and Mouw, Kent W and Szállási, Zoltán},
	doi = {10.1158/1078-0432.CCR-20-3316},
	journal-iso = {CLIN CANCER RES},
	journal = {CLINICAL CANCER RESEARCH},
	volume = {27},
	unique-id = {31781512},
	issn = {1078-0432},
	year = {2021},
	eissn = {1557-3265},
	pages = {2011-2022},
	orcid-numbers = {Rusz, Orsolya/0000-0001-5726-4072; Lózsa, Rita Bernadett/0000-0001-5957-906X; Szállási, Zoltán/0000-0001-5395-7509}
}

@article{MTMT:31518657,
	title = {E3 ligase RFWD3 is a novel modulator of stalled fork stability in BRCA2-deficient cells},
	url = {https://m2.mtmt.hu/api/publication/31518657},
	author = {Duan, Haohui and Mansour, Sarah and Reed, Rachel and Gillis, Margaret K. and Parent, Benjamin and Liu, Ben and Sztupinszki, Zsófia and Birkbak, Nicolai and Szállási, Zoltán and Elia, Andrew E. H. and Garber, Judy E. and Pathania, Shailja},
	doi = {10.1083/jcb.201908192},
	journal-iso = {J CELL BIOL},
	journal = {JOURNAL OF CELL BIOLOGY},
	volume = {219},
	unique-id = {31518657},
	issn = {0021-9525},
	abstract = {BRCA1/2 help maintain genomic integrity by stabilizing stalled forks. Here, we identify the E3 ligase RFWD3 as an essential modulator of stalled fork stability in BRCA2-deficient cells and show that codepletion of RFWD3 rescues fork degradation, collapse, and cell sensitivity upon replication stress. Stalled forks in BRCA2-deficient cells accumulate phosphorylated and ubiquitinated replication protein A (ubq-pRPA), the latter of which is mediated by RFWD3. Generation of this intermediate requires SMARCAL1, suggesting that it depends on stalled fork reversal. We show that in BRCA2-deficient cells, rescuing fork degradation might not be sufficient to ensure fork repair. Depleting MRE11 in BRCA2-deficient cells does block fork degradation, but it does not prevent fork collapse and cell sensitivity in the presence of replication stress. No such ubq-pRPA intermediate is formed in BRCA1-deficient cells, and our results suggest that BRCA1 may function upstream of BRCA2 in the stalled fork repair pathway. Collectively, our data uncover a novel mechanism by which RFWD3 destabilizes forks in BRCA2-deficient cells.},
	year = {2020},
	eissn = {1540-8140},
	orcid-numbers = {Birkbak, Nicolai/0000-0003-1613-9587; Szállási, Zoltán/0000-0001-5395-7509}
}

@article{MTMT:31409077,
	title = {Cross-reactivity between tumor MHC class I-restricted antigens and an enterococcal bacteriophage.},
	url = {https://m2.mtmt.hu/api/publication/31409077},
	author = {Fluckiger, Aurélie and Daillère, Romain and Sassi, Mohamed and Sixt, Barbara Susanne and Liu, Peng and Loos, Friedemann and Richard, Corentin and Rabu, Catherine and Alou, Maryam Tidjani and Goubet, Anne-Gaëlle and Lemaitre, Fabien and Ferrere, Gladys and Derosa, Lisa and Duong, Connie P M and Messaoudene, Meriem and Gagné, Andréanne and Joubert, Philippe and De Sordi, Luisa and Debarbieux, Laurent and Simon, Sylvain and Scarlata, Clara-Maria and Ayyoub, Maha and Palermo, Belinda and Facciolo, Francesco and Boidot, Romain and Wheeler, Richard and Boneca, Ivo Gomperts and Sztupinszki, Zsófia and Papp, Krisztián and Csabai, István and Pasolli, Edoardo and Segata, Nicola and Lopez-Otin, Carlos and Szállási, Zoltán and Andre, Fabrice and Iebba, Valerio and Quiniou, Valentin and Klatzmann, David and Boukhalil, Jacques and Khelaifia, Saber and Raoult, Didier and Albiges, Laurence and Escudier, Bernard and Eggermont, Alexander and Mami-Chouaib, Fathia and Nistico, Paola and Ghiringhelli, François and Routy, Bertrand and Labarrière, Nathalie and Cattoir, Vincent and Kroemer, Guido and Zitvogel, Laurence},
	doi = {10.1126/science.aax0701},
	journal-iso = {SCIENCE},
	journal = {SCIENCE},
	volume = {369},
	unique-id = {31409077},
	issn = {0036-8075},
	abstract = {Intestinal microbiota have been proposed to induce commensal-specific memory T cells that cross-react with tumor-associated antigens. We identified major histocompatibility complex (MHC) class I-binding epitopes in the tail length tape measure protein (TMP) of a prophage found in the genome of the bacteriophage Enterococcus hirae Mice bearing E. hirae harboring this prophage mounted a TMP-specific H-2Kb-restricted CD8+ T lymphocyte response upon immunotherapy with cyclophosphamide or anti-PD-1 antibodies. Administration of bacterial strains engineered to express the TMP epitope improved immunotherapy in mice. In renal and lung cancer patients, the presence of the enterococcal prophage in stools and expression of a TMP-cross-reactive antigen by tumors correlated with long-term benefit of PD-1 blockade therapy. In melanoma patients, T cell clones recognizing naturally processed cancer antigens that are cross-reactive with microbial peptides were detected.},
	year = {2020},
	eissn = {1095-9203},
	pages = {936-942},
	orcid-numbers = {Papp, Krisztián/0000-0003-0619-8233; Csabai, István/0000-0001-9232-9898; Szállási, Zoltán/0000-0001-5395-7509}
}

@article{MTMT:31194960,
	title = {Detection of molecular signatures of homologous recombination deficiency in prostate cancer with or without BRCA1/2 mutations},
	url = {https://m2.mtmt.hu/api/publication/31194960},
	author = {Sztupinszki, Zsófia and Diossy, Miklos and Krzystanek, Marcin and Börcsök, Judit and Pomerantz, Mark M and Tisza, Viktoria and Spisák, Sándor and Rusz, Orsolya and Csabai, István and Freedman, Matthew L and Szállási, Zoltán},
	doi = {10.1158/1078-0432.CCR-19-2135},
	journal-iso = {CLIN CANCER RES},
	journal = {CLINICAL CANCER RESEARCH},
	volume = {26},
	unique-id = {31194960},
	issn = {1078-0432},
	year = {2020},
	eissn = {1557-3265},
	pages = {2673-2680},
	orcid-numbers = {Rusz, Orsolya/0000-0001-5726-4072; Csabai, István/0000-0001-9232-9898; Szállási, Zoltán/0000-0001-5395-7509}
}

@article{MTMT:30625426,
	title = {Corrigendum to: Breast cancer brain metastases show increased levels of genomic aberration-based homologous recombination deficiency scores relative to their corresponding primary tumors},
	url = {https://m2.mtmt.hu/api/publication/30625426},
	author = {Diossy, M and Reiniger, Lilla and Sztupinszki, Zsófia and Krzystanek, M and Timms, K M and Neff, C and Solimeno, C and Pruss, D and Eklund, A C and Tóth, Erika and Kiss, O and Rusz, O and Cserni, G and Zombori, Tamás and Székely, Borbála and Kulka, Janina and Tímár, J and Csabai, István and Szállási, Zoltán},
	doi = {10.1093/annonc/mdz081},
	journal-iso = {ANN ONCOL},
	journal = {ANNALS OF ONCOLOGY},
	volume = {30},
	unique-id = {30625426},
	issn = {0923-7534},
	year = {2019},
	eissn = {1569-8041},
	pages = {1406-1406},
	orcid-numbers = {Reiniger, Lilla/0000-0003-2248-4264; Tóth, Erika/0000-0003-2054-8447; Zombori, Tamás/0000-0002-0654-563X; Kulka, Janina/0000-0001-6498-5943; Csabai, István/0000-0001-9232-9898; Szállási, Zoltán/0000-0001-5395-7509}
}

@article{MTMT:30417572,
	title = {The genomic imprint of cancer therapies helps timing the formation of metastases},
	url = {https://m2.mtmt.hu/api/publication/30417572},
	author = {Németh, Eszter and Krzystanek, Marcin and Reiniger, Lilla and Ribli, Dezső and Pipek, Orsolya Anna and Sztupinszki, Zsófia and Glasz, Tibor and Csabai, István and Moldvay, Judit and Szállási, Zoltán and Szüts, Dávid},
	doi = {10.1002/ijc.32159},
	journal-iso = {INT J CANCER},
	journal = {INTERNATIONAL JOURNAL OF CANCER},
	volume = {145},
	unique-id = {30417572},
	issn = {0020-7136},
	year = {2019},
	eissn = {1097-0215},
	pages = {694-704},
	orcid-numbers = {Reiniger, Lilla/0000-0003-2248-4264; Pipek, Orsolya Anna/0000-0001-8109-0340; Glasz, Tibor/0000-0003-2947-2733; Csabai, István/0000-0001-9232-9898; Szállási, Zoltán/0000-0001-5395-7509; Szüts, Dávid/0000-0001-7985-0136}
}

@mastersthesis{MTMT:30643683,
	title = {Szolid tumorok terápia szempontjából jelentős klinikai alcsoportokba való sorolása génexpressziós adatok alapján},
	url = {https://m2.mtmt.hu/api/publication/30643683},
	author = {Sztupinszki, Zsófia},
	doi = {10.14753/SE.2018.2114},
	unique-id = {30643683},
	year = {2018}
}