@article{MTMT:26935896,
	title = {Loss of BRCA1 or BRCA2 markedly increases the rate of base substitution mutagenesis and has distinct effects on genomic deletions (vol 36, pg 746, 2017)},
	url = {https://m2.mtmt.hu/api/publication/26935896},
	author = {Zamborszky, J and Szikriszt, B and Gervai, J Z and Pipek, Orsolya Anna and Póti, Ádám and Krzystanek, M and Ribli, D and Szalai-Gindl, J M and Csabai, I and Szállási, Zoltán and Swanton, C and Richardson, A L and Szüts, Dávid},
	doi = {10.1038/onc.2017.213},
	journal-iso = {ONCOGENE},
	journal = {ONCOGENE},
	volume = {36},
	unique-id = {26935896},
	issn = {0950-9232},
	year = {2017},
	eissn = {1476-5594},
	pages = {5085-5086},
	orcid-numbers = {Pipek, Orsolya Anna/0000-0001-8109-0340; 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:26513282,
	title = {Homologous Recombination Deficiency (HRD) Score Predicts Response to Platinum-Containing Neoadjuvant Chemotherapy in Patients with Triple-Negative Breast Cancer},
	url = {https://m2.mtmt.hu/api/publication/26513282},
	author = {Telli, ML and Timms, KM and Reid, J and Hennessy, B and Mills, GB and Jensen, KC and Szállási, Zoltán and Barry, WT and Winer, EP and Tung, N and Isakoff, SJ and Ryan, PD and Greene-Colozzi, A and Gutin, A and Sangale, Z and Iliev, D and Neff, C and Abkevich, V and Jones, JT and Lanchbury, JS and Hartman, AR and Garber, JE and Ford, JM and Silver, DP and Richardson, AL},
	doi = {10.1158/1078-0432.CCR-15-2477},
	journal-iso = {CLIN CANCER RES},
	journal = {CLINICAL CANCER RESEARCH},
	volume = {22},
	unique-id = {26513282},
	issn = {1078-0432},
	year = {2016},
	eissn = {1557-3265},
	pages = {3764-3773},
	orcid-numbers = {Szállási, Zoltán/0000-0001-5395-7509}
}

@article{MTMT:31826051,
	title = {Sequenza: allele-specific copy number and mutation profiles from tumor sequencing data},
	url = {https://m2.mtmt.hu/api/publication/31826051},
	author = {Favero, F and Joshi, T and Marquard, A M and Birkbak, N J and Krzystanek, M and Li, Q and Szállási, Zoltán and Eklund, A C},
	doi = {10.1093/annonc/mdu479},
	journal-iso = {ANN ONCOL},
	journal = {ANNALS OF ONCOLOGY},
	volume = {26},
	unique-id = {31826051},
	issn = {0923-7534},
	abstract = {Exome or whole-genome deep sequencing of tumor DNA along with paired normal DNA can potentially provide a detailed picture of the somatic mutations that characterize the tumor. However, analysis of such sequence data can be complicated by the presence of normal cells in the tumor specimen, by intratumor heterogeneity, and by the sheer size of the raw data. In particular, determination of copy number variations from exome sequencing data alone has proven difficult; thus, single nucleotide polymorphism (SNP) arrays have often been used for this task. Recently, algorithms to estimate absolute, but not allele-specific, copy number profiles from tumor sequencing data have been described.We developed Sequenza, a software package that uses paired tumor-normal DNA sequencing data to estimate tumor cellularity and ploidy, and to calculate allele-specific copy number profiles and mutation profiles. We applied Sequenza, as well as two previously published algorithms, to exome sequence data from 30 tumors from The Cancer Genome Atlas. We assessed the performance of these algorithms by comparing their results with those generated using matched SNP arrays and processed by the allele-specific copy number analysis of tumors (ASCAT) algorithm.Comparison between Sequenza/exome and SNP/ASCAT revealed strong correlation in cellularity (Pearson's r = 0.90) and ploidy estimates (r = 0.42, or r = 0.94 after manual inspecting alternative solutions). This performance was noticeably superior to previously published algorithms. In addition, in artificial data simulating normal-tumor admixtures, Sequenza detected the correct ploidy in samples with tumor content as low as 30%.The agreement between Sequenza and SNP array-based copy number profiles suggests that exome sequencing alone is sufficient not only for identifying small scale mutations but also for estimating cellularity and inferring DNA copy number aberrations.},
	keywords = {MUTATIONS; Software; Next-generation sequencing; CANCER GENOMICS; copy number alterations},
	year = {2015},
	eissn = {1569-8041},
	pages = {64-70},
	orcid-numbers = {Szállási, Zoltán/0000-0001-5395-7509}
}

@article{MTMT:22539074,
	title = {Telomeric Allelic Imbalance Indicates Defective DNA Repair and Sensitivity to DNA-Damaging Agents},
	url = {https://m2.mtmt.hu/api/publication/22539074},
	author = {Birkbak, NJ and Wang, ZGC and Kim, JY and Eklund, AC and Li, QY and Tian, RY and Bowman-Colin, C and Li, Y and Greene-Colozzi, A and Iglehart, JD and Tung, N and Ryan, PD and Garber, JE and Silver, DP and Szállási, Zoltán and Richardson, AL},
	doi = {10.1158/2159-8290.CD-11-0206},
	journal-iso = {CANCER DISCOV},
	journal = {CANCER DISCOVERY},
	volume = {2},
	unique-id = {22539074},
	issn = {2159-8274},
	year = {2012},
	eissn = {2159-8290},
	pages = {366-375},
	orcid-numbers = {Szállási, Zoltán/0000-0001-5395-7509}
}