@article{MTMT:34729974,
	title = {Profiling of copy number alterations using low-coverage whole-genome sequencing informs differential diagnosis and prognosis in primary cutaneous follicle center lymphoma.},
	url = {https://m2.mtmt.hu/api/publication/34729974},
	author = {Bátai, Bence and Kiss, Laura and Varga, Luca Petra and Nagy, Ákos and Househam, Jacob and Baker, Ann-Marie and László, Tamás and Udvari, Anna and Horváth, Róbert and Nagy, Tibor and Csomor, Judit and Szakonyi, József and Schneider, Tamás and Graham, Trevor A and Alpár, Donát and Fitzgibbon, Jude and Szepesi, Ágota and Bödör, Csaba},
	doi = {10.1016/j.modpat.2024.100465},
	journal-iso = {MODERN PATHOL},
	journal = {MODERN PATHOLOGY},
	volume = {37},
	unique-id = {34729974},
	issn = {0893-3952},
	abstract = {Primary cutaneous follicle center lymphoma (PCFCL) has an excellent prognosis using local treatment, while nodal follicular lymphoma (nFL) occasionally presenting with cutaneous spread, often requires systemic therapy. Distinction of the two diseases based on histopathology alone might be challenging. Copy number alterations (CNAs) have scarcely been explored on a genome-wide scale in PCFCL, yet they might serve as potential biomarkers during differential diagnosis and risk stratification. Low-coverage whole genome sequencing (lcWGS) is a robust, high-throughput method for genome-wide copy number profiling. In this study, we analyzed 28 PCFCL samples from 20 patients and compared the copy number profiles to a cohort of diagnostic samples of 64 nFL patients. Although the copy number profile of PCFCL was similar to that of nFL, PCFCL lacked amplifications of 18q, with the frequency peaking at 18q21.33 in nFL cases involving the BCL2 locus (PCFCL: 5.0% vs. nFL: 31.3%, p=0.018, Fisher's exact test). Development of distant cutaneous spread was significantly associated with higher genomic instability including the proportion of genome altered (0.02 vs. 0.13, p=0.033) and number of CNAs (2 vs. 9 p=0.017), as well as the enrichment of 2p22.2-p15 amplification involving REL and XPO1 (6.3% vs. 60.0%, p=0.005), 3q23-q24 amplification (0.0% vs. 50.0%, p=0.004), 6q16.1-q23.3 deletion (6.3% vs. 50.0%, p=0.018) and 9p21.3 deletion covering CDKN2A and CDKN2B loci (0.0% vs. 40.0%, p=0.014, all Fisher's exact test) in PCFCL. Analysis of sequential tumor samples in two cases harboring an unfavorable clinical course pointed to the acquisition of 2p amplification in the earliest common progenitor underlining its pivotal role in malignant transformation. By performing genome-wide copy number profiling on the largest patient cohort to date, we identified distinctive CNA alterations conceivably facilitating the differential diagnosis of PCFCL and secondary cutaneous involvement of nFL, and potentially aiding the risk stratification of patients with PCFCL in the future.},
	year = {2024},
	eissn = {1530-0285},
	orcid-numbers = {Varga, Luca Petra/0000-0002-6211-8245; Szakonyi, József/0000-0003-2463-8925; Szepesi, Ágota/0000-0002-0706-1178; Bödör, Csaba/0000-0002-0729-692X}
}

@article{MTMT:34430138,
	title = {Genetic Characterization of Primary Mediastinal B-Cell Lymphoma. Pathogenesis and Patient Outcomes},
	url = {https://m2.mtmt.hu/api/publication/34430138},
	author = {Noerenberg, Daniel and Briest, Franziska and Hennch, Cornelius and Yoshida, Kenichi and Hablesreiter, Raphael and Takeuchi, Yasuhide and Ueno, Hiroo and Staiger, Annette M and Ziepert, Marita and Asmar, Fazila and Locher, Benjamin N and Tóth, Erika and Weber, Thomas and Amini, Rose-Marie and Klapper, Wolfram and Bouzani, Maria and Poeschel, Viola and Rosenwald, Andreas and Held, Gerhard and Campo, Elías and Ishaque, Naveed and Stamatopoulos, Kostas and Kanellis, George and Anagnostopoulos, Ioannis and Bullinger, Lars and Goldschmidt, Neta and Zinzani, Pier Luigi and Bödör, Csaba and Rosenquist, Richard and Vassilakopoulos, Theodoros P and Ott, German and Ogawa, Seishi and Damm, Frederik},
	doi = {10.1200/JCO.23.01053},
	journal-iso = {J CLIN ONCOL},
	journal = {JOURNAL OF CLINICAL ONCOLOGY},
	volume = {42},
	unique-id = {34430138},
	issn = {0732-183X},
	abstract = {Primary mediastinal large B-cell lymphoma (PMBCL) is a rare aggressive lymphoma predominantly affecting young female patients. Large-scale genomic investigations and genetic markers for risk stratification are lacking.To elucidate the full spectrum of genomic alterations, samples from 340 patients with previously untreated PMBCL were investigated by whole-genome (n = 20), whole-exome (n = 78), and targeted (n = 308) sequencing. Statistically significant prognostic variables were identified using a multivariable Cox regression model and confirmed by L1/L2 regularized regressions.Whole-genome sequencing revealed a commonly disrupted p53 pathway with nonredundant somatic structural variations (SVs) in TP53-related genes (TP63, TP73, and WWOX) and identified novel SVs facilitating immune evasion (DOCK8 and CD83). Integration of mutation and copy-number data expanded the repertoire of known PMBCL alterations (eg, ARID1A, P2RY8, and PLXNC1) with a previously unrecognized role for epigenetic/chromatin modifiers. Multivariable analysis identified six genetic lesions with significant prognostic impact. CD58 mutations (31%) showed the strongest association with worse PFS (hazard ratio [HR], 2.52 [95% CI, 1.50 to 4.21]; P < .001) and overall survival (HR, 2.33 [95% CI, 1.14 to 4.76]; P = .02). IPI high-risk patients with mutated CD58 demonstrated a particularly poor prognosis, with 5-year PFS and OS rates of 41% and 58%, respectively. The adverse prognostic significance of the CD58 mutation status was predominantly observed in patients treated with nonintensified regimens, indicating that dose intensification may, to some extent, mitigate the impact of this high-risk marker. By contrast, DUSP2-mutated patients (24%) displayed durable responses (PFS: HR, 0.2 [95% CI, 0.07 to 0.55]; P = .002) and prolonged OS (HR, 0.11 [95% CI, 0.01 to 0.78]; P = .028). Upon CHOP-like treatment, these patients had very favorable outcome, with 5-year PFS and OS rates of 93% and 98%, respectively.This large-scale genomic characterization of PMBCL identified novel treatment targets and genetic lesions for refined risk stratification. DUSP2 and CD58 mutation analyses may guide treatment decisions between rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone and dose-adjusted etoposide, prednisone, vincristine, cyclophosphamide, doxorubicin, and rituximab.},
	year = {2024},
	eissn = {1527-7755},
	pages = {452-466},
	orcid-numbers = {Tóth, Erika/0000-0003-2054-8447; Bödör, Csaba/0000-0002-0729-692X}
}

@article{MTMT:34399695,
	title = {Low‐burden TP53 mutations represent frequent genetic events in CLL with an increased risk for treatment initiation},
	url = {https://m2.mtmt.hu/api/publication/34399695},
	author = {László, Tamás and Kotmayer, Lili and Fésüs, Viktória and Hegyi, Lajos and Gróf, Stefánia and Nagy, Ákos and Kajtár, Béla and Balogh, Alexandra and Weisinger, Júlia and Masszi, Tamás and Nagy, Zsolt and Farkas, Péter and Demeter, Judit and Istenes, Ildikó and Szász, Róbert and Gergely, Lajos and Sulák, Adrienn and Borbényi, Zita and Lévai, Dóra and Schneider, Tamás and Pettendi, Piroska and Bodai, Emese and Szerafin, László and Rejtő, László and Bátai, Árpád and Dömötör, Mária Á and Sánta, Hermina and Plander, Márk and Szendrei, Tamás and Hamed, Aryan and Lázár, Zsolt and Pauker, Zsolt and Radványi, Gáspár and Kiss, Adrienn and Körösmezey, Gábor and Jakucs, János and Dombi, Péter J and Simon, Zsófia and Klucsik, Zsolt and Gurzó, Mihály and Tiboly, Márta and Vidra, Tímea and Ilonczai, Péter and Bors, András and Andrikovics, Hajnalka and Egyed, Miklós and Székely, Tamás and Masszi, András and Alpár, Donát and Matolcsy, András and Bödör, Csaba},
	doi = {10.1002/cjp2.351},
	journal-iso = {J PATHOL CLIN RES},
	journal = {JOURNAL OF PATHOLOGY: CLINICAL RESEARCH},
	volume = {10},
	unique-id = {34399695},
	abstract = {TP53 aberrations predict chemoresistance and represent a contraindication for the use of standard chemoimmunotherapy in chronic lymphocytic leukaemia (CLL). Recent next‐generation sequencing (NGS)‐based studies have identified frequent low‐burden TP53 mutations with variant allele frequencies below 10%, but the clinical impact of these low‐burden TP53 mutations is still a matter of debate. In this study, we aimed to scrutinise the subclonal architecture and clinical impact of TP53 mutations using a sensitive, NGS‐based mutation analysis in a ‘real‐world’ cohort of 901 patients with CLL. In total, 225 TP53 mutations were identified in 17.5% (158/901) of the patients; 48% of these alterations represented high‐burden mutations, while 52% were low‐burden TP53 mutations. Low‐burden mutations as sole alterations were identified in 39% (62/158) of all mutated cases with 82% (51/62) of these being represented by a single low‐burden TP53 mutation. Patients harbouring low‐burden TP53 mutations had significantly lower time to first treatment compared to patients with wild‐type TP53 . Our study has expanded the knowledge on the frequency, clonal architecture, and clinical impact of low‐burden TP53 mutations. By demonstrating that patients with sole low‐burden TP53 variants represent more than one‐third of patients with TP53 mutations and have an increased risk for treatment initiation, our findings strengthen the need to redefine the threshold of TP53 variant reporting to below 10% in the routine diagnostic setting.},
	keywords = {chronic lymphocytic leukaemia; NGS; TP53},
	year = {2024},
	eissn = {2056-4538},
	orcid-numbers = {Kajtár, Béla/0000-0001-5551-3709; Masszi, Tamás/0000-0003-2322-9863; Nagy, Zsolt/0000-0002-9648-1851; Farkas, Péter/0000-0003-2840-2442; Demeter, Judit/0000-0001-8745-0757; Istenes, Ildikó/0000-0001-5582-6166; Szász, Róbert/0000-0003-1343-6017; Masszi, András/0000-0003-4303-764X; Matolcsy, András/0000-0002-5382-2150; Bödör, Csaba/0000-0002-0729-692X}
}

@article{MTMT:34395421,
	title = {Truncated titin is structurally integrated into the human dilated cardiomyopathic sarcomere},
	url = {https://m2.mtmt.hu/api/publication/34395421},
	author = {Kellermayer, Dalma Lucia and Tordai, Hedvig and Kiss, Balázs and Török, György and Péter, Dániel M. and Sayour, Alex Ali and Pólos, Miklós and Hartyánszky, István and Szilveszter, Bálint and Labeit, Siegfried and Gángó, Ambrus and Bedics, Gábor and Bödör, Csaba and Radovits, Tamás and Merkely, Béla Péter and Kellermayer, Miklós},
	doi = {10.1172/JCI169753},
	journal-iso = {J CLIN INVEST},
	journal = {JOURNAL OF CLINICAL INVESTIGATION},
	volume = {134},
	unique-id = {34395421},
	issn = {0021-9738},
	year = {2024},
	eissn = {1558-8238},
	orcid-numbers = {Kellermayer, Dalma Lucia/0000-0003-0398-0801; Tordai, Hedvig/0000-0002-0875-5569; Kiss, Balázs/0000-0002-2347-5928; Török, György/0000-0001-7616-5782; Sayour, Alex Ali/0000-0001-7728-4775; Hartyánszky, István/0000-0003-1909-6500; Szilveszter, Bálint/0000-0003-1530-4288; Labeit, Siegfried/0000-0002-9009-210X; Gángó, Ambrus/0000-0001-9127-5015; Bedics, Gábor/0000-0003-4628-2384; Bödör, Csaba/0000-0002-0729-692X; Merkely, Béla Péter/0000-0001-6514-0723; Kellermayer, Miklós/0000-0002-5553-6553}
}

@article{MTMT:34558244,
	title = {HU-LYGEN: A HAZAI DIFFÚZ NAGY B-SEJTES LYMPHOMA MOLEKULÁRIS PROFILOZÁS PROGRAM ELSŐ EREDMÉNYEI},
	url = {https://m2.mtmt.hu/api/publication/34558244},
	author = {Bátai, Bence and Varga, L and Weisinger, Júlia and Illyés, Gabriella and Masszi, András and Gergely, Lajos and Bátai, Á and Gurbity Pálfi, Timea and Rejtő, László and Plander, Márk and Egyed, Miklós and Nagy, Z and Masszi, Tamás and Alpár, Donát and Bödör, C},
	journal-iso = {MBA},
	journal = {MAGYAR BELORVOSI ARCHIVUM},
	volume = {76},
	unique-id = {34558244},
	issn = {0133-5464},
	year = {2023},
	pages = {300-301},
	orcid-numbers = {Masszi, András/0000-0003-4303-764X; Masszi, Tamás/0000-0003-2322-9863}
}

@misc{MTMT:34558230,
	title = {Bal kamra hypertrophiát okozó szívizombetegségek szív mágneses rezonanciás és genetikai jellegzetességei. Cardiac magnetic resonance and genetic characteristics of myocardial diseases causing left ventricular hypertrophy},
	url = {https://m2.mtmt.hu/api/publication/34558230},
	author = {Dohy, Zsófia and Fekete, Bálint András and Pozsonyi, Zoltán and Csonka, Katalin and Nagy, Beáta and Fintha, Attila and Balla, Dorottya and Szabó, Liliána and Juhász, Vencel and Czimbalmos, Csilla and Tóth, Attila and Matolcsy, András and Merkely, Béla Péter and Bödör, Csaba and Vágó, Hajnalka},
	unique-id = {34558230},
	year = {2023},
	orcid-numbers = {Dohy, Zsófia/0000-0002-0706-5179; Fekete, Bálint András/0000-0002-3895-477X; Pozsonyi, Zoltán/0000-0002-3098-2434; Fintha, Attila/0000-0002-0519-8170; Balla, Dorottya/0000-0002-5177-8483; Szabó, Liliána/0000-0002-4699-3648; Juhász, Vencel/0000-0001-9100-4952; Czimbalmos, Csilla/0000-0001-6311-9920; Matolcsy, András/0000-0002-5382-2150; Merkely, Béla Péter/0000-0001-6514-0723; Vágó, Hajnalka/0000-0002-3568-3572}
}

@article{MTMT:34452691,
	title = {A hazai onkohematológiai kutatás szolgálatában: A Molekuláris Onkohematológia Kutatócsoport első tíz éve},
	url = {https://m2.mtmt.hu/api/publication/34452691},
	author = {Bödör, Csaba and Alpár, Donát and Bátai, Bence and László, Tamás},
	journal-iso = {MAGYAR ONKOLÓGIA},
	journal = {MAGYAR ONKOLÓGIA},
	volume = {67},
	unique-id = {34452691},
	issn = {0025-0244},
	year = {2023},
	eissn = {2060-0399},
	pages = {260-265},
	orcid-numbers = {Bödör, Csaba/0000-0002-0729-692X}
}

@article{MTMT:34444932,
	title = {Gyermekkori agydaganatok: diagnózis és terápia – komprehenzív genomikai profilozás},
	url = {https://m2.mtmt.hu/api/publication/34444932},
	author = {Brückner, Edit and Bedics, Gábor and Reiniger, Lilla and Rajnai, Hajnalka and Jakab, Zsuzsanna and Bödör, Csaba and Scheich, Bálint and Garami, Miklós},
	journal-iso = {MAGYAR ONKOLÓGIA},
	journal = {MAGYAR ONKOLÓGIA},
	volume = {67},
	unique-id = {34444932},
	issn = {0025-0244},
	abstract = {With the advancement of molecular oncology, numerous new opportunities are available for the effective and efficient treatment of patients diagnosed with childhood brain tumors. This includes gene panel analysis aiding personalized treatment used in clinical trials, and the application of targeted therapy independent of tissue type (tumor agnostic therapy). Most personalized therapies inhibit certain kinases. In our review, we present the modern pathological diagnosis of childhood brain tumors, as well as the complex intracellular regulation of signal transduction pathways important from the point of view of clinical practice, and we describe their further targets defined on the basis of pharmacological characteristics of the pathway, based on international and our own results. Despite common mutations affecting kinases, personalized therapy is not available in many types of tumors. Through the example of childhood brain tumors, we demonstrate the expected future therapeutic significance of tyrosine kinases.},
	year = {2023},
	eissn = {2060-0399},
	pages = {315-320},
	orcid-numbers = {Brückner, Edit/0000-0002-2140-3357; Bedics, Gábor/0000-0003-4628-2384; Reiniger, Lilla/0000-0003-2248-4264; Rajnai, Hajnalka/0000-0003-0934-5366; Jakab, Zsuzsanna/0000-0002-8231-0357; Bödör, Csaba/0000-0002-0729-692X; Garami, Miklós/0000-0003-4298-2746}
}

@article{MTMT:34441434,
	title = {Pneumocystis diagnosztizálása nem ismert HIV fertőzött betegnél - Esetismertetés},
	url = {https://m2.mtmt.hu/api/publication/34441434},
	author = {Szűcs, Gergő and Komáromi, Tamás and Matics, Zsombor Zoltán and Erdélyi, Tamás and Pápay, Judit and Kristóf, Katalin and Bohács, Anikó and Müller, Veronika},
	journal-iso = {MED THORAC (BP)},
	journal = {MEDICINA THORACALIS (BUDAPEST)},
	volume = {76},
	unique-id = {34441434},
	issn = {0238-2571},
	year = {2023},
	pages = {323-326},
	orcid-numbers = {Szűcs, Gergő/0000-0002-3446-0406; Komáromi, Tamás/0000-0002-8083-7243; Erdélyi, Tamás/0000-0002-5025-8769; Pápay, Judit/0000-0003-2642-2060; Kristóf, Katalin/0000-0002-5189-4636; Bohács, Anikó/0000-0002-8229-4254; Müller, Veronika/0000-0002-1398-3187}
}

@article{MTMT:34406243,
	title = {A Magyar Diffúz Nagy B-sejtes Lymphoma Molekuláris Profilozási Projekt (HU-LyGen): ismertető és első eredmények},
	url = {https://m2.mtmt.hu/api/publication/34406243},
	author = {Varga, Luca Petra and Bödör, Csaba and Bátai, Bence},
	doi = {10.1556/2068.2023.00178},
	journal-iso = {HEMATOLÓGIA-TRANSZFUZIOLÓGIA},
	journal = {HEMATOLÓGIA-TRANSZFUZIOLÓGIA},
	volume = {56},
	unique-id = {34406243},
	issn = {1786-5913},
	year = {2023},
	pages = {104-109},
	orcid-numbers = {Varga, Luca Petra/0000-0002-6211-8245; Bödör, Csaba/0000-0002-0729-692X}
}