@article{MTMT:34866822,
	title = {Dietary sulfur amino acid restriction in humans with overweight and obesity: Evidence of an altered plasma and urine sulfurome, and a novel metabolic signature that correlates with loss of fat mass and adipose tissue gene expression},
	url = {https://m2.mtmt.hu/api/publication/34866822},
	author = {Olsen, Thomas and Vinknes, Kathrine J. and Barvíková, Kristýna and Stolt, Emma and Lee-Ødegård, Sindre and Troensegaard, Hannibal and Johannessen, Hanna and Elshorbagy, Amany and Sokolová, Jitka and Krijt, Jakub and Křížková, Michaela and Ditrói, Tamás and Nagy, Péter and Øvrebø, Bente and Refsum, Helga and Thoresen, Magne and Retterstøl, Kjetil and Kožich, Viktor},
	doi = {10.1016/j.redox.2024.103192},
	journal-iso = {REDOX BIOL},
	journal = {REDOX BIOLOGY},
	volume = {73},
	unique-id = {34866822},
	issn = {2213-2317},
	year = {2024},
	eissn = {2213-2317},
	pages = {103192},
	orcid-numbers = {Olsen, Thomas/0000-0003-1805-5221; Nagy, Péter/0000-0003-3393-235X}
}

@article{MTMT:34854434,
	title = {Sulfite oxidase deficiency causes persulfidation loss and H2S release},
	url = {https://m2.mtmt.hu/api/publication/34854434},
	author = {Chun-Yu, Fu and Joshua, Benedict Kohl and Filip, Liebsch and Davide, D`Andrea and Max, Mai and Anna, Theresa Mellis and Emilia, Kouroussis and Ditrói, Tamás and José, Angel Santamaria-Araujo and Sin, Yuin Yeo and Heike, Endepols and Michaela, Křížkov and Viktor, Kožich and Uladzimir, Barayeu and Takaaki, Akaike and Julia, B. Hennermann and Nagy, Péter and Milos, Filipovic and Günter, Schwarz},
	doi = {10.1101/2024.03.13.584820},
	journal = {bioRxive},
	volume = {&},
	unique-id = {34854434},
	year = {2024},
	eissn = {2692-8205},
	pages = {&},
	orcid-numbers = {Nagy, Péter/0000-0003-3393-235X}
}

@article{MTMT:34852051,
	title = {Lactoperoxidase catalytically oxidize hydrogen sulfide via intermediate formation of sulfheme derivatives},
	url = {https://m2.mtmt.hu/api/publication/34852051},
	author = {Ríos-González, Bessie B. and Domán, Andrea and Ditrói, Tamás and Garai, Dorottya and Crespo, Leishka D. and Gerfen, Gary J. and Furtmüller, Paul G. and Nagy, Péter and López-Garriga, Juan},
	doi = {10.1016/j.rbc.2024.100021},
	journal-iso = {Redox Biochem Chem},
	journal = {Redox Biochemistry and Chemistry},
	volume = {8},
	unique-id = {34852051},
	year = {2024},
	eissn = {2773-1766},
	pages = {100021},
	orcid-numbers = {Domán, Andrea/0000-0002-5762-5998; Furtmüller, Paul G./0000-0002-1199-2469; Nagy, Péter/0000-0003-3393-235X}
}

@article{MTMT:34839142,
	title = {High-throughput molecular assays for inclusion in personalised oncology trials - State-of-the-art and beyond.},
	url = {https://m2.mtmt.hu/api/publication/34839142},
	author = {Edsjö, Anders and Russnes, Hege G and Lehtiö, Janne and Tamborero, David and Hovig, Eivind and Stenzinger, Albrecht and Rosenquist, Richard},
	doi = {10.1111/joim.13785},
	journal-iso = {J INTERN MED},
	journal = {JOURNAL OF INTERNAL MEDICINE},
	volume = {295},
	unique-id = {34839142},
	issn = {0954-6820},
	abstract = {In the last decades, the development of high-throughput molecular assays has revolutionised cancer diagnostics, paving the way for the concept of personalised cancer medicine. This progress has been driven by the introduction of such technologies through biomarker-driven oncology trials. In this review, strengths and limitations of various state-of-the-art sequencing technologies, including gene panel sequencing (DNA and RNA), whole-exome/whole-genome sequencing and whole-transcriptome sequencing, are explored, focusing on their ability to identify clinically relevant biomarkers with diagnostic, prognostic and/or predictive impact. This includes the need to assess complex biomarkers, for example microsatellite instability, tumour mutation burden and homologous recombination deficiency, to identify patients suitable for specific therapies, including immunotherapy. Furthermore, the crucial role of biomarker analysis and multidisciplinary molecular tumour boards in selecting patients for trial inclusion is discussed in relation to various trial concepts, including drug repurposing. Recognising that today's exploratory techniques will evolve into tomorrow's routine diagnostics and clinical study inclusion assays, the importance of emerging technologies for multimodal diagnostics, such as proteomics and in vivo drug sensitivity testing, is also discussed. In addition, key regulatory aspects and the importance of patient engagement in all phases of a clinical trial are described. Finally, we propose a set of recommendations for consideration when planning a new precision cancer medicine trial.},
	keywords = {Biomarkers; Clinical Trials; omics technologies; precision cancer medicine; personalised oncology; precision diagnostics},
	year = {2024},
	eissn = {1365-2796},
	pages = {785-803},
	orcid-numbers = {Patócs, Attila Balázs/0000-0001-7506-674X; Nagy, Péter/0000-0003-3393-235X; Grolmusz, Vince Kornél/0000-0002-5677-895X}
}

@article{MTMT:34805400,
	title = {Global burden of bladder cancer mortality in 2020 and 2040 according to GLOBOCAN estimates.},
	url = {https://m2.mtmt.hu/api/publication/34805400},
	author = {Wéber, András and Vignat, Jerome and Shah, Richa and Morgan, Eileen and Laversanne, Mathieu and Nagy, Péter and Kenessey, István and Znaor, Ariana},
	doi = {10.1007/s00345-024-04949-8},
	journal-iso = {WORLD J UROL},
	journal = {WORLD JOURNAL OF UROLOGY},
	volume = {42},
	unique-id = {34805400},
	issn = {0724-4983},
	abstract = {In 2020, bladder cancer (BC) was the seventh most prevalent cancer in the world, with 5-year prevalence of more than 1.7 million cases. Due to the main risk factors-smoking and chemical exposures-associated with BC, it is considered a largely preventable and avoidable cancer. An overview of BC mortality can allow an insight not only into the prevalence of global risk factors, but also into the varying efficiency of healthcare systems worldwide. For this purpose, this study analyzes the national mortality estimates for 2020 and projected future trends up to 2040.Age-standardized mortality rates per 100,000 person-years of BC for 185 countries by sex were obtained from the GLOBOCAN 2020 database, operated by the International Agency for Research on Cancer (IARC). Mortality rates were stratified according to sex and Human Development Index (HDI). BC deaths were projected up to 2040 on the basis of demographic changes, alongside different scenarios of annually increasing, stable or decreasing mortality rates from the baseline year of 2020.In 2020, nearly three times more men died from BC than women, with more than 210,000 deaths in both sexes combined, worldwide. Regardless of gender, more than half of the total BC deaths were from countries with a very high HDI. According to our projections, while the number of deaths for men can only increase up to 54% (from 159 to around 163-245 thousand), for women it is projected to increase two- to three-fold (from 50 to around 119-176 thousand) by 2040. The burden of BC mortality in countries with a very high HDI versus high HDI appears to converge by 2040 for both sexes.Opposite mortality trends by gender highlight the urgent need for immediate interventions to expand anti-tobacco strategies, especially for women. The implementation of more strict occupational health and safety regulations could also prevent exposures associated with BC. Improving the ability to detect BC earlier and access to treatment can have a significant positive impact on reducing mortality rates, minimizing economic costs, and enhancing the quality of life for patients.},
	keywords = {MORTALITY; bladder cancer; PROJECTION},
	year = {2024},
	eissn = {1433-8726},
	orcid-numbers = {Wéber, András/0000-0003-1605-8226; Nagy, Péter/0000-0003-3393-235X; Kenessey, István/0000-0002-6963-8489}
}

@article{MTMT:34778874,
	title = {Neurobehavioral dysfunction in a mouse model of Down syndrome. upregulation of cystathionine β-synthase, H2S overproduction, altered protein persulfidation, synaptic dysfunction, endoplasmic reticulum stress, and autophagy},
	url = {https://m2.mtmt.hu/api/publication/34778874},
	author = {Panagaki, Theodora and Janickova, Lucia and Petrovic, Dunja and Zuhra, Karim and Ditrói, Tamás and Jurányi, Eszter Petra and Bremer, Olivier and Ascenção, Kelly and Philipp, Thilo M and Nagy, Péter and Filipovic, Milos R and Szabo, Csaba},
	doi = {10.1007/s11357-024-01146-8},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	unique-id = {34778874},
	issn = {2509-2715},
	abstract = {Down syndrome (DS) is a genetic condition where the person is born with an extra chromosome 21. DS is associated with accelerated aging; people with DS are prone to age-related neurological conditions including an early-onset Alzheimer's disease. Using the Dp(17)3Yey/ + mice, which overexpresses a portion of mouse chromosome 17, which encodes for the transsulfuration enzyme cystathionine β-synthase (CBS), we investigated the functional role of the CBS/hydrogen sulfide (H2S) pathway in the pathogenesis of neurobehavioral dysfunction in DS. The data demonstrate that CBS is higher in the brain of the DS mice than in the brain of wild-type mice, with primary localization in astrocytes. DS mice exhibited impaired recognition memory and spatial learning, loss of synaptosomal function, endoplasmic reticulum stress, and autophagy. Treatment of mice with aminooxyacetate, a prototypical CBS inhibitor, improved neurobehavioral function, reduced the degree of reactive gliosis in the DS brain, increased the ability of the synaptosomes to generate ATP, and reduced endoplasmic reticulum stress. H2S levels in the brain of DS mice were higher than in wild-type mice, but, unexpectedly, protein persulfidation was decreased. Many of the above alterations were more pronounced in the female DS mice. There was a significant dysregulation of metabolism in the brain of DS mice, which affected amino acid, carbohydrate, lipid, endocannabinoid, and nucleotide metabolites; some of these alterations were reversed by treatment of the mice with the CBS inhibitor. Thus, the CBS/H2S pathway contributes to the pathogenesis of neurological dysfunction in DS in the current animal model.},
	keywords = {Brain; metabolism; ASTROCYTES; cognition; gliosis; gasotransmitters; Persulfidation},
	year = {2024},
	eissn = {2509-2723},
	orcid-numbers = {Jurányi, Eszter Petra/0000-0002-0563-4876; Nagy, Péter/0000-0003-3393-235X}
}

@article{MTMT:34720278,
	title = {Versatile roles of cysteine persulfides in tumor biology.},
	url = {https://m2.mtmt.hu/api/publication/34720278},
	author = {Galambos, Klaudia and Czikora, Ágnes and Erdélyi, Katalin and Nagy, Péter},
	doi = {10.1016/j.cbpa.2024.102440},
	journal-iso = {CURR OPIN CHEM BIOL},
	journal = {CURRENT OPINION IN CHEMICAL BIOLOGY},
	volume = {79},
	unique-id = {34720278},
	issn = {1367-5931},
	abstract = {Rewiring the transsulfuration pathway is recognized as a rapid adaptive metabolic response to environmental conditions in cancer cells to support their increased cysteine demand and to produce Reactive Sulfur Species (RSS) including hydrogen sulfide (H2S) and cysteine persulfide. This can directly (via RSS) or indirectly (by supplying Cys) trigger chemical or enzyme catalyzed persulfidation on critical protein cysteine residues to protect them from oxidative damage and to orchestrate protein functions, and thereby contribute to cancer cell plasticity. In this review key aspects of persulfide-mediated biological processes are highlighted and critically discussed in relation to cancer cell survival, bioenergetics, proliferation as well as in tumor angiogenesis, adaptation to hypoxia and oxidative stress, and regulation of epithelial to mesenchymal transition.},
	keywords = {CANCER; CYSTEINE; Transsulfuration; Persulfidation; persulfide},
	year = {2024},
	eissn = {1879-0402},
	pages = {102440},
	orcid-numbers = {Erdélyi, Katalin/0000-0001-8802-1292; Nagy, Péter/0000-0003-3393-235X}
}

@article{MTMT:34538356,
	title = {Effectiveness of SARS-CoV-2 primary vaccines and boosters in patients with type 2 diabetes mellitus in Hungary (HUN-VE 4 Study)},
	url = {https://m2.mtmt.hu/api/publication/34538356},
	author = {Molnár, Gergő Attila and Vokó, Zoltán and Sütő, Gábor and Rokszin, György Aurél and Nagy, Dávid and Surján, György and Surján, Orsolya and Nagy, Péter and Kenessey, István and Wéber, András and Pálosi, Mihály and Müller, Cecília and Kásler, Miklós and Wittmann, István and Kiss, Zoltán},
	doi = {10.1136/bmjdrc-2023-003777},
	journal-iso = {BMJ OPEN DIAB RES CA},
	journal = {BMJ OPEN DIABETES RESEARCH & CARE},
	volume = {12},
	unique-id = {34538356},
	abstract = {Introduction Type 2 diabetes mellitus is a risk factor for severe COVID-19 infection and is associated with increased risk of complications. The present study aimed to investigate effectiveness and persistence of different COVID vaccines in persons with or without diabetes during the Delta wave in Hungary.Research design and methods Data sources were the national COVID-19 registry data from the National Public Health Center and the National Health Insurance Fund on the total Hungarian population. The adjusted incidence rate ratios and corresponding 95% CIs were derived from a mixed-effect negative binomial regression model.Results A population of 672 240 cases with type 2 diabetes and a control group of 2 974 102 non-diabetic persons free from chronic diseases participated. Unvaccinated elderly persons with diabetes had 2.68 (95% CI 2.47 to 2.91) times higher COVID-19-related mortality rate as the ‘healthy’ controls. Primary immunization effectively equalized the risk of COVID-19 mortality between the two groups. Vaccine effectiveness declined over time, but the booster restored the effectiveness against mortality to over 90%. The adjusted vaccine effectiveness of the primary Pfizer-BioNTech against infection in the 14–120 days of postvaccination period was 71.6 (95% CI 66.3 to 76.1)% in patients aged 65–100 years with type 2 diabetes and 64.52 (95% CI 59.2 to 69.2)% in the controls. Overall, the effectiveness tended to be higher in individuals with diabetes than in controls. The booster vaccines could restore vaccine effectiveness to over 80% concerning risk of infection (eg, patients with diabetes aged 65–100 years: 89.1 (88.1–89.9)% with Pfizer-on-Pfizer, controls 65–100 years old: 86.9 (85.8–88.0)% with Pfizer-on-Pfizer, or patients with diabetes aged 65–100 years: 88.3 (87.2–89.2)% with Pfizer-on-Sinopharm, controls 65–100 years old: 87.8 (86.8–88.7)% with Pfizer-on-Sinopharm).Conclusions Our data suggest that people with type 2 diabetes may have even higher health gain when getting vaccinated as compared with non-diabetic persons, eliminating the marked, COVID-19-related excess risk of this population. Boosters could restore protection.Data are available upon reasonable request.},
	year = {2024},
	eissn = {2052-4897},
	orcid-numbers = {Molnár, Gergő Attila/0000-0001-6052-5907; Vokó, Zoltán/0000-0002-1004-1848; Surján, György/0000-0001-5836-7647; Nagy, Péter/0000-0003-3393-235X; Kenessey, István/0000-0002-6963-8489; Wéber, András/0000-0003-1605-8226; Kásler, Miklós/0000-0002-7235-8787; Kiss, Zoltán/0000-0002-4752-8529}
}

@article{MTMT:34523883,
	title = {UNCAN.eu: Toward a European Federated Cancer Research Data Hub},
	url = {https://m2.mtmt.hu/api/publication/34523883},
	author = {Boutros, Michael and Baumann, Michael and Bigas, Anna and Chaabane, Linda and Guérin, Julien and Habermann, Jens K and Jobard, Aurélien and Pelicci, Pier Giuseppe and Stegle, Oliver and Tonon, Giovanni and Valencia, Alfonso and Winkler, Eva C and Blanc, Patricia and De Maria, Ruggero and Medema, Rene H and Nagy, Péter and Tabernero, Josep and Solary, Eric},
	doi = {10.1158/2159-8290.CD-23-1111},
	journal-iso = {CANCER DISCOV},
	journal = {CANCER DISCOVERY},
	volume = {14},
	unique-id = {34523883},
	issn = {2159-8274},
	abstract = {To enable a collective effort that generates a new level of UNderstanding CANcer (UNCAN.eu) [Cancer Discov (2022) 12 (11): OF1], the European Union supports the creation of a sustainable platform that connects cancer research across Member States. A workshop hosted in Heidelberg gathered European cancer experts to identify ongoing initiatives that may contribute to building this platform and discuss the governance and long-term evolution of a European Federated Cancer Data Hub.},
	year = {2024},
	eissn = {2159-8290},
	pages = {30-35},
	orcid-numbers = {Nagy, Péter/0000-0003-3393-235X}
}

@article{MTMT:34450816,
	title = {Strategies to decrease inequalities in cancer therapeutics, care and prevention.},
	url = {https://m2.mtmt.hu/api/publication/34450816},
	author = {Ringborg, Ulrik and von Braun, Joachim and Celis, Julio and Baumann, Michael and Berns, Anton and Eggermont, Alexander and Heard, Edith and Heitor, Manuel and Chandy, Mammen and Chen, Chien-Jen and Costa, Alberto and De Lorenzo, Francesco and De Robertis, Edward M and Dubee, Frederick Charles and Ernberg, Ingemar and Gabriel, Mariya and Helland, Åslaug and Henrique, Rui and Jönsson, Bengt and Kallioniemi, Olli and Korbel, Jan and Krause, Mechthild and Lowy, Douglas R and Michielin, Olivier and Nagy, Péter and Oberst, Simon and Paglia, Vincenzo and Parker, M Iqbal and Ryan, Kevin and Sawyers, Charles L and Schüz, Joachim and Silkaitis, Katherine and Solary, Eric and Thomas, David and Turkson, Peter and Weiderpass, Elisabete and Yang, Huanming},
	doi = {10.1002/1878-0261.13575},
	journal-iso = {MOL ONCOL},
	journal = {MOLECULAR ONCOLOGY},
	volume = {18},
	unique-id = {34450816},
	issn = {1574-7891},
	abstract = {Analyses of inequalities related to prevention and cancer therapeutics/care show disparities between countries with different economic standing, and within countries with high Gross Domestic Product. The development of basic, technological and biological research provides clinical and prevention opportunities that make their implementation into healthcare systems more complex, mainly due to the growth of Personalized/Precision Cancer Medicine (PCM). Initiatives like the US-Cancer Moonshot and the EU-Mission on Cancer and Europe´s Beating Cancer Plan are initiated to boost cancer prevention and therapeutics/care innovation and to mitigate present inequalities. The conference organised by the Pontifical Academy of Sciences in collaboration with the European Academy of Cancer Sciences discussed the inequality problem, dependent on the economic status of a country, the increasing demands for infrastructure supportive of innovative research and its implementation in healthcare and prevention programs. Establishing translational research and a coherent cancer research continuum is still a challenge. Research has to cover the entire continuum from basic to outcomes research for clinical and prevention components. Comprehensive Cancer Centres (CCCs) are of critical importance for integrating research innovations to preclinical and early clinical research, as for ensuring state-of-the-art patient care within healthcare systems. International collaborative networks between CCCs are necessary to reach the critical mass of infrastructures and patients for PCM research, and for introducing prevention modalities and new treatments effectively. Outcomes and health economics research are required to assess the cost-effectiveness of new interventions, currently a missing element in the research portfolio. Data sharing and critical mass are essential for innovative research to develop PCM. Despite advances in cancer research, cancer incidence and prevalence is growing. Making cancer research infrastructures accessible for all patients, considering the increasing inequalities, requires science policy actions incentivising research aimed at prevention and cancer therapeutics/care with an increased focus on patients´ needs and cost-effective healthcare.},
	keywords = {INEQUALITIES; cancer prevention; Healthcare; Science policy; Cancer therapeutics/care; translational cancer research},
	year = {2024},
	eissn = {1878-0261},
	pages = {245-279},
	orcid-numbers = {Nagy, Péter/0000-0003-3393-235X}
}