@article{MTMT:36868436,
	title = {Analysis of Soft Tissue N-Glycome Profiles in Oral Squamous Cell Carcinoma, a Pilot Study},
	url = {https://m2.mtmt.hu/api/publication/36868436},
	author = {Gebri, Eniko and Hogyor, Kinga and Szabo, Adrienne and Guttman, András},
	doi = {10.3390/ijms27020740},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {27},
	unique-id = {36868436},
	issn = {1661-6596},
	abstract = {Oral squamous cell carcinoma (OSCC) is an aggressive disease with a glycoproteomically unmapped progression and a low five-year survival rate. Thus, the aim of this pilot study was to explore the N-glycosylation pattern differences in malignant, adjacent mucosal and healthy tissues in the context of OSCC. Oral mucosal soft tissue samples was obtained by incisional biopsy from five patients with OSCC, both from the malignant and the opposite healthy gingival sides, and from seven age-sex-matched healthy controls. The collected tissues were homogenized, followed by N-glycan profiling of the endoglycosidase-released and fluorophore-labeled carbohydrates using capillary electrophoresis with ultra-sensitive laser-induced fluorescent detection (CE-LIF). Six out of the twenty-two identified N-glycan structures, including glycogens, showed significant (p < 0.05) differences between the malignant tissue samples of the OSCC patients and the healthy controls. Comparing the healthy and the positive control oral mucosal samples, differences in four N-glycan structures were revealed, while only one alteration was observed between the N-glycan profiles of the malignant tumor and positive control samples. However, the results are presented descriptively, reflecting the limited sample size of the pilot study, it shows the potential of high-resolution CE-LIF-based glyocoanalytical protocol to be highly efficient and sensitive for glycobiomarker-based molecular diagnostics of oral malignant lesions.},
	year = {2026},
	eissn = {1422-0067},
	pages = {740},
	orcid-numbers = {Szabo, Adrienne/0000-0002-0135-739X; Guttman, András/0000-0002-7838-082X}
}

@article{MTMT:35663024,
	title = {Sex-specific mechanisms in vascular aging: exploring cellular and molecular pathways in the pathogenesis of age-related cardiovascular and cerebrovascular diseases},
	url = {https://m2.mtmt.hu/api/publication/35663024},
	author = {Ungvári, Anna Sára and Gulej, Rafal and Patai, Roland and Papp, Zoltán and Tóth, Attila and Szabó, Attila Ádám and Podesser, Bruno K. and Sótonyi, Péter and Benyó, Zoltán and Yabluchanskiy, Andriy and Tarantini, Stefano and Maier, Andrea B. and Csiszar, Anna and Ungvári, Zoltán István},
	doi = {10.1007/s11357-024-01489-2},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	volume = {47},
	unique-id = {35663024},
	issn = {2509-2715},
	abstract = {Aging remains the foremost risk factor for cardiovascular and cerebrovascular diseases, surpassing traditional factors in epidemiological significance. This review elucidates the cellular and molecular mechanisms underlying vascular aging, with an emphasis on sex differences that influence disease progression and clinical outcomes in older adults. We discuss the convergence of aging processes at the macro- and microvascular levels and their contributions to the pathogenesis of vascular diseases. Critical analysis of both preclinical and clinical studies reveals significant sex-specific variations in these mechanisms, which could be pivotal in understanding the disparity in disease morbidity and mortality between sexes. The review highlights key molecular pathways, including oxidative stress, inflammation, and autophagy, and their differential roles in the vascular aging of males and females. We argue that recognizing these sex-specific differences is crucial for developing targeted therapeutic strategies aimed at preventing and managing age-related vascular pathologies. The implications for personalized medicine and potential areas for future research are also explored, emphasizing the need for a nuanced approach to the study and treatment of vascular aging.},
	year = {2025},
	eissn = {2509-2723},
	pages = {301-337},
	orcid-numbers = {Sótonyi, Péter/0000-0002-2216-4298; Benyó, Zoltán/0000-0001-6015-0359; Tarantini, Stefano/0000-0001-5627-1430; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:35676767,
	title = {Cerebromicrovascular mechanisms contributing to long COVID: implications for neurocognitive health},
	url = {https://m2.mtmt.hu/api/publication/35676767},
	author = {Fekete, Mónika and Lehoczki, Andrea Marianna and Szappanos, Ágnes and Tóth, Attila and Mahdi, Mohamed and Sótonyi, Péter and Benyó, Zoltán and Yabluchanskiy, Andriy and Tarantini, Stefano and Ungvári, Zoltán István},
	doi = {10.1007/s11357-024-01487-4},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	volume = {47},
	unique-id = {35676767},
	issn = {2509-2715},
	abstract = {Long COVID (also known as post-acute sequelae of SARS-CoV-2 infection [PASC] or post-COVID syndrome) is characterized by persistent symptoms that extend beyond the acute phase of SARS-CoV-2 infection, affecting approximately 10% to over 30% of those infected. It presents a significant clinical challenge, notably due to pronounced neurocognitive symptoms such as brain fog. The mechanisms underlying these effects are multifactorial, with mounting evidence pointing to a central role of cerebromicrovascular dysfunction. This review investigates key pathophysiological mechanisms contributing to cerebrovascular dysfunction in long COVID and their impacts on brain health. We discuss how endothelial tropism of SARS-CoV-2 and direct vascular infection trigger endothelial dysfunction, impaired neurovascular coupling, and blood-brain barrier disruption, resulting in compromised cerebral perfusion. Furthermore, the infection appears to induce mitochondrial dysfunction, enhancing oxidative stress and inflammation within cerebral endothelial cells. Autoantibody formation following infection also potentially exacerbates neurovascular injury, contributing to chronic vascular inflammation and ongoing blood-brain barrier compromise. These factors collectively contribute to the emergence of white matter hyperintensities, promote amyloid pathology, and may accelerate neurodegenerative processes, including Alzheimer's disease. This review also emphasizes the critical role of advanced imaging techniques in assessing cerebromicrovascular health and the need for targeted interventions to address these cerebrovascular complications. A deeper understanding of the cerebrovascular mechanisms of long COVID is essential to advance targeted treatments and mitigate its long-term neurocognitive consequences.},
	keywords = {AUTOANTIBODIES; endothelial dysfunction; mitochondrial dysfunction; Neurovascular coupling; Long COVID; long-haul COVID; Cerebromicrovascular dysfunction; Persistent COVID symptoms},
	year = {2025},
	eissn = {2509-2723},
	pages = {745-779},
	orcid-numbers = {Fekete, Mónika/0000-0001-8632-2120; Sótonyi, Péter/0000-0002-2216-4298; Benyó, Zoltán/0000-0001-6015-0359; Tarantini, Stefano/0000-0001-5627-1430; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:35701407,
	title = {Effect of the operational parameters on the electromigration of proteins in sodium dodecyl sulfate capillary gel electrophoresis in the presence of propidium iodide fluorescent dye},
	url = {https://m2.mtmt.hu/api/publication/35701407},
	author = {Auer, Felícia and Guttman, András},
	doi = {10.1016/j.talanta.2025.127601},
	journal-iso = {TALANTA},
	journal = {TALANTA},
	volume = {287},
	unique-id = {35701407},
	issn = {0039-9140},
	year = {2025},
	eissn = {1873-3573},
	pages = {127601},
	orcid-numbers = {Auer, Felícia/0000-0001-8347-7637; Guttman, András/0000-0002-7838-082X}
}

@article{MTMT:35721307,
	title = {Predicting the effectiveness of chemotherapy treatment in lung cancer utilizing artificial intelligence-supported serum N-glycome analysis},
	url = {https://m2.mtmt.hu/api/publication/35721307},
	author = {Török, Rebeka and Mészáros, Brigitta and Gombás, Veronika and Fogarassyné Vathy, Ágnes and Szabó, Miklós and Csánky, Eszter and Járvás, Gábor and Guttman, András},
	doi = {10.1016/j.compbiomed.2025.109681},
	journal-iso = {COMPUT BIOL MED},
	journal = {COMPUTERS IN BIOLOGY AND MEDICINE},
	volume = {186},
	unique-id = {35721307},
	issn = {0010-4825},
	year = {2025},
	eissn = {1879-0534},
	orcid-numbers = {Gombás, Veronika/0009-0007-3091-1402; Fogarassyné Vathy, Ágnes/0000-0002-5524-1675; Járvás, Gábor/0000-0002-9289-6304; Guttman, András/0000-0002-7838-082X}
}

@article{MTMT:35775490,
	title = {Multifaceted Approaches in Epithelial Cell Adhesion Molecule-Mediated Circulating Tumor Cell Isolation},
	url = {https://m2.mtmt.hu/api/publication/35775490},
	author = {Szerényi, Dóra and Járvás, Gábor and Guttman, András},
	doi = {10.3390/molecules30050976},
	journal-iso = {MOLECULES},
	journal = {MOLECULES},
	volume = {30},
	unique-id = {35775490},
	issn = {1431-5157},
	abstract = {Circulating tumor cells (CTCs) are pivotal in cancer metastasis and serve as valuable biomarkers for diagnosis, prognosis, and treatment monitoring. Traditional CTC capture methods predominantly utilize the epithelial cell adhesion molecule (EpCAM) as a marker for isolation. However, the heterogeneity of these circulating cells and the epithelial-to-mesenchymal transition process (wherein epithelial cells acquire mesenchymal characteristics) limit the efficacy of EpCAM-based capture techniques. In this paper, we critically review the role of the EpCAM in CTC capture, explore the impact of epithelial-to-mesenchymal transition on EpCAM expression, and discuss alternative biomarkers and strategies to enhance CTC isolation. By evaluating the limitations of EpCAM-mediated capture and the challenges posed by epithelial-to-mesenchymal transition, we aim to provide insights into the development of more comprehensive liquid biopsy approaches for cancer management.},
	year = {2025},
	eissn = {1420-3049},
	orcid-numbers = {Szerényi, Dóra/0000-0002-4615-1926; Járvás, Gábor/0000-0002-9289-6304; Guttman, András/0000-0002-7838-082X}
}

@article{MTMT:35795725,
	title = {Potential Glycobiomarkers in Maternal Obesity and Gestational Diabetes During Human Pregnancy},
	url = {https://m2.mtmt.hu/api/publication/35795725},
	author = {Farkas, Anna and Surányi, Andrea and Kolcsár, Bálint and Gyurkovits, Zita and Kozinszky, Zoltán and Sandor, G. Vari and Guttman, András},
	doi = {10.3390/jcm14051626},
	journal-iso = {J CLIN MED},
	journal = {JOURNAL OF CLINICAL MEDICINE},
	volume = {14},
	unique-id = {35795725},
	abstract = {Introduction: Obesity is a rapidly growing common health problem worldwide that can lead to the development of gestational diabetes mellitus (GDM). However, GDM not only affects women with obesity but can also develop at any time, even after the OGTT test; therefore, an increasing number of complications related to GDM can be seen in both mothers and their children. It is necessary to discover biomarkers capable of indicating the development of GDM or complications during/after pregnancy. Since the N-glycosylation motif of human IgG has been described to change under many physiological and pathological conditions, it is a promising target for biomarker research. In our study, the effects of obesity and GDM were investigated on human serum IgG N-linked glycosylation patterns during human pregnancy. Materials and Methods: The study participants were categorized into four groups according to their body mass index (BMI) and GDM status: normal weight as control, obese (BMI > 30 kg/m2), normal weight with GDM, and obese with GDM. The released N-glycan components of IgG were separated with capillary electrophoresis and detected using a laser-induced fluorescence detector. Results: The result revealed several differences between the N-glycosylation patterns of the four study groups. Of this, 17 of the 20 identified structures differed significantly between the groups. The ratios of sialylated to non-sialylated structures were not changed significantly, but the core fucosylation level showed a significant decrease in the GDM and obese GDM groups compared to the control subjects. The lowest degree of core fucosylation was observed in the GDM group. Conclusions: The findings indicate that obesity in isolation does not have a significant impact on the IgG N-glycosylation pattern in pregnancy. Conversely, alterations in the N-glycan profile of antibodies may serve as biomarkers for the diagnosis of GDM in mothers with a normal BMI, although more evidence is needed. By incorporating glycan-based biomarkers into clinical practice, healthcare providers can improve early detection, personalize management strategies, and potentially mitigate adverse pregnancy outcomes associated with obesity and GDM.
		Keywords:
		capillary electrophoresis; gestational diabetes mellitus; human IgG N-glycome; maternal obesity; molecular diagnostics},
	year = {2025},
	eissn = {2077-0383},
	orcid-numbers = {Surányi, Andrea/0000-0002-1168-7261; Gyurkovits, Zita/0000-0002-7069-9473; Kozinszky, Zoltán/0000-0001-7485-9895; Guttman, András/0000-0002-7838-082X}
}

@article{MTMT:36123222,
	title = {Rapid baseline hump-free analysis of therapeutic proteins in a wide molecular weight range by SDS - capillary agarose gel electrophoresis},
	url = {https://m2.mtmt.hu/api/publication/36123222},
	author = {Sárközy, Dániel and Farkas, Anna and Guttman, András},
	doi = {10.1016/j.aca.2025.344147},
	journal-iso = {ANAL CHIM ACTA},
	journal = {ANALYTICA CHIMICA ACTA},
	volume = {2025},
	unique-id = {36123222},
	issn = {0003-2670},
	year = {2025},
	eissn = {1873-4324},
	pages = {344147},
	orcid-numbers = {Guttman, András/0000-0002-7838-082X}
}

@article{MTMT:36172614,
	title = {Improved analytical workflow towards machine learning supported N-glycomics-based biomarker discovery},
	url = {https://m2.mtmt.hu/api/publication/36172614},
	author = {Fogarassyné Vathy, Ágnes and Gombás, Veronika and Török, Rebeka and Járvás, Gábor and Guttman, András},
	doi = {10.1016/j.talanta.2025.128389},
	journal-iso = {TALANTA},
	journal = {TALANTA},
	volume = {295},
	unique-id = {36172614},
	issn = {0039-9140},
	year = {2025},
	eissn = {1873-3573},
	pages = {128389},
	orcid-numbers = {Fogarassyné Vathy, Ágnes/0000-0002-5524-1675; Járvás, Gábor/0000-0002-9289-6304; Guttman, András/0000-0002-7838-082X}
}

@article{MTMT:36189639,
	title = {Hypoxia-Induced Changes in Endothelial Cell Phenotype and Function},
	url = {https://m2.mtmt.hu/api/publication/36189639},
	author = {Tóth, Andrea and Jeney, Viktória},
	doi = {10.1089/ars.2025.1022},
	journal-iso = {ANTIOXID REDOX SIGNAL},
	journal = {ANTIOXIDANTS & REDOX SIGNALING},
	unique-id = {36189639},
	issn = {1523-0864},
	abstract = {Significance: Endothelial cells (ECs) are specialized cells lining the interior surface of blood vessels, playing a crucial role in vascular biology. They exhibit remarkable versatility, adapting to various tissue requirements. Their ability to respond to physiological and pathological stimuli ensures proper tissue function and homeostasis. Recent Advances: Hypoxia is when the oxygen level in a given organ, tissue, or cell type drops below the physiological level and is insufficient to maintain adequate homeostasis. ECs respond to hypoxia by activating various mechanisms. Hypoxia-induced changes in ECs can promote survival in low-oxygen environments by altering cellular metabolism and inducing neoangiogenesis. However, hypoxia-induced EC responses can also be detrimental, leading to increased production of reactive oxygen species, heightened inflammation, changes in vascular tone, increased permeability of the endothelial barrier, and a higher risk of coagulation. Critical Issues: Hypoxia-induced EC responses contribute to the pathogenesis of various diseases, including metabolic diseases (e.g., diabetes, chronic kidney disease), infectious diseases, chronic inflammation, neoplastic diseases, cardiovascular diseases (e.g., atherosclerosis, myocardial infarction, and stroke) lung diseases (e.g., chronic obstructive pulmonary disease and pulmonary hypertension), eye diseases (age-related macular degeneration and retinopathy), and neurodegenerative diseases (e.g., Alzheimer’s disease and Parkinson’s disease). Future Directions: Detailed, disease-specific investigations are essential to delineate how endothelial hypoxia responses contribute to various pathologies. Understanding these mechanisms could reveal whether targeting endothelial hypoxia holds therapeutic potential. Antioxid. Redox Signal. 00, 000-000. Copyright 2025, Mary Ann Liebert, Inc., publishers.},
	keywords = {Inflammation; ATHEROSCLEROSIS; metabolism; Reactive oxygen species; HYPOXIA; Endothelial cell},
	year = {2025},
	eissn = {1557-7716}
}