@article{MTMT:34820368,
	title = {In Vivo Imaging of Acute Hindlimb Ischaemia in Rat Model: A Pre-Clinical PET Study},
	url = {https://m2.mtmt.hu/api/publication/34820368},
	author = {Farkasinszky, Gergely and Péliné Szabó, Judit and Károlyi, Péter and Rácz, Szilvia and Dénes, Noémi and Papp, Tamás and Király, József and Szabó, Zsuzsanna and Kertész, István and Mező, Gábor and Halmos, Gábor and Képes, Zita and Trencsényi, György},
	doi = {10.3390/pharmaceutics16040542},
	journal-iso = {PHARMACEUTICS},
	journal = {PHARMACEUTICS},
	volume = {16},
	unique-id = {34820368},
	issn = {1999-4923},
	abstract = {Background: To better understand ischaemia-related molecular alterations, temporal changes in angiogenic Aminopeptidase N (APN/CD13) expression and glucose metabolism were assessed with PET using a rat model of peripheral arterial disease (PAD). Methods: The mechanical occlusion of the base of the left hindlimb triggered using a tourniquet was applied to establish the ischaemia/reperfusion injury model in Fischer-344 rats. 2-[18F]FDG and [68Ga]Ga-NOTA-c(NGR) PET imaging performed 1, 3, 5, 7, and 10 days post-ischaemia induction was followed by Western blotting and immunohistochemical staining for APN/CD13 in ischaemic and control muscle tissue extracts. Results: Due to a cellular adaptation to hypoxia, a gradual increase in [68Ga]Ga-NOTA-c(NGR) and 2-[18F]FDG uptake was observed from post-intervention day 1 to 7 in the ischaemic hindlimbs, which was followed by a drop on day 10. Conforming pronounced angiogenic recovery, the NGR accretion of the ischaemic extremities differed significantly from the controls 5, 7, and 10 days after ischaemia induction (p ≤ 0.05), which correlated with the Western blot and immunohistochemical results. No remarkable radioactivity was depicted between the normally perfused hindlimbs of either the ischaemic or the control groups. Conclusions: The PET-based longitudinal assessment of angiogenesis-associated APN/CD13 expression and glucose metabolism during ischaemia may continue to broaden our knowledge on the pathophysiology of PAD.},
	year = {2024},
	eissn = {1999-4923},
	orcid-numbers = {Mező, Gábor/0000-0002-7618-7954; Képes, Zita/0000-0003-2889-8521; Trencsényi, György/0000-0001-6456-6212}
}

@article{MTMT:34534306,
	title = {DNA methylome, R-loop and clinical exome profiling of patients with sporadic amyotrophic lateral sclerosis},
	url = {https://m2.mtmt.hu/api/publication/34534306},
	author = {Feró, Orsolya and Varga, Dóra and Nagy, Éva and Karányi, Zsolt and Sipos, Éva and Engelhardt, József and Török, Nóra and Balogh, István and Vető, Borbála and Likó, István and Fóthi, Ábel and Szabó, Zoltán and Halmos, Gábor and Vécsei, László and Arányi, Tamás and Székvölgyi, Lóránt},
	doi = {10.1038/s41597-024-02985-y},
	journal-iso = {SCI DATA},
	journal = {SCIENTIFIC DATA},
	volume = {11},
	unique-id = {34534306},
	abstract = {Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by the death of motor neurons, the aetiology of which is essentially unknown. Here, we present an integrative epigenomic study in blood samples from seven clinically characterised sporadic ALS patients to elucidate molecular factors associated with the disease. We used clinical exome sequencing (CES) to study DNA variants, DNA-RNA hybrid immunoprecipitation sequencing (DRIP-seq) to assess R-loop distribution, and reduced representation bisulfite sequencing (RRBS) to examine DNA methylation changes. The above datasets were combined to create a comprehensive repository of genetic and epigenetic changes associated with the ALS cases studied. This repository is well-suited to unveil new correlations within individual patients and across the entire patient cohort. The molecular attributes described here are expected to guide further mechanistic studies on ALS, shedding light on the underlying genetic causes and facilitating the development of new epigenetic therapies to combat this life-threatening disease.},
	year = {2024},
	eissn = {2052-4463},
	orcid-numbers = {Fóthi, Ábel/0000-0001-7398-9700; Vécsei, László/0000-0001-8037-3672}
}

@{MTMT:34212323,
	title = {Signaling mechanism of growth hormone-releasing hormone receptor},
	url = {https://m2.mtmt.hu/api/publication/34212323},
	author = {Halmos, Gábor and Szabó, Zsuzsanna and Juhász, Éva and Andrew, V. Schally},
	booktitle = {Hormone Receptors: Structures and Functions},
	doi = {10.1016/bs.vh.2023.06.004},
	unique-id = {34212323},
	year = {2023},
	pages = {1-26}
}

@article{MTMT:34162579,
	title = {Shikonin Causes an Apoptotic Effect on Human Kidney Cancer Cells through Ras/MAPK and PI3K/AKT Pathways},
	url = {https://m2.mtmt.hu/api/publication/34162579},
	author = {Király, József and Szabó, Erzsébet Katalin and Fodor, Petra and Fejes, Zsolt and Nagy, Béla and Juhász, Éva and Vass, Anna and Choudhury, Mahua and Kónya, Gábor and Halmos, Gábor and Szabó, Zsuzsanna},
	doi = {10.3390/molecules28186725},
	journal-iso = {MOLECULES},
	journal = {MOLECULES},
	volume = {28},
	unique-id = {34162579},
	issn = {1420-3049},
	abstract = {(1) Background: Shikonin, the main ingredient in Chinese herbal medicine, is described as a novel angiogenesis inhibitor, and its anticancer effects have already been studied. Shikonin and its derivatives induce apoptosis and suppress metastasis, which further enhance the effectiveness of chemotherapy. However, their mechanism of function has not been completely elucidated on human renal cancer cells. (2) Methods: In our study, CAKI-2 and A-498 cells were treated with increasing concentrations (2.5–40 µM) of shikonin, when colony formation ability and cytotoxic activity were tested. The changes in the expression of the main targets of apoptotic pathways were measured by RT-qPCR and Western blot. The intracellular levels of miR-21 and miR-155 were quantified by RT-qPCR. (3) Results: Shikonin exerted a dose-dependent effect on the proliferation of the cell lines examined. In 5 µM concentration of shikonin in vitro elevated caspase-3 and -7 levels, the proteins of the Ras/MAPK and PI3K/AKT pathways were activated. However, no significant changes were detected in the miR-21 and miR-155 expressions. (4) Conclusions: Our findings indicated that shikonin causes apoptosis of renal cancer cells by activating the Ras/MAPK and PI3K/AKT pathways. These effects of shikonin on renal cancer cells may bear important potential therapeutic implications for the treatment of renal cancer.},
	year = {2023},
	eissn = {1420-3049}
}

@article{MTMT:34131187,
	title = {Radiolabeled NGR-Based Heterodimers for Angiogenesis Imaging : a Review of Preclinical Studies},
	url = {https://m2.mtmt.hu/api/publication/34131187},
	author = {Trencsényi, György and Halmos, Gábor and Képes, Zita},
	doi = {10.3390/cancers15184459},
	journal-iso = {CANCERS},
	journal = {CANCERS},
	volume = {15},
	unique-id = {34131187},
	abstract = {Since angiogenesis/neoangiogenesis has a major role in tumor development, progression and metastatic spread, the establishment of angiogenesis-targeting imaging and therapeutic vectors is of utmost significance. Aminopeptidase N (APN/CD13) is a pivotal biomarker of angiogenic processes abundantly expressed on the cell surface of active vascular endothelial and various neoplastic cells, constituting a valuable target for cancer diagnostics and therapy. Since the asparagine–glycine–arginine (NGR) sequence has been shown to colocalize with APN/CD13, the research interest in NGR-peptide-mediated vascular targeting is steadily growing. Earlier preclinical experiments have already demonstrated the imaging and therapeutic feasibility of NGR-based probes labeled with different positron emission tomography (PET) and single-photon emission computed tomography (SPECT) radionuclides, including Gallium-68 (68Ga), Copper-64 (64Cu), Technetium-99m (99mTc), Lutetium-177 (177Lu), Rhenium-188 (188Re) or Bismuth-213 (213Bi). To improve the tumor binding affinity and the retention time of single-receptor targeting peptides, NGR motifs containing heterodimers have been introduced to identify multi-receptor overexpressing malignancies. Preclinical studies with various tumor-bearing experimental animals provide useful tools for the investigation of the in vivo imaging behavior of NGR-based heterobivalent ligands. Herein, we review the reported preclinical achievements on NGR heterodimers that could be highly relevant for the development of further target-specific multivalent compounds in diagnostic and therapeutic settings.},
	year = {2023},
	eissn = {2072-6694},
	orcid-numbers = {Trencsényi, György/0000-0001-6456-6212; Képes, Zita/0000-0003-2889-8521}
}

@article{MTMT:34083399,
	title = {Potential Role of VHL, PTEN, and BAP1 Mutations in Renal Tumors},
	url = {https://m2.mtmt.hu/api/publication/34083399},
	author = {Szegedi, Krisztián Gábor and Szabó, Zsuzsanna and Kállai, Judit and Király, József and Szabó, Erzsébet and Bereczky, Zsuzsanna and Juhász, Éva and Dezső, Balázs and Szász, Csaba and Zsebik, Barbara and Flaskó, Tibor and Halmos, Gábor},
	doi = {10.3390/jcm12134538},
	journal-iso = {J CLIN MED},
	journal = {JOURNAL OF CLINICAL MEDICINE},
	volume = {12},
	unique-id = {34083399},
	abstract = {The genetic profiling of renal tumors has revealed genomic regions commonly affected by structural changes and a general genetic heterogeneity. The VHL, PTEN, and BAP1 genes are often mutated in renal tumors. The frequency and clinical relevance of these mutations in renal tumors are still being researched. In our study, we investigated VHL, PTEN, and BAP1 genes and the sequencing of 24 samples of patients with renal tumors, revealing that VHL was mutated at a noticeable frequency (25%). Six of the investigated samples showed mutations, and one genetic polymorphism (rs779805) was detected in both heterozygote and homozygote forms. PTEN gene mutation was observed in only one sample, and one specimen showed genetic polymorphism. In the case of the BAP1 gene, all of the samples were wild types. Interestingly, VHL mutation was detected in two female patients diagnosed with AML and in one with oncocytoma. We assume that VHL or PTEN mutations may contribute to the development of human renal cancer. However, the overall mutation rate was low in all specimens investigated, and the development and prognosis of the disease were not exclusively associated with these types of genetic alterations.},
	year = {2023},
	eissn = {2077-0383},
	orcid-numbers = {Bereczky, Zsuzsanna/0000-0002-1483-3703}
}

@CONFERENCE{MTMT:33998813,
	title = {miRNS-ek és angiogenezis markerek kapcsolatának vizsgálata humán vese karcinómában},
	url = {https://m2.mtmt.hu/api/publication/33998813},
	author = {Király, József and Fodor, Petra and Szenthe, Kálmán and Szabó, Erzsébet and Flaskó, Tibor and Szegedi, Krisztián and Zsebik, Barbara and Szász, Csaba and Halmos, Gábor and Szabó, Zsuzsanna},
	booktitle = {Abstract book of the 6th International Cholnoky Symposium},
	unique-id = {33998813},
	year = {2022},
	pages = {10}
}

@article{MTMT:33644566,
	title = {Angiogenezismarkerek és miRNS-ek kapcsolatának vizsgálata humán vesekarcinómában},
	url = {https://m2.mtmt.hu/api/publication/33644566},
	author = {Király, József and Fodor, Petra and Szenthe, Kálmán and Szabó, Erzsébet and Flaskó, Tibor and Szegedi, Krisztián and Zsebik, Barbara and Szász, Csaba and Halmos, Gábor and Szabó, Zsuzsanna},
	journal-iso = {MAGYAR ONKOLÓGIA},
	journal = {MAGYAR ONKOLÓGIA},
	volume = {66},
	unique-id = {33644566},
	issn = {0025-0244},
	year = {2022},
	eissn = {2060-0399},
	pages = {249-250}
}

@CONFERENCE{MTMT:33644517,
	title = {The potential applicability of quercetin in the treatment of uveal melanoma tumour metastases},
	url = {https://m2.mtmt.hu/api/publication/33644517},
	author = {Fodor, Petra and Király, József and Szabó, Zsuzsanna and Halmos, Gábor and Zsebik, Barbara},
	booktitle = {Abstract book of the 6th International Cholnoky Symposium},
	unique-id = {33644517},
	keywords = {PROLIFERATION; MIGRATION; Quercetin; Uveal melanoma; MM28 cells},
	year = {2022},
	pages = {25}
}

@article{MTMT:33604518,
	title = {Quercetin hatásának vizsgálata metasztatikus uveális melanóma sejtvonalon},
	url = {https://m2.mtmt.hu/api/publication/33604518},
	author = {Fodor, Petra and Király, József and Szabó, Zsuzsanna and Halmos, Gábor and Zsebik, Barbara},
	journal-iso = {MAGYAR ONKOLÓGIA},
	journal = {MAGYAR ONKOLÓGIA},
	volume = {66},
	unique-id = {33604518},
	issn = {0025-0244},
	year = {2022},
	eissn = {2060-0399},
	pages = {249}
}