@article{MTMT:34875002,
	title = {Extracellular vesicles promote migration despite BRAF inhibitor treatment in malignant melanoma cells.},
	url = {https://m2.mtmt.hu/api/publication/34875002},
	author = {Németh, Afrodité and Bányai, Gréta L and Dobos, Nikolett K and Kós, Tamás and Gaál, Anikó and Varga, Zoltán and Buzás, Edit Irén and Khamari, Delaram and Dank, Magdolna and Takács, István and Szász, Attila Marcell and Garay, Tamás},
	doi = {10.1186/s12964-024-01660-4},
	journal-iso = {CELL COMM SIGN},
	journal = {CELL COMMUNICATION AND SIGNALING},
	volume = {22},
	unique-id = {34875002},
	issn = {1478-811X},
	abstract = {Extracellular vesicles (EVs) constitute a vital component of intercellular communication, exerting significant influence on metastasis formation and drug resistance mechanisms. Malignant melanoma (MM) is one of the deadliest forms of skin cancers, because of its high metastatic potential and often acquired resistance to oncotherapies. The prevalence of BRAF mutations in MM underscores the importance of BRAF-targeted therapies, such as vemurafenib and dabrafenib, alone or in combination with the MEK inhibitor, trametinib. This study aimed to elucidate the involvement of EVs in MM progression and ascertain whether EV-mediated metastasis promotion persists during single agent BRAF (vemurafenib, dabrafenib), or MEK (trametinib) and combined BRAF/MEK (dabrafenib/trametinib) inhibition.Using five pairs of syngeneic melanoma cell lines, we assessed the impact of EVs - isolated from their respective supernatants - on melanoma cell proliferation and migration. Cell viability and spheroid growth assays were employed to evaluate proliferation, while migration was analyzed through mean squared displacement (MSD) and total traveled distance (TTD) measurements derived from video microscopy and single-cell tracking.Our results indicate that while EV treatments had remarkable promoting effect on cell migration, they exerted only a modest effect on cell proliferation and spheroid growth. Notably, EVs demonstrated the ability to mitigate the inhibitory effects of BRAF inhibitors, albeit they were ineffective against a MEK inhibitor and the combination of BRAF/MEK inhibitors. In summary, our findings contribute to the understanding of the intricate role played by EVs in tumor progression, metastasis, and drug resistance in MM.},
	keywords = {cell migration; Melanoma; Extracellular vesicles; Vemurafenib; Trametinib; dabrafenib; Single cell tracking},
	year = {2024},
	eissn = {1478-811X},
	orcid-numbers = {Buzás, Edit Irén/0000-0002-3744-206X; Dank, Magdolna/0000-0002-4442-8733; Takács, István/0000-0002-7810-4833; Szász, Attila Marcell/0000-0003-2739-4196; Garay, Tamás/0000-0003-0329-9207}
}

@article{MTMT:34857935,
	title = {Can long-read sequencing tackle the barriers, which the next-generation could not? A review},
	url = {https://m2.mtmt.hu/api/publication/34857935},
	author = {Szakállas, Nikolett and Barták, Barbara Kinga and Valcz, Gábor and Nagy, Zsófia Brigitta and Takács, István and Molnár, Béla},
	doi = {10.3389/pore.2024.1611676},
	journal-iso = {PATHOL ONCOL RES},
	journal = {PATHOLOGY AND ONCOLOGY RESEARCH},
	volume = {30},
	unique-id = {34857935},
	issn = {1219-4956},
	abstract = {The large-scale heterogeneity of genetic diseases necessitated the deeper examination of nucleotide sequence alterations enhancing the discovery of new targeted drug attack points. The appearance of new sequencing techniques was essential to get more interpretable genomic data. In contrast to the previous short-reads, longer lengths can provide a better insight into the potential health threatening genetic abnormalities. Long-reads offer more accurate variant identification and genome assembly methods, indicating advances in nucleotide deflect-related studies. In this review, we introduce the historical background of sequencing technologies and show their benefits and limits, as well. Furthermore, we highlight the differences between short- and long-read approaches, including their unique advances and difficulties in methodologies and evaluation. Additionally, we provide a detailed description of the corresponding bioinformatics and the current applications.},
	year = {2024},
	eissn = {1532-2807},
	orcid-numbers = {Valcz, Gábor/0000-0002-7109-3529; Takács, István/0000-0002-7810-4833; Molnár, Béla/0000-0001-6655-7942}
}

@{MTMT:34817497,
	title = {Kalcium-anyagcsere zavarai, osteoporosis},
	url = {https://m2.mtmt.hu/api/publication/34817497},
	author = {Horváth, Csaba and Takács, István},
	booktitle = {Belgyógyászat 1 tantárgyi jegyzet},
	unique-id = {34817497},
	year = {2024},
	pages = {170-185},
	orcid-numbers = {Horváth, Csaba/0000-0002-0490-7932; Takács, István/0000-0002-7810-4833}
}

@{MTMT:34804137,
	title = {A mellékpajzsmirigy betegségei},
	url = {https://m2.mtmt.hu/api/publication/34804137},
	author = {Takács, István},
	booktitle = {Belgyógyászat 1 tantárgyi jegyzet},
	unique-id = {34804137},
	year = {2024},
	pages = {70-72},
	orcid-numbers = {Takács, István/0000-0002-7810-4833}
}

@{MTMT:34804134,
	title = {Pajzsmirigyhormon-adaptációs szindróma (nonthyroidal illness – PASz)},
	url = {https://m2.mtmt.hu/api/publication/34804134},
	author = {Takács, István},
	booktitle = {Belgyógyászat 1 tantárgyi jegyzet},
	unique-id = {34804134},
	year = {2024},
	pages = {68-69},
	orcid-numbers = {Takács, István/0000-0002-7810-4833}
}

@{MTMT:34803088,
	title = {Hyperthyreosis},
	url = {https://m2.mtmt.hu/api/publication/34803088},
	author = {Bakos, Bence and Takács, István},
	booktitle = {Belgyógyászat 1 tantárgyi jegyzet},
	unique-id = {34803088},
	year = {2024},
	pages = {46-49},
	orcid-numbers = {Bakos, Bence/0000-0003-2073-6536; Takács, István/0000-0002-7810-4833}
}

@book{MTMT:34802851,
	title = {Belgyógyászat 1 tantárgyi jegyzet},
	url = {https://m2.mtmt.hu/api/publication/34802851},
	isbn = {9789633316122},
	editor = {Takács, István},
	publisher = {Semmelweis Kiadó és Multimédia Stúdió},
	unique-id = {34802851},
	year = {2024},
	orcid-numbers = {Takács, István/0000-0002-7810-4833}
}

@article{MTMT:34795043,
	title = {Analysis of SIRT1 Gene SNPs and Clinical Characteristics in Medication-Related Osteonecrosis of the Jaw},
	url = {https://m2.mtmt.hu/api/publication/34795043},
	author = {Bojtor, Bence and Vaszilkó, Mihály Tamás and Ármós, Richárd Levente and Tóbiás, Bálint and Podani, János and Szentpéteri, Szófia Katalin and Balla, Bernadett and Lengyel, Balazs and Pikó, Henriett and Illés, Anett and Kiss, András and Putz, Zsuzsanna and Takács, István and Kósa, János and Lakatos, Péter},
	doi = {10.3390/ijms25073646},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {25},
	unique-id = {34795043},
	issn = {1661-6596},
	abstract = {Certain genetic factors, including single-nucleotide polymorphisms (SNPs) in the SIRT1 gene, have been linked to medication-related osteonecrosis of the jaw (MRONJ). This study examined four SNPs in the SIRT1 gene and implemented multivariate statistical analysis to analyze genetic and clinical factors in MRONJ patients. Genomic DNA was isolated from peripheral blood samples of 63 patients of European origin treated for MRONJ, and four SNP genotypes in the gene encoding the SIRT-1 protein were determined by Sanger sequencing. The allele frequencies measured in the MRONJ population were compared with allele frequencies measured in the European population in the National Center for Biotechnology Information Allele Frequency Aggregator (NCBI ALFA) database. Genetic and clinical factors were examined with multivariate statistical analysis. A C:A allele distribution ratio of 77.8:22.2 was measured in the rs932658 SNP. In the ALFA project, a C:A allele distribution ratio of 59.9:40.1 was detected in the European population, which was found to be a significant difference (p = 4.5 × 10−5). Multivariate statistical analysis revealed a positive correlation (0.275) between the genotype of SNP rs932658 and the number of stages improved during appropriate MRONJ therapy. It is concluded that allele A in SNP rs932658 in the SIRT1 gene acts as a protective factor in MRONJ.},
	year = {2024},
	eissn = {1422-0067},
	orcid-numbers = {Vaszilkó, Mihály Tamás/0000-0002-2570-0009; Tóbiás, Bálint/0000-0003-4343-1866; Podani, János/0000-0002-1452-1486; Szentpéteri, Szófia Katalin/0000-0003-0073-4154; Balla, Bernadett/0000-0003-2465-1804; Pikó, Henriett/0000-0002-3579-5451; Illés, Anett/0000-0001-5351-9015; Putz, Zsuzsanna/0000-0002-0674-337X; Takács, István/0000-0002-7810-4833; Lakatos, Péter/0000-0002-7652-3671}
}

@article{MTMT:34780698,
	title = {Az első hazai tapasztalatok összegzése kromoszomális microarray-analízis és teljesexom-szekvenálás módszerekkel a magzati diagnosztikában},
	url = {https://m2.mtmt.hu/api/publication/34780698},
	author = {Pikó, Henriett and Illés, Anett and Nagy, Sándor and Beke, Artúr and Árvai, Kristóf and Elekes, Tibor and Ferdinandyné Horváth, Emese and Ferenczy, Miklós and Mosonyi, Péter and Lukács, Valéria and Klujber, Valéria and Török, Olga and Kiss, Zsuzsanna and P Tardy, Erika and Tidrenczel, Zsolt and Tóbiás, Bálint and Balla, Bernadett and Lakatos, Péter and Kósa, János and Takács, István},
	doi = {10.1556/650.2024.33028},
	journal-iso = {ORV HETIL},
	journal = {ORVOSI HETILAP},
	volume = {165},
	unique-id = {34780698},
	issn = {0030-6002},
	abstract = {Bevezetés: Az elmúlt évtized egyik jelentős technológiai újdonsága az ún. ’high-throughput’ molekuláris genetikai vizsgálati módszerek – mint a kromoszomális microarray-analízis (chromosomal microarray analysis, CMA) és a teljesexom-szekvenálás (whole-exome sequencing, WES) – elterjedése a praenatalis diagnosztikában. Célkitűzés: Az elmúlt 5 évben munkacsoportunk több mint 252 praenatalis vizsgálatot végzett hazai laboratóriumi háttérrel, amelyek indikációját különböző súlyosságú strukturális magzati ultrahangeltérések képezték. A klasszikus citogenetikai vizsgálatok eredményétől függően végeztük el a nagy felbontású CMA- és WES-analíziseket a praenatalis diagnosztika érdekében. Módszer: A CMA-vizsgálatokat a „GeneChip System 3000 Instrument” platformmal végeztük az SNP-alapú komparatív hibridizálás módszerével. Az általunk elvégzett újgenerációs szekvenálás során a teljes humán exom szekvenciájának meghatározása IonTorrent és Illumina platformokkal történt. Eredmények: Összesen 252 magzati CMA-vizsgálatot végeztünk, és 42%-ban mutattunk ki valamilyen hiányt vagy többletet, ebből 22%-ban igazoltunk kóros eltérést. 42 esetben végeztünk WES-t, amelyből 9 esetben (21,4%) azonosítottunk kóros eltérést az öröklésmenetet támogató, a magzati fenotípussal feltételezhetően összefüggésben lévő, a ClinVar adatbázis vagy az ACMG-klasszifikáció alapján. Megbeszélés: Tekintettel arra, hogy a magzati fenotípus értékelése közvetett, a praenatalis CMA- és WES-elemzésnek elsősorban a magzati ultrahangvizsgálat során azonosítható strukturális anomáliákkal összefüggő génekre, kromoszomális régiókra kell korlátozódnia. A szülők vizsgálata mind a CMA-, mind a WES-analízisek során kiemelt jelentőséggel bír, főleg azokban az esetekben, amelyeknél a kapott eltérés nem hozható egyértelmű összefüggésbe az ultrahangeltérésekkel. Következtetés: Fontos meghatározni azokat a paramétereket, amelyek alapján a magzati mintában talált kópiaszám-eltéréseket és WES-vizsgálattal igazolt variánsokat a leletben közöljük (figyelembe véve a nemzetközi ajánlásokat). Ezek alapján a praenatalis klinikai genetikai tanácsadáskor sokkal használhatóbb információk adhatók. Orv Hetil. 2024; 165(14): 523–530.},
	year = {2024},
	eissn = {1788-6120},
	pages = {523-530},
	orcid-numbers = {Pikó, Henriett/0000-0002-3579-5451; Illés, Anett/0000-0001-5351-9015; Beke, Artúr/0000-0002-6826-7751; Árvai, Kristóf/0000-0001-8774-937X; Tidrenczel, Zsolt/0000-0001-7223-1551; Tóbiás, Bálint/0000-0003-4343-1866; Balla, Bernadett/0000-0003-2465-1804; Lakatos, Péter/0000-0002-7652-3671; Takács, István/0000-0002-7810-4833}
}

@article{MTMT:34729561,
	title = {An Open-Label Phase 2 Study of Eneboparatide, a Novel PTH Receptor 1 Agonist, in Hypoparathyroidism},
	url = {https://m2.mtmt.hu/api/publication/34729561},
	author = {Takács, István and Mezősi, Emese and Soto, Alfonso and Kamenický, Peter and Figueres, Lucile and Galvez Moreno, Maria Angeles and Lemoine, Sandrine and Borson-Chazot, Francoise and Capel, Ismael and Ouldrouis, Taha and Lucas, Nadège and Allas, Soraya and Sumeray, Mark and Ovize, Michel and Mannstadt, Michael},
	doi = {10.1210/clinem/dgae121},
	journal-iso = {J CLIN ENDOCR METAB},
	journal = {JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM},
	unique-id = {34729561},
	issn = {0021-972X},
	abstract = {Hypoparathyroidism is a rare disorder characterized by a deficiency in parathyroid hormone (PTH) resulting in hypocalcemia, hyperphosphatemia, and hypercalciuria. Eneboparatide is an investigational peptide agonist of the PTH1 receptor for the treatment of chronic hypoparathyroidism (HP).To evaluate the efficacy, safety, and tolerability of eneboparatide in HP patients.Open-label, phase 2 study.Twenty-eight patients (21 women, 7 men), mean age (range): 58 years (28-72), with HP were enrolled into 2 consecutive cohorts (C1, n = 12, and C2, n = 16).Following an optimization period, daily subcutaneous injections of eneboparatide were administered for 3 months at 20 µg/day (C1) or 10 µg/day (C2) starting dose. Conventional therapy was progressively removed and eneboparatide could be titrated up to 60 µg (C1) or 80 µg (C2).Proportion of patients achieving independence from conventional therapy, albumin-adjusted serum calcium (ADsCa), 24-h urine calcium (uCa), serum bone turnover markers (s-CTX and P1NP), bone mineral density (BMD), and adverse events (AEs).After 3 months,  ≥ 88% patients achieved independence from conventional therapy while mean ADsCa was maintained within target range (7.8-9 mg/dL). Eneboparatide induced a rapid and sustained reduction of mean 24-hour uCa, even among patients with hypercalciuria. Bone turnover markers slightly increased and BMD remained unchanged, consistent with progressive resumption of physiologic bone turnover. Eneboparatide was well tolerated with no serious AEs.Eneboparatide allowed independence from conventional therapy and maintenance of serum calcium within a target range, while normalizing uCa excretion and producing a balanced resumption of bone turnover.},
	keywords = {calcium; REPLACEMENT THERAPY; Parathyroid Hormone; hypoparathyroidism; bone biomarkers; eneboparatide},
	year = {2024},
	eissn = {1945-7197},
	orcid-numbers = {Takács, István/0000-0002-7810-4833; Mezősi, Emese/0000-0001-9367-3877}
}