TY - JOUR AU - Sápi, Johanna TI - Finding Maximum Tolerated Dose in Phase I Oncology Clinical Trials with Bayesian Methods JF - ACTA POLYTECHNICA HUNGARICA J2 - ACTA POLYTECH HUNG VL - 21 PY - 2024 IS - 6 SP - 129 EP - 145 PG - 17 SN - 1785-8860 UR - https://m2.mtmt.hu/api/publication/34718775 ID - 34718775 LA - English DB - MTMT ER - TY - JOUR AU - Sápi, Zoltán AU - Lippai, Zoltán AU - Papp, Gergő AU - Hegyi, Lajos AU - Sápi, Johanna AU - Dezső, Katalin AU - Szuhai, Károly TI - Nodular fasciitis: a comprehensive, time-correlated investigation of 17 cases JF - MODERN PATHOLOGY J2 - MODERN PATHOL VL - 34 PY - 2021 IS - 12 SP - 2192 EP - 2199 PG - 8 SN - 0893-3952 DO - 10.1038/s41379-021-00883-x UR - https://m2.mtmt.hu/api/publication/32127306 ID - 32127306 N1 - Export Date: 22 April 2024; CODEN: MODPE LA - English DB - MTMT ER - TY - JOUR AU - Drexler, Dániel András AU - Sápi, Johanna AU - Kovács, Levente TI - H∞ control of nonlinear systems with positive input with application to antiangiogenic therapy JF - IFAC PAPERSONLINE J2 - IFACOL VL - 51 PY - 2018 IS - 25 SP - 146 EP - 151 PG - 6 SN - 2405-8971 DO - 10.1016/j.ifacol.2018.11.096 UR - https://m2.mtmt.hu/api/publication/31546506 ID - 31546506 AB - There are many systems in practice that can have only positive (nonnegative) input, typical examples for such systems are physiological systems. Moreover, the parameters of these systems are usually not known exactly or may vary over time, thus application of robust controllers represents a reasonable possibility. Most model-based controller design methods are developed for systems that can (or must) have negative and positive inputs as well, thus a dynamical extension is given here to the original system that ensures that the input of the original system is positive but the extended system can have negative input as well. The current paper investigates a robust control design method with positive input for an automatic therapy possibility in the case of antiangiogenic targeted molecular therapy using a recently published tumor growth model based on mice experiments. The extended system is transformed into an integrator series that is further modified using state-feedback to prepare the system for H-infinity norm-based controller synthesis. The simulations demonstrate the robustness of the controller and the positivity of the input. (C) 2018, IFAC (International Federation of Automatic Control) Hosting by Elsevier Ltd. All rights reserved. LA - English DB - MTMT ER - TY - JOUR AU - Czakó, Bence Géza AU - Sápi, Johanna AU - Kovács, Levente TI - Optimal PID Based Computed Torque Control of Tumor Growth Models JF - IFAC PAPERSONLINE J2 - IFACOL VL - 51 PY - 2018 IS - Ghent SP - 900 EP - 905 PG - 6 SN - 2405-8971 DO - 10.1016/j.ifacol.2018.06.109 UR - https://m2.mtmt.hu/api/publication/27606372 ID - 27606372 LA - English DB - MTMT ER - TY - JOUR AU - Mihály, Dóra AU - Papp, Gergő AU - Mervai, Zsolt AU - Reszegi, Andrea AU - Tátrai, Péter AU - Szalóki, Gábor AU - Sápi, Johanna AU - Sápi, Zoltán TI - The oncomir face of microRNA-206: A permanent miR-206 transfection study. JF - EXPERIMENTAL BIOLOGY AND MEDICINE J2 - EXP BIOL MED VL - 243 PY - 2018 IS - 12 SP - 1014 EP - 1023 PG - 10 SN - 1535-3702 DO - 10.1177/1535370218795406 UR - https://m2.mtmt.hu/api/publication/3407974 ID - 3407974 N1 - 1st Department of Pathology and Experimental Cancer Research, Semmelweis University, Budapest, H-1085, Hungary Solvo Biotechnology, Budaörs, H-2040, Hungary Óbuda University, University Research, Innovation and Service Center, Physiological Controls Research Center, Budapest, H-1034, Hungary Cited By :1 Export Date: 11 March 2020 CODEN: EBMMB Correspondence Address: Sápi, Z.; 1st Department of Pathology and Experimental Cancer Research, Semmelweis UniversityHungary; email: sapi.zoltan.dr@gmail.com 1st Department of Pathology and Experimental Cancer Research, Semmelweis University, Budapest, H-1085, Hungary Solvo Biotechnology, Budaörs, H-2040, Hungary Óbuda University, University Research, Innovation and Service Center, Physiological Controls Research Center, Budapest, H-1034, Hungary Cited By :1 Export Date: 16 June 2020 CODEN: EBMMB Correspondence Address: Sápi, Z.; 1st Department of Pathology and Experimental Cancer Research, Semmelweis UniversityHungary; email: sapi.zoltan.dr@gmail.com Chemicals/CAS: glucose 6 phosphate dehydrogenase, 37259-83-9, 9001-40-5; MicroRNAs; MIRN206 microRNA, human; SMARCB1 Protein; SMARCB1 protein, human 1st Department of Pathology and Experimental Cancer Research, Semmelweis University, Budapest, H-1085, Hungary Solvo Biotechnology, Budaörs, H-2040, Hungary Óbuda University, University Research, Innovation and Service Center, Physiological Controls Research Center, Budapest, H-1034, Hungary Cited By :3 Export Date: 10 May 2021 CODEN: EBMMB Correspondence Address: Sápi, Z.; 1st Department of Pathology and Experimental Cancer Research, Hungary; email: sapi.zoltan.dr@gmail.com AB - MiR-206 is a remarkable miRNA because it functions as a suppressor miRNA in rhabdomyosarcoma while at the same time, as previously showed, it can act as an oncomiRNA in SMARCB1 immunonegative soft tissue sarcomas. The aim of this study was to investigate the effect of miR-206 on its several target genes in various human tumorous and normal cell lines. In the current work, we created miR-206-overexpressing cell lines (HT-1080, Caco2, iASC, and SS-iASC) using permanent transfection. mRNA expression of the target genes of miR-206 (SMARCB1, ACTL6A, CCND1, POLA1, NOTCH3, MET, and G6PD) and SMARCB1 protein expression were examined with quantitative real-time polymerase chain reaction, immunoblotting, immunocytochemistry, and flow cytometry. MiRNA inhibition was used to validate our results. We found a diverse silencing effect of miR-206 on its target genes. While an overall tendency of downregulation was noted, expression profiles of individual cell lines showed large variability. Only CCND1 and MET were consistently downregulated. MiR-206 had an antiproliferative effect on a normal human fibroblast cell line. A strong silencing effect of SMARCB1 in miR-206 transfected SS-iASC was most likely caused by the synergic influence of the SS18-SSX1 fusion protein and miR-206. In the same cell line, a moderate decrease of SMARCB1 protein expression could be observed with immunocytochemistry and flow cytometry. In the most comprehensive analysis of miR-206 effects so far, a modest but significant downregulation of miR-206 targets on the mRNA level was confirmed across all cell lines. However, the variability of the effect shows that the action of this miRNA is largely cell context-dependent. Our results also support the conception that the oncomiR effect of miR-206 on SMARCB1 plays an important but not exclusive role in SMARCB1 immunonegative soft tissue sarcomas so it can be considered important in planning the targeted therapy of these tumors in the future. Impact statement Mir-206 is a very unique microRNA because it can act as a suppressor miRNA or as an oncomiRNA depending on the tumor tissue. In SMARCB1 negative soft tissue sarcomas miR-206 is overexpressed, so thus in epithelioid and synovial sarcomas it functions as an oncomiRNA. MiR-206 has diverse silencing effects on its target genes. We found that the action of miR-206 is largely cell context dependent. The oncomiR role of miR-206 is crucial but not exclusive in SMARCB1 negative soft tissue sarcomas and miR-206 has an antiproliferative effect on a normal human fibroblast cell line. Expressions of miR-206 targets observed in tumors can only be reproduced in the corresponding tumorous cell lines. This is the first study which examined the permanent effect of miR-206 on its target genes in normal, tumor, and genetically engineered cell lines. LA - English DB - MTMT ER - TY - CHAP AU - Csercsik, Dávid AU - Sápi, Johanna AU - Kovács, Levente ED - Jakob, Stoustrup ED - Thomas, Parisini ED - Kristin, Y Pettersen TI - Model-based simulation and comparison of open-loop and closed-loop combined therapies for tumor treatment T2 - Proceedings of the 2018 IEEE Conference on Control Technology and Applications PB - IEEE CY - New York, New York SN - 9781538676974 PY - 2018 SP - 1383 EP - 1388 PG - 6 DO - 10.1109/CCTA.2018.8511526 UR - https://m2.mtmt.hu/api/publication/3407348 ID - 3407348 AB - Targeted molecular therapies opened new ways and increased the efficiency of cancer therapies. Antiangiogenic therapy focuses against the growth of tumor by blocking the blood vessel formation of it. Its control engineering perspective has been presented several times, but its key point represents modeling the tumor growth. The purpose of our research is to go beyond the already published minimalistic approach and set up a bi-compartmental (vasculature-dependent tumor growth and angiogenesis) model. The aim of the current paper is to extend our recently published dynamical bicompartmetal model to include the effect of not only for antiangiogenic, but also cytotoxic drugs as well as input. We compare the effect of the two different inputs on the model dynamics in the context of final tumor volume, which can be used as a measure of therapy effectiveness. According to the model prediction, the combination of drugs is more efficient compared to either monotherapy. Furthermore, we compare an optimized open-loop protocol with a very simple intuitive feedback therapy solution. LA - English DB - MTMT ER - TY - CHAP AU - Csercsik, Dávid AU - Sápi, Johanna AU - Tamás, Gönczy AU - Kovács, Levente ED - IEEE, , TI - Bi-compartmental modelling of tumor and supporting vasculature growth dynamics for cancer treatment optimization purpose T2 - 2017 IEEE 56th Annual Conference on Decision and Control, CDC 2017 PB - IEEE CY - Piscataway (NJ) SN - 9781509028733 PY - 2018 SP - 4698 EP - 4702 PG - 5 DO - 10.1109/CDC.2017.8264353 UR - https://m2.mtmt.hu/api/publication/3320070 ID - 3320070 LA - English DB - MTMT ER - TY - JOUR AU - Drexler, Dániel András AU - Sápi, Johanna AU - Kovács, Levente TI - Optimal discrete time control of antiangiogenic tumor therapy JF - IFAC PAPERSONLINE J2 - IFACOL VL - 50 PY - 2017 IS - 1 SP - 13504 EP - 13509 PG - 6 SN - 2405-8971 DO - 10.1016/j.ifacol.2017.08.2337 UR - https://m2.mtmt.hu/api/publication/27348698 ID - 27348698 LA - English DB - MTMT ER - TY - JOUR AU - Drexler, Dániel András AU - Sápi, Johanna AU - Kovács, Levente TI - Modeling of Tumor Growth Incorporating the Effects of Necrosis and the Effect of Bevacizumab JF - COMPLEXITY J2 - COMPLEXITY VL - 2017 PY - 2017 PG - 10 SN - 1076-2787 DO - 10.1155/2017/5985031 UR - https://m2.mtmt.hu/api/publication/3309515 ID - 3309515 LA - English DB - MTMT ER - TY - JOUR AU - Csercsik, Dávid AU - Sápi, Johanna AU - Kovács, Levente TI - A bicompartmental dynamic tumor growth model JF - IFAC PAPERSONLINE J2 - IFACOL VL - 50 PY - 2017 IS - 1 SP - 12216 EP - 12221 PG - 6 SN - 2405-8971 DO - 10.1016/j.ifacol.2017.08.2119 UR - https://m2.mtmt.hu/api/publication/3307426 ID - 3307426 LA - English DB - MTMT ER -