14 results on '"Sarosi V"'
Search Results
2. MODERATED POSTER SESSION: Athletes heart systemic diseases, pulmonary heart disease, miscelaneous disease: Thursday 4 December 2014, 08: 30–18: 00Location: Moderated Poster area
- Author
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Faludi, R, Varga-Nagy, N, Vertes, V, Hajdu, M, Illes, MB, Sarosi, V, and Alexy, G
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- 2014
3. Mitochondrial dysfunction is a key determinant of the rare disease lymphangioleiomyomatosis and provides a novel therapeutic target
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Abdelwahab, E. M. M., primary, Pal, S., additional, Kvell, K., additional, Sarosi, V., additional, Bai, P., additional, Rue, R., additional, Krymskaya, V., additional, McPhail, D., additional, Porter, A., additional, and Pongracz, J. E., additional
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- 2018
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4. 45P Analysis of lung cancer patient pathway: A 6-year nationwide analysis from Hungary
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Bogos, K., Gaffly, G., Kiss, Z., Tamási, L., Ostoros, G., Müller, V., Urbán, L., Bittner, N., Sárosi, V., Vastag, A., Polányi, Z., Daniel, A., Nagy, B., Rokszin, G., Abonyi-Tóth, Z., Barcza, Z., Moldvay, J., and Vokó, Z.
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- 2021
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5. Increased Wnt5a in squamous cell lung carcinoma inhibits endothelial cell motility
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Rapp, J., primary, Kiss, E., additional, Meggyes, M., additional, Szabo-Meleg, E., additional, Feller, D., additional, Smuk, G., additional, Laszlo, T., additional, Sarosi, V., additional, Molnar, T. F., additional, Kvell, K., additional, and Pongracz, J. E., additional
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- 2016
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6. 9175 The effectiveness of erlotinib (Tarceva®) treatment in KRAS negative lung adenocarcinomas – preliminary results of an observational cohort study
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Ostoros, G., Sárosi, V., Losonczy, G., Tolnay, E., and Molnár, L.
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- 2009
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7. MODERATED POSTER SESSION: Athletes heart systemic diseases, pulmonary heart disease, miscelaneous disease: Thursday 4 December 2014, 08:30-18:00 * Location: Moderated Poster area
- Author
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D'ascenzi, F, Cameli, M, Lisi, M, Focardi, M, Andrei, V, Incampo, E, Bonifazi, M, Mondillo, S, Przewlocka-Kosmala, M, Rojek, A, Mysiak, A, Kosmala, W, Spethmann, S, Dreger, H, Meyn, R, Mueller, E, Baumann, G, Quinkler, M, Knebel, F, Enescu, OA, Rimbas, RC, Cinteza, M, Vinereanu, D, 28338/2013, Grant, Addetia, K, Maffessanti, F, Yamat, M, Weinert, L, Mor-Avi, V, Lang, RM, Faludi, R, Varga-Nagy, N, Vertes, V, Hajdu, M, Illes, MB, Sarosi, V, Alexy, G, Hamodraka, E, Kontogiannis, N, Kallistratos, M, Zacharopoulou, I, Zamfir, T, Manetos, C, Siama, K, Tsoukas, A, Skyrlas, A, Manolis, A, Garcia Fuertes, D, Crespin Crespin, M, Villanueva Fernandez, E, Krisdinarti, L, Tarigan, L, Mumpuni, H, Anggrahini, DW, Van De Bruaene, A, La Gerche, A, Claessen, G, De Meester, P, Devroe, S, Bogaert, J, Claus, P, Heidbuchel, H, Gewillig, M, and Budts, W
- Abstract
Purpose: Atrial fibrosis and increased atrial stiffness as substrates for atrial arrhythmias have been supposed in athletes. However, although supported by experimental data, this hypothesis has not been confirmed in humans. Recently, a new non-invasive estimation of left atrial (LA) stiffness, using tissue Doppler imaging and speckle tracking echocardiography (STE), has been validated. The aim of this study was to determine LA stiffness in athletes and to compare it with controls. Methods. 150 top-level athletes and 90 age and sex-matched sedentary subjects were analyzed. STE was use to obtain peak atrial longitudinal strain (PALS) and peak atrial contraction strain (PACS). LA stiffness was determined using E/e’ ratio in conjunction with PALS. Left ventricular (LV) stiffness was also calculated. Results: LA volume index was higher in athletes as compared with controls (24.6±7.3 vs. 18.4±7.8 mL/m2, p<.0001). Both global PALS and global PACS were lower (p<.05 and p≤.001,respectively) and E/e’ ratio was lower in athletes in comparison with controls (4.9±1.2 vs. 6.1±1.4, p<.0001). Although LA size was greater in athletes, they showed a lower LA stiffness as compared with sedentary subjects (0.13±0.04 vs. 0.16±0.06, p≤.001). A lower LV stiffness was also found in athletes (0.84±0.27 vs. 1.07±0.46, p≤.001). LV stiffness was the only independent predictor of LA stiffness (β=0.46, p<.0001) while LV end-systolic volume index was the only independent predictor of LA volume index (β=0.250, p=.002). Conclusions: Competitive athletes had a lower LA stiffness as compared with controls, despite a greater LA size. Thus, our data do not support the concept of an increased LA stiffness in athletes. 2D STE was a reliable and simple tool to non-invasively investigate left atrial stiffness in athletes.
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- 2014
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8. KRAS and EGFR Mutations Differentially Alter ABC Drug Transporter Expression in Cisplatin-Resistant Non-Small Cell Lung Cancer.
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Jaromi L, Csongei V, Vesel M, Abdelwahab EMM, Soltani A, Torok Z, Smuk G, Sarosi V, and Pongracz JE
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- A549 Cells, Aged, Carcinoma, Non-Small-Cell Lung drug therapy, Cell Line, Cell Line, Tumor, Cisplatin pharmacology, ErbB Receptors genetics, Female, Gene Expression genetics, Human Umbilical Vein Endothelial Cells, Humans, Lung Neoplasms drug therapy, Male, Middle Aged, Tumor Microenvironment genetics, ATP-Binding Cassette Transporters genetics, Carcinoma, Non-Small-Cell Lung genetics, Drug Resistance, Multiple genetics, Drug Resistance, Neoplasm genetics, Lung Neoplasms genetics, Mutation genetics, Proto-Oncogene Proteins p21(ras) genetics
- Abstract
Lung carcinoma is still the most common malignancy worldwide. One of the major subtypes of non-small cell lung cancer (NSCLC) is adenocarcinoma (AC). As driver mutations and hence therapies differ in AC subtypes, we theorized that the expression and function of ABC drug transporters important in multidrug resistance (MDR) would correlate with characteristic driver mutations KRAS or EGFR. Cisplatin resistance (CR) was generated in A549 (KRAS) and PC9 (EGFR) cell lines and gene expression was tested. In three-dimensional (3D) multicellular aggregate cultures, both ABCB1 and ABCG2 transporters, as well as the WNT microenvironment, were investigated. ABCB1 and ABCG2 gene expression levels were different in primary AC samples and correlated with specific driver mutations. The drug transporter expression pattern of parental A549 and PC9, as well as A549-CR and PC9-CR, cell lines differed. Increased mRNA levels of ABCB1 and ABCG2 were detected in A549-CR cells, compared to parental A549, while the trend observed in the case of PC9 cells was different. Dominant alterations were observed in LEF1, RHOU and DACT1 genes of the WNT signalling pathway in a mutation-dependent manner. The study confirmed that, in lung AC-s, KRAS and EGFR driver mutations differentially affect both drug transporter expression and the cisplatin-induced WNT signalling microenvironment.
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- 2021
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9. Cisplatin treatment induced interleukin 6 and 8 production alters lung adenocarcinoma cell migration in an oncogenic mutation dependent manner.
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Kiss E, Abdelwahab EHMM, Steib A, Papp E, Torok Z, Jakab L, Smuk G, Sarosi V, and Pongracz JE
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- A549 Cells, Antineoplastic Agents pharmacology, Antineoplastic Agents therapeutic use, Carcinoma, Non-Small-Cell Lung drug therapy, Carcinoma, Non-Small-Cell Lung genetics, Cell Movement drug effects, Cell Movement genetics, Cell Survival drug effects, Cell Survival physiology, Cisplatin pharmacology, Humans, Interleukin-6 genetics, Interleukin-8 genetics, Lung Neoplasms drug therapy, Lung Neoplasms genetics, Mutation drug effects, Carcinoma, Non-Small-Cell Lung metabolism, Cisplatin therapeutic use, Interleukin-6 metabolism, Interleukin-8 metabolism, Lung Neoplasms metabolism, Mutation physiology
- Abstract
Background: The predominant metastatic site of lung cancer (LC) is the brain. Although outdated, conventional cisplatin treatment is still the main therapeutic approach for patients with advanced non-small cell lung cancer (NSCLC), since targeted therapy that offers better tumor control is not always possible. In the present study brain metastasis associated cytokine expression was investigated in primary NSCLC adenocarcinoma (AC) tissues with known oncogenic mutations in the presence or absence of platina based and tyrosine kinase inhibitor (TKI) drugs., Methods: Primary lung tumor samples were isolated, DNA was sequenced and then the samples were grouped based on mutation. Experiments were also performed using KRAS mutant A549 and EGFR mutant PC-9 cells. Drug response was analyzed in three dimensional (3D) tissue cultures. We assessed drug response and IL-6 and IL-8 cytokine expression in relation to cellular invasion using ATP dependent cell viability, qRT-PCR analysis, cytokine bead array, and migration assay., Results: In 3D co-cultures, primary NSCLC derived cells harboring EGFR mutation responded better to erlotinib treatment than KRAS mutant or KRAS/EGFR wild type (WT) cancer cells. In contrast, under the same culture conditions KRAS/EGFR WT or KRAS mutant cancer cells are more sensitive to cisplatin than EGFR mutant cells. Drug response and pro-inflammatory cytokine production varied depending on the driver mutations. Cisplatin but not erlotinib increased both IL-6 and IL-8 secretion and only IL-6 increased cellular migration and proliferation., Conclusion: In vitro assays are available to determine the response to planned therapeutic approach of lung cancer subtypes. The sequence of administration of therapeutic drugs determines cytokine production and therefore therapeutic response.
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- 2020
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10. Cigarette Smoke-Induced Pulmonary Inflammation Becomes Systemic by Circulating Extracellular Vesicles Containing Wnt5a and Inflammatory Cytokines.
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Feller D, Kun J, Ruzsics I, Rapp J, Sarosi V, Kvell K, Helyes Z, and Pongracz JE
- Abstract
Chronic obstructive pulmonary disease (COPD) is a devastating, irreversible pathology affecting millions of people worldwide. Clinical studies show that currently available therapies are insufficient, have no or little effect on elevated comorbidities and on systemic inflammation. To develop alternative therapeutic options, a better understanding of the molecular background of COPD is essential. In the present study, we show that non-canonical and pro-inflammatory Wnt5a is up-regulated by cigarette smoking with parallel up-regulation of pro-inflammatory cytokines in both mouse and human model systems. Wnt5a is not only a pro-inflammatory Wnt ligand but can also inhibit the anti-inflammatory peroxisome proliferator-activated receptor gamma transcription and affect M1/M2 macrophage polarization. Both Wnt5a and pro-inflammatory cytokines can be transported in lipid bilayer sealed extracellular vesicles that reach and deliver their contents to every organ measured in the blood of COPD patients, therefore, demonstrating a potential mechanism for the systemic nature of this crippling disease.
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- 2018
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11. L-Arginine Pathway in COPD Patients with Acute Exacerbation: A New Potential Biomarker.
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Ruzsics I, Nagy L, Keki S, Sarosi V, Illes B, Illes Z, Horvath I, Bogar L, and Molnar T
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- Biomarkers blood, C-Reactive Protein metabolism, Chromatography, High Pressure Liquid, Disease Progression, Female, Follow-Up Studies, Forced Expiratory Flow Rates, Humans, Male, Middle Aged, Prospective Studies, Pulmonary Disease, Chronic Obstructive diagnosis, Pulmonary Disease, Chronic Obstructive physiopathology, Severity of Illness Index, Tandem Mass Spectrometry, Time Factors, Arginine blood, Pulmonary Disease, Chronic Obstructive blood
- Abstract
Background: Acute exacerbation of chronic obstructive pulmonary disease (AECOPD) remains a major cause of mortality. Clinical criteria of AECOPD are subjective. Biomarkers for AECOPD may aid in the initiation of early treatment. Increased production of asymmetric and symmetric dimethylarginine (ADMA, SDMA) is related to hypoxia. In COPD, a rise in ADMA results in a shift of L-arginine breakdown, contributing to airway obstruction. We aimed to compare serum levels of ADMA, SDMA and L-arginine in patients with and without AECOPD., Methods: L-arginine metabolites quantified by high-performance liquid chromatography in venous blood samples and partial capillary oxygen pressure were prospectively investigated in 32 patients with COPD, 12 with AECOPD and 30 healthy subjects., Results: Both ADMA and SDMA were significantly higher in AECOPD compared to stable COPD (p = 0.004 and p < 0.001, respectively). Oxygen content in capillaries correlated with serum ADMA concentration. However, the concentration of L-arginine was not different between AECOPD and stable COPD. Both ADMA and SDMA separated AECOPD with high sensitivity and specificity (AUC: 0.81, p = 0.001; AUC: 0.91, p < 0.001, respectively). A cut-off value ≥0.57 for SDMA was an independent variable to confirm AECOPD in a regression model (OR: 1.632, p = 0.001). All markers were significantly higher in the sera of both patient groups compared to the controls (p < 0.05, respectively)., Conclusions: COPD is associated with elevated L-arginine, ADMA and SDMA serum levels. In patients with AECOPD, production of ADMA and SDMA are more pronounced presumably due to more severe hypoxic insult. Methylated arginine derivatives in the sera may help early recognition of AECOPD.
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- 2016
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12. Alteration in the Wnt microenvironment directly regulates molecular events leading to pulmonary senescence.
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Kovacs T, Csongei V, Feller D, Ernszt D, Smuk G, Sarosi V, Jakab L, Kvell K, Bartis D, and Pongracz JE
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- Animals, Humans, Lung cytology, Mice, Mice, Inbred BALB C, Cellular Senescence physiology, Lung metabolism, PPAR gamma metabolism, Wnt Proteins metabolism
- Abstract
In the aging lung, the lung capacity decreases even in the absence of diseases. The progenitor cells of the distal lung, the alveolar type II cells (ATII), are essential for the repair of the gas-exchange surface. Surfactant protein production and survival of ATII cells are supported by lipofibroblasts that are peroxisome proliferator-activated receptor gamma (PPARγ)-dependent special cell type of the pulmonary tissue. PPARγ levels are directly regulated by Wnt molecules; therefore, changes in the Wnt microenvironment have close control over maintenance of the distal lung. The pulmonary aging process is associated with airspace enlargement, decrease in the distal epithelial cell compartment and infiltration of inflammatory cells. qRT-PCR analysis of purified epithelial and nonepithelial cells revealed that lipofibroblast differentiation marker parathyroid hormone-related protein receptor (PTHrPR) and PPARγ are reduced and that PPARγ reduction is regulated by Wnt4 via a β-catenin-dependent mechanism. Using a human in vitro 3D lung tissue model, a link was established between increased PPARγ and pro-surfactant protein C (pro-SPC) expression in pulmonary epithelial cells. In the senile lung, both Wnt4 and Wnt5a levels increase and both Wnt-s increase myofibroblast-like differentiation. Alteration of the Wnt microenvironment plays a significant role in pulmonary aging. Diminished lipo- and increased myofibroblast-like differentiation are directly regulated by specific Wnt-s, which process also controls surfactant production and pulmonary repair mechanisms., (© 2014 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.)
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- 2014
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13. Effectiveness of erlotinib treatment in advanced KRAS mutation-negative lung adenocarcinoma patients: Results of a multicenter observational cohort study (MOTIVATE).
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Sarosi V, Losonczy G, Francovszky E, Tolnay E, Torok S, Galffy G, Hegedus B, Dome B, and Ostoros G
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- Adenocarcinoma mortality, Adenocarcinoma pathology, Adenocarcinoma of Lung, Adult, Aged, Antineoplastic Agents administration & dosage, Antineoplastic Agents adverse effects, Cohort Studies, Erlotinib Hydrochloride, Female, Humans, Lung Neoplasms mortality, Lung Neoplasms pathology, Male, Middle Aged, Neoplasm Staging, Protein Kinase Inhibitors administration & dosage, Protein Kinase Inhibitors adverse effects, Quinazolines administration & dosage, Quinazolines adverse effects, Risk Factors, Treatment Outcome, Adenocarcinoma drug therapy, Adenocarcinoma genetics, Antineoplastic Agents therapeutic use, Genes, ras, Lung Neoplasms drug therapy, Lung Neoplasms genetics, Mutation, Protein Kinase Inhibitors therapeutic use, Quinazolines therapeutic use
- Abstract
Objectives: Erlotinib is an epidermal growth factor receptor tyrosine-kinase inhibitor (EGFR-TKI), used for the treatment of non-small cell lung cancer. As the clinical significance of KRAS mutational status has not yet been clearly determined in this setting, our aim was to investigate the efficacy of erlotinib in advanced KRAS mutation-negative lung adenocarcinoma patients., Materials and Methods: MOTIVATE is an open-label, multicenter, observational trial with Tarceva(®) (erlotinib) monotherapy. Enrolled patients with advanced (stage IIIB/IV) KRAS wild type (WT) lung adenocarcinoma refractory to one or two courses of prior chemotherapy were treated with erlotinib at 150mg/day. The primary endpoint was progression-free survival (PFS). Secondary endpoints were overall survival (OS) and best tumor response rate (RR)., Results and Conclusion: In total, 327 patients were included. Median PFS and OS were 3.3 and 14.4 months, respectively. Three patients (1.2%) had complete response, 51 patients (20.2%) had partial response and 123 patients (48.8%) had SD. Significantly longer median PFS and OS were observed in Eastern Oncology Cooperative Group Performance Status (ECOG PS) 0-1 patients, as compared to ECOG PS 2-3 patients. The longest median OS (20.5 months) was found in patients with ECOG PS 0-1 who received erlotinib as a second-line therapy. There was no difference in median OS in cohorts stratified to disease stage and smoking status. Female patients had both longer median PFS and OS. Disease control rate was 70.2%. Our results suggest that erlotinib represents a valid treatment option for patients with KRAS WT lung adenocarcinoma and, moreover, that KRAS mutation analysis could help to identify clinically relevant subgroups of NSCLC patients that may benefit from EGFR-TKI therapy., (Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.)
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- 2014
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14. PET-CT imaging and reality.
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Baliko Z, Sarosi V, Illes MB, Varga Z, Hegedus G, Molnar P, and Szakall S
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- Adenocarcinoma complications, Adenocarcinoma pathology, Colonic Neoplasms complications, Colonic Neoplasms pathology, Diagnosis, Differential, Humans, Invasive Pulmonary Aspergillosis complications, Lung Neoplasms diagnosis, Male, Middle Aged, Positron-Emission Tomography, Tomography, X-Ray Computed, Invasive Pulmonary Aspergillosis diagnosis
- Abstract
The spectrum of human diseases caused by members of the Aspergillus genus is extensive. It ranges from allergic reactions to colonization of preexisting pulmonary cavities to invasion and destruction of lung parenchyma with pyemic spread to brain, skin, and other organs, causing rapid death. The immune status of the host is a crucial factor in determining the phenotype and severity of the disease. In this case report Chronic Necrotizing Pulmonary Aspergillosis (CNPA), a rare, locally- or semi-invasive variant of pulmonary Aspergillosis, mimicking lung metastasis is presented. The 60-year-old male patient had earlier received multiple cycles of systemic chemotherapy due to colorectal carcinoma. Our case report focuses on the benefits and the possible disadvantages of PET-CT imaging in CNPA.
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- 2011
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