TY - JOUR AU - Harisi, Revekka AU - Kenessey, István AU - Olah, JN AU - Timar, F AU - Babo, I AU - Pogany, G AU - Paku, Sándor AU - Jeney, András TI - Differential inhibition of single and cluster type tumor cell migration. JF - ANTICANCER RESEARCH J2 - ANTICANCER RES VL - 29 PY - 2009 IS - 8 SP - 2981 EP - 2985 PG - 5 SN - 0250-7005 UR - https://m2.mtmt.hu/api/publication/1425345 ID - 1425345 N1 - Cited By :22 Export Date: 28 September 2021 CODEN: ANTRD Correspondence Address: Jeney, A.; First Institute of Pathology and Experimental Cancer Research, 26 Ulloi ut, H-1085, Budapest, Hungary; email: ajeney@korbl.sote.hu AB - For the control of tumor metastasis it is important to identify chemical compounds with antimigratory potency. Agents acting against single cell and cluster type migration are necessary for successful antimetastatic therapy. In the present study, the migration of HT-1080 fibrosarcoma cells and OSCORT osteosarcoma cells was compared in a Boyden chamber and in an extracellular matrix (ECM)-based three-dimensional cell culture (3-DCC) model system. The Boyden chamber offers a model of single tumor cell migration, whereas the 3-DCC model system demonstrates invasive growth in the form of a cluster. Since PD98059 (MEK inhibitor) exclusively reduced migration in the 3-DCC model, it may be plausible that the ERK/MAPK signaling pathway is essential for cluster type migration. Interestingly, single cell migration was stimulated upon blocking phosphatidylinositol 3-kinase (PI3K) and also p38-MAPK by treatment with LY294002 and SB203580 respectively. A remarkable reduction of single cell migration was observed following treatment with okadaic acid, a phosphatase 1 (PP1) and 2A (PP2A) inhibitor, which was rather intriguing. This study provided evidence that certain cytotoxic/cytostatic agents at appropriate concentrations were able to preferentially inhibit certain types of migration relative to cell proliferation. Single cell migration was selectively inhibited by taxol at very low subtoxic concentration, whereas 5-hexyl-2'-deoxyuridine (HUdR) exclusively inhibited the cluster type of migration. The borrelidin compound was able to inhibit both types of tumor cell migration, but single tumor cell migration was much less affected. It is interesting that migration was more reduced than proliferation by borrelidin, especially at the advanced growth stage. Taxol is recommended as an agent acting against single cell migration, as well as HUdR and borrelidin as leading compounds for developing antimetastatic drugs against cluster type migration. LA - English DB - MTMT ER - TY - JOUR AU - Lódi, Csaba AU - Szabó, Erzsébet AU - Holczbauer, Ágnes AU - Batmunkh, E AU - Szijártó, Attila AU - Kupcsulik, Péter Károly AU - Kovalszky, Ilona AU - Paku, Sándor AU - Illyes, G AU - Kiss, András AU - Schaff, Zsuzsa TI - Claudin-4 differentiates biliary tract cancers from hepatocellular carcinomas JF - MODERN PATHOLOGY J2 - MODERN PATHOL VL - 19 PY - 2006 IS - 3 SP - 460 EP - 469 PG - 10 SN - 0893-3952 DO - 10.1038/modpathol.3800549 UR - https://m2.mtmt.hu/api/publication/1242486 ID - 1242486 N1 - Kiss András és Schaff Zsuzsa megosztott utolsó szerzők. AB - The recently identified claudins are dominant components of tight junctions, responsible for cell adhesion, polarity and paracellular permeability. Certain claudins have been shown to have relevance in tumor development, with some of them, especially claudin-4, even suggested as future therapeutic target. The aim of the present study was to analyze the expression of claudin-4 in the biliary tree, biliary tract cancers and hepatocellular carcinomas. A total of 107 cases were studied: 53 biliary tract cancers, 50 hepatocellular carcinomas, 10 normal liver and 10 normal extrahepatic biliary duct samples. Immunohistochemical analysis was performed on conventional specimens and on tissue microarrays as well. Claudin-4 was further investigated by Western blot analysis and real-time RT-PCR. Intense membranous immunolabeling was found for claudin-4 in all biliary tract cancers unrelated to the primary site of origin, namely intrahepatic, extrahepatic or gallbladder cancers. Normal biliary epithelium showed weak positivity for claudin-4. In contrast, normal hepatocytes and tumor cells of hepatocellular carcinomas did not express claudin-4. The results of Western immunoblot analysis and real-time RT-PCR were in correlation with the immunohistochemical findings. Cytokeratins, as CK7 (92%) and CK19 (83%) were mostly positive in biliary tract cancers, however, one-third of hepatocellular carcinomas also expressed CK7 (34%). HSA antibody (HepPar1) reacted with the majority of hepatocellular carcinomas (86%), while being positive in a low percentage of the biliary tract cancers (8%). In conclusion, this is the first report of a significantly increased claudin-4 expression in biliary tract cancers, which represents a novel feature of tumors of biliary tract origin. Claudin-4 expression seems to be a useful marker in differentiating biliary tract cancers from hepatocellular carcinomas and could well become a potential diagnostic tool. LA - English DB - MTMT ER - TY - JOUR AU - Döme, Balázs AU - Tímár, József AU - Dobos, Judit AU - Rásó-Barnett, Lívia AU - Rásó, Erzsébet AU - Paku, Sándor AU - Kenessey, István AU - Ostoros, Gyula AU - Magyar, M AU - Ladányi, Andrea AU - Bogos, Krisztina AU - Tóvári, József TI - Identification and clinical significance of circulating endothelial progenitor cells in human non-small cell lung cancer JF - CANCER RESEARCH J2 - CANCER RES VL - 66 PY - 2006 IS - 14 SP - 7341 EP - 7347 PG - 7 SN - 0008-5472 DO - 10.1158/0008-5472.CAN-05-4654 UR - https://m2.mtmt.hu/api/publication/1072475 ID - 1072475 AB - Until recently, it was generally accepted that vascularization of tumors arises exclusively from endothelial sprouting. Whether circulating bone marrow-derived endothelial progenitor cells (EPC) participate in the progression of non-small cell lung cancer (NSCLC) has not yet been evaluated. EPCs labeled with CD34, CD133, and vascular endothelial growth factor receptor-2 (VEGFR2) antibodies were counted by flow cytometry in the peripheral blood of 53 NSCLC patients. Furthermore, by means of a quantitative reverse transcription-PCR approach, we measured VEGFR2, CD133, CD34, and VE-cadherin mRNA in the peripheral blood samples of the same patient population. EPCs in tumor samples were identified by confocal microscopy using CD31, CD34. CD133, and VEGFR2 antibodies. Although immunofluorescent labeling of microvessels made clear that incorporation of EPCs is a rare phenomenon in NSCLC tissue (9 of 22 cases), circulating EPC levels before therapeutic intervention were increased in NSCLC patients (P < 0.002, versus healthy controls), and high pretreatment circulating EPC numbers correlated with poor overall survival (P < 0.001). Furthermore, in the subgroup of responders to treatment, the posttreatment EPC numbers in the peripheral blood were significantly lower compared with nonresponding patients. Interestingly, pretreatment mRNA levels of CD133, VE-cadherin, and CD34 were not significantly increased in NSCLC patients, whereas VEGFR2 expression was increased by 80-fold. Moreover, posttreatment VEGFR2 mRNA level in the peripheral blood was significantly higher in the subgroup of nonresponding patients when compared with posttreatment level of patients responding to antitumor therapy. Circulating levels of bone marrow-derived EPCs are significantly increased in NSCLC patients and correlate with clinical behavior. LA - English DB - MTMT ER - TY - JOUR AU - Peták, István AU - Houghton, JA AU - Kopper, László TI - Molecular Targeting of Cell Death Signal Transduction Pathways in Cancer JF - CURRENT SIGNAL TRANSDUCTION THERAPY J2 - CURR SIGNAL TRANSDUCT THER VL - 1 PY - 2006 IS - 1 SP - 113 EP - 131 PG - 19 SN - 1574-3624 DO - 10.2174/157436206775269217 UR - https://m2.mtmt.hu/api/publication/1047090 ID - 1047090 N1 - Megjegyzés-23483804 Megjegyzés-22364987 LA - English DB - MTMT ER - TY - JOUR AU - Reiniger, Lilla AU - Bödör, Csaba AU - Bognar, A AU - Balogh, Zsófia AU - Csomor, Judit AU - Szepesi, Ágota AU - Kopper, László AU - Matolcsy, András TI - Richter's and prolymphocytic transformation of chronic lymphocytic leukemia are associated with high mRNA expression of activation-induced cytidine deaminase and aberrant somatic hypermutation JF - LEUKEMIA J2 - LEUKEMIA VL - 20 PY - 2006 IS - 6 SP - 1089 EP - 1095 PG - 7 SN - 0887-6924 DO - 10.1038/sj.leu.2404183 UR - https://m2.mtmt.hu/api/publication/1038547 ID - 1038547 LA - English DB - MTMT ER - TY - JOUR AU - Füle, Tibor AU - Máthé, Miklós AU - Suba, Zsuzsanna AU - Csapó, Zsolt AU - Szarvas, Tibor AU - Tátrai, Péter AU - Paku, Sándor AU - Kovalszky, Ilona TI - The presence of human papillomavirus 16 in neural structures and vascular endothelial cells JF - VIROLOGY J2 - VIROLOGY VL - 348 PY - 2006 IS - 2 SP - 289 EP - 296 PG - 8 SN - 0042-6822 DO - 10.1016/j.virol.2005.12.043 UR - https://m2.mtmt.hu/api/publication/154557 ID - 154557 LA - English DB - MTMT ER - TY - CHAP AU - Kopper, László AU - Matolcsy, A AU - Udvardy, Miklós ED - Matolcsy, András ED - Udvardy, Miklós ED - Kopper, László TI - A haemopoesesis sejtjei T2 - Hematológiai betegségek atlasza PB - Medicina Könyvkiadó CY - Budapest SN - 9632260260 PY - 2006 SP - 48 EP - 67 PG - 20 UR - https://m2.mtmt.hu/api/publication/154556 ID - 154556 LA - Hungarian DB - MTMT ER - TY - JOUR AU - Kövesi, György AU - Szende, Béla TI - Prognostic value of cyclin D1, p27, and p63 in oral leukoplakia JF - JOURNAL OF ORAL PATHOLOGY AND MEDICINE J2 - J ORAL PATHOL MED VL - 35 PY - 2006 IS - 5 SP - 274 EP - 277 PG - 4 SN - 0904-2512 DO - 10.1111/j.1600-0714.2006.00396.x UR - https://m2.mtmt.hu/api/publication/154555 ID - 154555 N1 - Megjegyzés-21240874 PubMed ID: 16630290 Chemicals/CAS: CKAP4 protein, human; Cyclin D1, 136601-57-5; Membrane Proteins; Neoplasm Proteins; p27 antigen; Proliferating Cell Nuclear Antigen; Tumor Markers, Biological Megjegyzés-21371335 Chemicals/CAS: CKAP4 protein, human; Cyclin D1, 136601-57-5; Membrane Proteins; Neoplasm Proteins; p27 antigen; Proliferating Cell Nuclear Antigen; Tumor Markers, Biological Megjegyzés-21240799 PubMed ID: 16630290 Chemicals/CAS: CKAP4 protein, human; Cyclin D1, 136601-57-5; Membrane Proteins; Neoplasm Proteins; p27 antigen; Proliferating Cell Nuclear Antigen; Tumor Markers, Biological LA - English DB - MTMT ER - TY - JOUR AU - Mihalik, Rudolf AU - Imre, G TI - Kaszpázok, apoptózis, sejtelhalás: (jel) útvesztőben JF - ORVOSKÉPZÉS J2 - ORVOSKÉPZÉS VL - 81 PY - 2006 IS - 3 SP - 151 EP - 157 PG - 7 SN - 0030-6037 UR - https://m2.mtmt.hu/api/publication/154553 ID - 154553 LA - Hungarian DB - MTMT ER - TY - JOUR AU - Nagy, K AU - Szekely-Szűcs, K AU - Izeradjene, K AU - Douglas, L AU - Tillman, M AU - Barti-Juhász, Helga AU - Dominici, M AU - Spano, C AU - Luca, Cervo G AU - Conte, P AU - Houghton, JA AU - Mihalik, Rudolf AU - Kopper, László AU - Peták, István TI - Proteasome inhibitors sensitize colon carcinoma cells to TRAIL-induced apoptosis via enhanced release of Smac/DIABLO from the mitochondria JF - PATHOLOGY AND ONCOLOGY RESEARCH J2 - PATHOL ONCOL RES VL - 12 PY - 2006 IS - 3 SP - 133 EP - 142 PG - 10 SN - 1219-4956 DO - 10.1007/BF02893359 UR - https://m2.mtmt.hu/api/publication/154552 ID - 154552 N1 - Ist Department of Pathology and Experimental Cancer Research, Semmelweis University, Budapest, Hungary Molecular Pathology Research Group, Joint Research Organization of the Hungarian Academy of Science, Semmelweis University, Budapest, Hungary Szentágothai János Knowledge Center, Budapest, Hungary Department of Oncology and Hematology, University of Modena and Reggio Emilia, Modena, Italy Division of Molecular Therapeutics, Department of Hematology-Oncology, St. Jude Children's Research Hospital, Memphis, TN, United States 1st Department of Pathology and Experimental Cancer Research, Semmelweis University, Ülloi út 26, Budapest, H-1085, Hungary Cited By :31 Export Date: 2 June 2021 CODEN: POREF Correspondence Address: Peták, I.; 1st Department of Pathology and Experimental Cancer Research, Ülloi út 26, Budapest, H-1085, Hungary; email: petak@kkk.org.hu Chemicals/CAS: benzyloxycarbonylleucylleucylleucinal, 133407-82-6; bortezomib, 179324-69-7, 197730-97-5; caspase 3, 169592-56-7; caspase 8; cytochrome c, 9007-43-6, 9064-84-0; epoxomicin, 134381-21-8; protein bcl 2, 219306-68-0; protein bcl xl, 151033-38-4 Tradenames: mg 132, Calbiochem; ps 341 Manufacturers: Boston Biochemicals; Calbiochem Funding details: 118/2001 Funding details: National Institutes of Health, NIH Funding details: National Cancer Institute, NCI, R01CA032613, R01CA087952, R25CA023944 Funding details: American Lebanese Syrian Associated Charities, ALSAC, ETT 145/2003, OMFB-01634/2001, T046665, TET I-48/2003 Funding details: Nemzeti Kutatási és Technológiai Hivatal, NKTH Funding text 1: R.M. was supported by OTKA T029611, OTKA T049008 and ETT 197/2000 grants. L.K. was supported by OTKA T34892, ETT 193/2000, NKFP-1A/20/2002, OTKA TS 049887 grants. A.S. was supported by FKFP 0150/2001, ETT 192/2000 grants and the Békési Foundation 118/2001. M.D. and P.C. were supported by the Region Emilia Romagna. J.H. was supported by NIH Awards CA 87952, CA 32613, CA 23944, and by the American Lebanese Syrian Associated Charities. I.P. was supported by Zoltán Magyary Scholarship, Terry Fox Foundation, ETT 145/2003, OTKA T046665, TET I-48/2003, OMFB-01634/2001 grants and by the National Office for Research and Technology (NKTH), Hungary. The authors would like to thank Balázs Sarkadi for his most valuable suggestions. LA - English DB - MTMT ER -