@article{MTMT:1425345,
	title = {Differential inhibition of single and cluster type tumor cell migration.},
	url = {https://m2.mtmt.hu/api/publication/1425345},
	author = {Harisi, Revekka and Kenessey, István and Olah, JN and Timar, F and Babo, I and Pogany, G and Paku, Sándor and Jeney, András},
	journal-iso = {ANTICANCER RES},
	journal = {ANTICANCER RESEARCH},
	volume = {29},
	unique-id = {1425345},
	issn = {0250-7005},
	abstract = {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.},
	keywords = {Adolescent; Male; Humans; signal transduction; Tumor Cells, Cultured; Enzyme Inhibitors/pharmacology; Pyridines/pharmacology; Okadaic Acid/pharmacology; Flavonoids/pharmacology; *Cell Proliferation; Cell Culture Techniques; Imidazoles/pharmacology; Morpholines/pharmacology; p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors/metabolism; Phosphatidylinositol 3-Kinases/antagonists & inhibitors/metabolism; Paclitaxel/pharmacology; Osteosarcoma/drug therapy/*pathology; Fibrosarcoma/drug therapy/*pathology; Extracellular Signal-Regulated MAP Kinases/antagonists & inhibitors/metabolism; Deoxyuridine/analogs & derivatives/pharmacology; Chromones/pharmacology; *Cell Movement; Bone Neoplasms/drug therapy/*secondary},
	year = {2009},
	eissn = {1791-7530},
	pages = {2981-2985},
	orcid-numbers = {Kenessey, István/0000-0002-6963-8489; Paku, Sándor/0000-0003-2664-7729}
}

@article{MTMT:1242486,
	title = {Claudin-4 differentiates biliary tract cancers from hepatocellular carcinomas},
	url = {https://m2.mtmt.hu/api/publication/1242486},
	author = {Lódi, Csaba and Szabó, Erzsébet and Holczbauer, Ágnes and Batmunkh, E and Szijártó, Attila and Kupcsulik, Péter Károly and Kovalszky, Ilona and Paku, Sándor and Illyes, G and Kiss, András and Schaff, Zsuzsa},
	doi = {10.1038/modpathol.3800549},
	journal-iso = {MODERN PATHOL},
	journal = {MODERN PATHOLOGY},
	volume = {19},
	unique-id = {1242486},
	issn = {0893-3952},
	abstract = {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.},
	keywords = {Humans; immunohistochemistry; Diagnosis, Differential; Blotting, Western; Gene Expression; reverse transcriptase polymerase chain reaction; Adenocarcinoma/genetics/metabolism/pathology; RNA, Messenger/genetics/metabolism; Keratin-7; Laminin/analysis; Liver/metabolism/pathology; Membrane Proteins/genetics/*metabolism; Keratins/analysis; Claudin-4; Tissue Array Analysis/methods; Liver Neoplasms/genetics/metabolism/*pathology; Carcinoma, Hepatocellular/genetics/metabolism/*pathology; Biliary Tract Neoplasms/genetics/metabolism/*pathology},
	year = {2006},
	eissn = {1530-0285},
	pages = {460-469},
	orcid-numbers = {Lódi, Csaba/0000-0003-3525-6922; Kovalszky, Ilona/0000-0002-0179-3378; Paku, Sándor/0000-0003-2664-7729; Kiss, András/0000-0002-7453-3163; Schaff, Zsuzsa/0000-0002-6429-8059}
}

@article{MTMT:1072475,
	title = {Identification and clinical significance of circulating endothelial progenitor cells in human non-small cell lung cancer},
	url = {https://m2.mtmt.hu/api/publication/1072475},
	author = {Döme, Balázs and Tímár, József and Dobos, Judit and Rásó-Barnett, Lívia and Rásó, Erzsébet and Paku, Sándor and Kenessey, István and Ostoros, Gyula and Magyar, M and Ladányi, Andrea and Bogos, Krisztina and Tóvári, József},
	doi = {10.1158/0008-5472.CAN-05-4654},
	journal-iso = {CANCER RES},
	journal = {CANCER RESEARCH},
	volume = {66},
	unique-id = {1072475},
	issn = {0008-5472},
	abstract = {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.},
	year = {2006},
	eissn = {1538-7445},
	pages = {7341-7347},
	orcid-numbers = {Döme, Balázs/0000-0001-8799-8624; Tímár, József/0000-0001-9183-0859; Rásó, Erzsébet/0000-0002-4589-5771; Paku, Sándor/0000-0003-2664-7729; Kenessey, István/0000-0002-6963-8489; Ladányi, Andrea/0000-0001-9304-8473; Tóvári, József/0000-0002-5543-3204}
}

@article{MTMT:1047090,
	title = {Molecular Targeting of Cell Death Signal Transduction Pathways in Cancer},
	url = {https://m2.mtmt.hu/api/publication/1047090},
	author = {Peták, István and Houghton, JA and Kopper, László},
	doi = {10.2174/157436206775269217},
	journal-iso = {CURR SIGNAL TRANSDUCT THER},
	journal = {CURRENT SIGNAL TRANSDUCTION THERAPY},
	volume = {1},
	unique-id = {1047090},
	issn = {1574-3624},
	year = {2006},
	pages = {113-131},
	orcid-numbers = {Peták, István/0000-0003-0422-9286; Kopper, László/0000-0002-4921-3678}
}

@article{MTMT:1038547,
	title = {Richter's and prolymphocytic transformation of chronic lymphocytic leukemia are associated with high mRNA expression of activation-induced cytidine deaminase and aberrant somatic hypermutation},
	url = {https://m2.mtmt.hu/api/publication/1038547},
	author = {Reiniger, Lilla and Bödör, Csaba and Bognar, A and Balogh, Zsófia and Csomor, Judit and Szepesi, Ágota and Kopper, László and Matolcsy, András},
	doi = {10.1038/sj.leu.2404183},
	journal-iso = {LEUKEMIA},
	journal = {LEUKEMIA},
	volume = {20},
	unique-id = {1038547},
	issn = {0887-6924},
	year = {2006},
	eissn = {1476-5551},
	pages = {1089-1095},
	orcid-numbers = {Reiniger, Lilla/0000-0003-2248-4264; Bödör, Csaba/0000-0002-0729-692X; Szepesi, Ágota/0000-0002-0706-1178; Kopper, László/0000-0002-4921-3678; Matolcsy, András/0000-0002-5382-2150}
}

@article{MTMT:154557,
	title = {The presence of human papillomavirus 16 in neural structures and vascular endothelial cells},
	url = {https://m2.mtmt.hu/api/publication/154557},
	author = {Füle, Tibor and Máthé, Miklós and Suba, Zsuzsanna and Csapó, Zsolt and Szarvas, Tibor and Tátrai, Péter and Paku, Sándor and Kovalszky, Ilona},
	doi = {10.1016/j.virol.2005.12.043},
	journal-iso = {VIROLOGY},
	journal = {VIROLOGY},
	volume = {348},
	unique-id = {154557},
	issn = {0042-6822},
	year = {2006},
	eissn = {1096-0341},
	pages = {289-296},
	orcid-numbers = {Szarvas, Tibor/0000-0002-6321-0799; Tátrai, Péter/0000-0001-9726-1992; Paku, Sándor/0000-0003-2664-7729; Kovalszky, Ilona/0000-0002-0179-3378}
}

@inbook{MTMT:154556,
	title = {A haemopoesesis sejtjei},
	url = {https://m2.mtmt.hu/api/publication/154556},
	author = {Kopper, László and Matolcsy, A and Udvardy, Miklós},
	booktitle = {Hematológiai betegségek atlasza},
	unique-id = {154556},
	year = {2006},
	pages = {48-67},
	orcid-numbers = {Kopper, László/0000-0002-4921-3678}
}

@article{MTMT:154555,
	title = {Prognostic value of cyclin D1, p27, and p63 in oral leukoplakia},
	url = {https://m2.mtmt.hu/api/publication/154555},
	author = {Kövesi, György and Szende, Béla},
	doi = {10.1111/j.1600-0714.2006.00396.x},
	journal-iso = {J ORAL PATHOL MED},
	journal = {JOURNAL OF ORAL PATHOLOGY AND MEDICINE},
	volume = {35},
	unique-id = {154555},
	issn = {0904-2512},
	year = {2006},
	eissn = {1600-0714},
	pages = {274-277},
	orcid-numbers = {Kövesi, György/0000-0002-6398-6474}
}

@article{MTMT:154553,
	title = {Kaszpázok, apoptózis, sejtelhalás: (jel) útvesztőben},
	url = {https://m2.mtmt.hu/api/publication/154553},
	author = {Mihalik, Rudolf and Imre, G},
	journal-iso = {ORVOSKÉPZÉS},
	journal = {ORVOSKÉPZÉS},
	volume = {81},
	unique-id = {154553},
	issn = {0030-6037},
	year = {2006},
	pages = {151-157}
}

@article{MTMT:154552,
	title = {Proteasome inhibitors sensitize colon carcinoma cells to TRAIL-induced apoptosis via enhanced release of Smac/DIABLO from the mitochondria},
	url = {https://m2.mtmt.hu/api/publication/154552},
	author = {Nagy, K and Szekely-Szűcs, K and Izeradjene, K and Douglas, L and Tillman, M and Barti-Juhász, Helga and Dominici, M and Spano, C and Luca, Cervo G and Conte, P and Houghton, JA and Mihalik, Rudolf and Kopper, László and Peták, István},
	doi = {10.1007/BF02893359},
	journal-iso = {PATHOL ONCOL RES},
	journal = {PATHOLOGY AND ONCOLOGY RESEARCH},
	volume = {12},
	unique-id = {154552},
	issn = {1219-4956},
	year = {2006},
	eissn = {1532-2807},
	pages = {133-142},
	orcid-numbers = {Kopper, László/0000-0002-4921-3678; Peták, István/0000-0003-0422-9286}
}