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001-es BibID:	BIBFORM065333
Első szerző:	Cerisano, Vanessa
Cím:	Molecular mechanisms of CD99-induced caspase-independent cell death and cell-cell adhesion in Ewing's sarcoma cells : actin and zyxin as key intracellular mediators / Vanessa Cerisano, Yan Aalto, Stefania Perdichizzi, Ghislaine Bernard, Maria Cristina Manara, Stefania Benini, Giovanna Cenacchi, Paola Preda, Giovanna Lattanzi, Bálint Nagy, Sakari Knuutila, Mario Paolo Colombo, Alain Bernard, Piero Picci, Katia Scotlandi
Dátum:	2004
ISSN:	0950-9232
Megjegyzések:	CD99 is a unique 32-kDa cell surface molecule with broad cellular expression but still poorly understood biological functions. In cancer cells, CD99 is highly expressed in virtually all Ewing's sarcoma (ES). Engagement of CD99 induces fast homotypic aggregation of ES cells and caspase-independent apoptosis. In this study, we analysed signal transduction after CD99 engagement on ES cells. Findings obtained with selective inhibitors indicated that only actin cytoskeleton integrity was essential for cell-cell adhesion and apoptosis of ES cells. Indeed, CD99 stimulation induced actin repolymerization, further supporting the role of cytoskeleton in CD99 signaling. Gene expression profiling of ES cells after CD99 engagement showed modulation in the expression of 32 genes. Among the pool of upregulated genes reported to be involved in cell adhesion, we chose to analyse the role of zyxin, a cytoplasmic adherens junction protein found to play a role in the regulation of the actin cytoskeleton. Overexpression of zyxin after CD99 ligation was confirmed by real-time PCR and Western blot. Treatment of ES cells with zyxin antisense oligonucleotides inhibited CD99-induced cell aggregation and apoptosis, suggesting a functional role for this protein. Therefore, our findings indicate that CD99 functions occur through reorganization of cytoskeleton and identify actin and zyxin as the early signaling events driven by CD99 engagement.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban CD-99 induced caspase independent cell death Ewing's sarcoma
Megjelenés:	Oncogene. - 23 : 33 (2004), p. 5664-5674. -
További szerzők:	Aalto, Yan Perdichizzi, Stefania Bernard, Ghislaine Manara, Maria Cristina Benini, Stefania Cenacchi, Giovanna Preda, Paola Lattanzi, Giovanna Nagy Bálint (1956-) (molekuláris genetikus) Knuutila, Sakari Colombo, Mario Paolo Bernard, Alain Picci, Piero Scotlandi, Katia
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM065323
Első szerző:	Myllykangas, Samuel
Cím:	DNA copy number amplification profiling of human neoplasms / S. Myllykangas, J. Himberg, T. Böhling, B. Nagy, J. Hollmén, S. Knuutila
Dátum:	2006
ISSN:	0950-9232
Megjegyzések:	DNA copy number amplifications activate oncogenes and are hallmarks of nearly all advanced tumors. Amplified genes represent attractive targets for therapy, diagnostics and prognostics. To investigate DNA amplifications in different neoplasms, we performed a bibliomics survey using 838 published chromosomal comparative genomic hybridization studies and collected amplification data at chromosome band resolution from more than 4500 cases. Amplification profiles were determined for 73 distinct neoplasms. Neoplasms were clustered according to the amplification profiles, and frequently amplified chromosomal loci (amplification hot spots) were identified using computational modeling. To investigate the site specificity and mechanisms of gene amplifications, colocalization of amplification hot spots, cancer genes, fragile sites, virus integration sites and gene size cohorts were tested in a statistical framework. Amplification-based clustering demonstrated that cancers with similar etiology, cell-of-origin or topographical location have a tendency to obtain convergent amplification profiles. The identified amplification hot spots were colocalized with the known fragile sites, cancer genes and virus integration sites, but global statistical significance could not be ascertained. Large genes were significantly overrepresented on the fragile sites and the reported amplification hot spots. These findings indicate that amplifications are selected in the cancer tissue environment according to the qualitative traits and localization of cancer genes.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban DNA copy number profiling human neoplasms
Megjelenés:	Oncogene. - 25 : 55 (2006), p. 7324-7332. -
További szerzők:	Himberg, J. Böhling, T. Nagy Bálint (1956-) (molekuláris genetikus) Hollmén, Jaakko Knuutila, Sakari
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM065337
Első szerző:	Xie, Yuntao
Cím:	Gene expression profile by blocking the SYT-SSX fusion gene in synovial sarcoma cells. Identification of XRCC4 as a putative SYT-SSX target gene / Yuntao Xie, Maria Törnkvist, Yan Aalto, Gunnar Nilsson, Leonard Girnita, Bálint Nagy, Sakari Knuutila, Olle Larsson
Dátum:	2003
ISSN:	0950-9232
Megjegyzések:	Increasing evidence suggests that the SYT-SSX fusion gene plays an important role in synovial sarcoma development and progression. However, very little is known about the downstream targets of SYT-SSX. In this study, we used antisense oligonucleotides to block the expression of the SYT-SSX fusion gene in synovial sarcoma cells. By comparing SYT-SSX inhibited cells with noninhibited cells, the gene expression profile was analysed using cDNA microarray and established by real-time PCR. Herewith, using a filter containing 1176 cancer-relevant genes, we found that the DNA repair gene XRCC4 and the DNA mismatch repair gene MSH2 were downregulated, whereas the gene encoding for the serine/threonine protein kinase PRK (also known as CNK), and the macrophage inhibitory cytokine MICI (also known as PLAB) were upregulated after the inhibition of SYT-SSX. In comparison, expression of the XRCC4 gene was undergoing the strongest alteration. Consistently, the protein expression of XRCC4 was found to be decreased after SYT-SSX inhibition, whereas there were no detectable changes for the other gene products. Our study provides some clues to elucidate the signaling pathways of the SYT-SSX fusion gene, as well as it demonstrates a valuable model system for search for other SYT-SSX targets.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban gene expression synovial carcinoma SYT-SSX fusion gene
Megjelenés:	Oncogene. - 22 : 48 (2003), p. 7628-7631. -
További szerzők:	Törnkvist, Maria Aalto, Yan Nilsson, Gunnar Girnita, Leonard Nagy Bálint (1956-) (molekuláris genetikus) Knuutila, Sakari Larsson, Olle
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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