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001-es BibID:	BIBFORM065233
Első szerző:	Canestraro, Martina
Cím:	Synergistic antiproliferative effect of arsenic trioxide combined with bortezomib in HL60 cell line and primary blasts from patients affected by myeloproliferative disorders / Martina Canestraro, Sara Galimberti, Hakan Savli, Giuseppe Alberto Palumbo, Daniele Tibullo, Balint Nagy, Francesca Guerrini, Simona Piaggi, Naci Cine, Maria Rita Metelli, Mario Petrini
Dátum:	2010
ISSN:	0165-4608
Megjegyzések:	Both arsenic trioxide (ATO) and bortezomib show separate antileukemic activity. With the purpose of evaluating whether the combination of ATO and bortezomib would be an option for patients with acute leukemia, we incubated HL60 leukemic cells with ATO alone and in combination with bortezomib. ATO and bortezomib cooperated to induce cell death and to inhibit proliferation and apoptosis in a synergistic way. The combined treatment resulted in a stronger activation of caspase 8 and 9, moderate activation of caspase 3, and increased expression of Fas and tumor necrosis factor?related apoptosis-inducing ligand (TRAIL)-DR5 receptors. When bortezomib was added, some proapoptotic genes (CARD9, TRAIL) were upregulated, and some antiapoptotic genes (BCL2, BCL3, FLICE) were downregulated. When coincubated, approximately 80% of cells showed altered mitochondrial membrane permeability. Moreover, ATO alone and in combination with bortezomib abrogated DNA-binding activity of nuclear factor kappa beta (NF-?B). Gene expression assays showed that more deregulated genes were related to proliferation of leukocytes, tumorigenesis, control of cell cycle, hypoxia and oxidative stress, cytokines, PI3K-AKT, ERK-MAPK, EGF pathways, and ubiquitination. Finally, in three cases of acute myeloid leukemia, the addition of bortezomib to ATO significantly increased cytotoxicity. We conclude that the combination of bortezomib and ATO may be efficacious in the treatment of myeloid disorders.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban bortezomib synergestic antiproliferative
Megjelenés:	Cancer Genetics And Cytogenetics 199 : 2 (2010), p. 110-120. -
További szerzők:	Galimberti, Sara Savlı, Hakan Palumbo, Giuseppe Alberto Tibullo, Daniele Nagy Bálint (1956-) (molekuláris genetikus) Guerrini, Francesca Piaggi, Simona Cine, Naci Metelli, Maria Rita Petrini, Mario
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001-es BibID:	BIBFORM073620
Első szerző:	Galimberti, Sara
Cím:	Vascular Endothelial Growth Factor Polymorphisms in Mantle Cell Lymphoma / Galimberti S., Nagy B., Palumbo G. A., Ciancia E., Buda G., Orciuolo E., Melosi A., Lambelet P., Ronca F., Petrini M.
Dátum:	2010
ISSN:	0001-5792
Megjegyzések:	In this study, we determined the allele and genotype frequencies of vascular endothelial growth factor (VEGF) G+405C, C-460T, C+936T and C-2578A single nucleotide polymorphisms (SNPs) in 32 patients affected by mantle cell lymphoma (MCL) and 58 healthy controls. Real-time PCR combined with melting curve analysis was used for the determination of SNP alleles. A significant difference in the allele frequency of VEGFC-460T and C+936T SNPs in MCL and healthy cases was not observed. On the contrary, VEGF G+405C and C-2578A SNP allele distribution was significantly lower in the patient group than among normal controls (p = 0.014, p = 0.001). This observation suggests that further investigation is warranted, both in vitro and in a larger series of patients, to further examine the role of VEGF polymorphisms in the pathogenesis of MCL. In addition, the use of quantitative real-time PCR combined with a melting curve analysis method in the detection of the 4 VEGF SNPs may have the potential to replace older and more time-consuming PCR-RFLP methods and bears further investigation.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban VEGF Mantle cell lymphoma
Megjelenés:	Acta Haematologica 123 : 2 (2010), p. 91-95. -
További szerzők:	Nagy Bálint (1956-) (molekuláris genetikus) Palumbo, Giuseppe Alberto Ciancia, Eugenio Buda, G. Orciuolo, E. Melosi, A. Lambelet, P. Ronca, F. Petrini, Mario
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001-es BibID:	BIBFORM065229
035-os BibID:	(PMID)21115902
Első szerző:	Galimberti, Sara
Cím:	ITF2357 Interferes with Apoptosis and Inflammatory Pathways in the HL-60 Model : a Gene Expression Study / Sara Galimberti, Martina Canestraro, Hakan Savli, Giuseppe Alberto Palumbo, Daniele Tibullo, Balint Nagy, Simona Piaggi, Francesca Guerrini, Naci Cine, Maria Rita Metelli, Mario Petrini
Dátum:	2010
ISSN:	0250-7005
Megjegyzések:	Background: Cytotoxic and pro-apoptotic effectsexerted by the histone deacetylase inhibitor ITF2357 havebeen reported in acute myeloid leukemia HL-60 cells. In thecurrent study, its mechanism of action was investigated at themolecular level. Materials and Methods: Cell proliferationwas evaluated by methyl thiazol tetrazolium bromidereduction; apoptosis by annexin V, mitochondrialtransmembrane potential by tetramethylrhodamine ethylester. Functional experiments and gene expressionevaluations were performed by flow cytometry, microarray,and quantitative polymerase chain reaction. Results:Significant cell growth inhibition and increased apoptosiswere observed. ITF2357 reduced protein levels of BCL-2,MCL-1, and BCL-X, and increased levels of BAK. Exposureto ITF2357 did not abrogate NF-?B DNA binding. Aftermicroarray analysis, interleukin-10, interleukin-6, epidermalgrowth factor, peroxisome proliferator-activated receptor(PPAR), transforming growth factor ?, P38 mitogenactivatedprotein kinase, aryl hydrocarbon receptor,xenobiotic metabolism, PPAR/retinoic acid receptor, NF-?B,apoptosis, lipopolysaccharide/interleukin-1, G-proteinreceptor, T-cell receptor, and platelet-derived growth factorwere the de-regulated pathways. Conclusion: This studyshows that ITF2357 influences both proliferation andinflammatory pathways in HL-60 cells; this observationcould have possible applications in clinical practice.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban gene expression pathways apoptosis Inflammatory
Megjelenés:	Anticancer Research. - 30 (2010), p. 4025-4035. -
További szerzők:	Canestraro, Martina Savlı, Hakan Palumbo, Giuseppe Alberto Tibullo, Daniele Nagy Bálint (1956-) (molekuláris genetikus) Piaggi, Simona Guerrini, Francesca Cine, Naci Metelli, Maria Rita Petrini, Mario
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM074834
Első szerző:	Savlı, Hakan
Cím:	Bortezomib and Arsenic Trioxide Activity on a Myelodysplastic Cell Line (P39) : a Gene Expression Study / Hakan Savlı, Sara Galimberti, Deniz Sünnetçi, Martina Canestraro, Giuseppe Palumbo, Balint Nagy, Francesco Di Raimondo, Mario Petrini
Dátum:	2015
ISSN:	1300-7777
Megjegyzések:	NTRODUCTION:We aimed to understand the molecular pathways affected by bortezomib and arsenic trioxide treatment on myelomonocytoid cell line P39.METHODS:Oligonucleotide microarray platforms were used for gene expression and pathway analysis. Confirmation studies were performed using quantitative real time PCR.RESULTS:Bortezomib treatment has shown upregulated DIABLO and NF-?BIB (a NF-?B inhibitor) and downregulated NF-?B1, NF-?B2, and BIRC1 gene expressions. Combination treatment of the two compounds showed gene expression deregulations in concordance by the results of single bortezomib treatment. Especially, P53 was a pathway more significantly modified and a gene network centralized around the beta estradiol gene. Beta estradiol, BRCA2, and FOXA1 genes were remarkable deregulations in our findings.DISCUSSION AND CONCLUSION:Results support the suggestions about possible use of proteasome inhibitors in the treatment of high-risk myelodysplastic syndrome (MDS). NF-?B was observed as an important modulator in leukemic transformation of MDS.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban bortezomib gene expression myelodyplastic
Megjelenés:	Turkish Journal of Hematology. - 32 : 3 (2015), p. 206-212. -
További szerzők:	Galimberti, Sara Sünnetçi, Deniz Canesastraro, Martina Palumbo, Giuseppe Alberto Nagy Bálint (1956-) (molekuláris genetikus) Raimondo, Francesco Di Petrini, Mario
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