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17 results on '"Di Giulio, Stefano"'

3. SMO-M2 mutation does not support cell-autonomous Hedgehog activity in cerebellar granule cell precursors

Author

Petroni, Marialaura, Sahùn Roncero, Maria, Ramponi, Valentina, Fabretti, Francesca, Nicolis Di Robilant, Vittoria, Moretti, Marta, Alfano, Vincenzo, Corsi, Alessandro, De Panfilis, Simone, Giubettini, Maria, Di Giulio, Stefano, Capalbo, Carlo, Belardinilli, Francesca, Coppa, Anna, Sardina, Francesca, Colicchia, Valeria, Pedretti, Flaminia, Infante, Paola, Cardinali, Beatrice, Tessitore, Alessandra, Canettieri, Gianluca, De Smaele, Enrico, and Giannini, Giuseppe

Published
2019
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4. MRE11 inhibition highlights a replication stress-dependent vulnerability of MYCN-driven tumors

Author

Petroni, Marialaura, Sardina, Francesca, Infante, Paola, Bartolazzi, Armando, Locatelli, Erica, Fabretti, Francesca, Di Giulio, Stefano, Capalbo, Carlo, Cardinali, Beatrice, Coppa, Anna, Tessitore, Alessandra, Colicchia, Valeria, Sahùn Roncero, Maria, Belardinilli, Francesca, Di Marcotullio, Lucia, Soddu, Silvia, Comes Franchini, Mauro, Petricci, Elena, Gulino, Alberto, and Giannini, Giuseppe

Published
2018
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5. A gene dosage‐dependent effect unveils NBS1 as both a haploinsufficient tumour suppressor and an essential gene for SHH‐medulloblastoma

Author

Petroni, Marialaura, primary, Fabretti, Francesca, additional, Di Giulio, Stefano, additional, Nicolis di Robilant, Vittoria, additional, La Monica, Veronica, additional, Moretti, Marta, additional, Belardinilli, Francesca, additional, Bufalieri, Francesca, additional, Coppa, Anna, additional, Paci, Paola, additional, Corsi, Alessandro, additional, De Smaele, Enrico, additional, Coni, Sonia, additional, Canettieri, Gianluca, additional, Di Marcotullio, Lucia, additional, Wang, Zhao‐Qi, additional, and Giannini, Giuseppe, additional

Published
2022
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6. A combination of PARP and CHK1 inhibitors efficiently antagonizes MYCN-driven tumors

Author

Di Giulio, Stefano, primary, Colicchia, Valeria, additional, Pastorino, Fabio, additional, Pedretti, Flaminia, additional, Fabretti, Francesca, additional, Nicolis di Robilant, Vittoria, additional, Ramponi, Valentina, additional, Scafetta, Giorgia, additional, Moretti, Marta, additional, Licursi, Valerio, additional, Belardinilli, Francesca, additional, Peruzzi, Giovanna, additional, Infante, Paola, additional, Goffredo, Bianca Maria, additional, Coppa, Anna, additional, Canettieri, Gianluca, additional, Bartolazzi, Armando, additional, Ponzoni, Mirco, additional, Giannini, Giuseppe, additional, and Petroni, Marialaura, additional

Published
2021
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7. Clinical Multigene Panel Sequencing Identifies Distinct Mutational Association Patterns in Metastatic Colorectal Cancer

Author

Belardinilli, Francesca, primary, Capalbo, Carlo, additional, Malapelle, Umberto, additional, Pisapia, Pasquale, additional, Raimondo, Domenico, additional, Milanetti, Edoardo, additional, Yasaman, Mahdavian, additional, Liccardi, Carlotta, additional, Paci, Paola, additional, Sibilio, Pasquale, additional, Pepe, Francesco, additional, Bonfiglio, Caterina, additional, Mezi, Silvia, additional, Magri, Valentina, additional, Coppa, Anna, additional, Nicolussi, Arianna, additional, Gradilone, Angela, additional, Petroni, Marialaura, additional, Di Giulio, Stefano, additional, Fabretti, Francesca, additional, Infante, Paola, additional, Coni, Sonia, additional, Canettieri, Gianluca, additional, Troncone, Giancarlo, additional, and Giannini, Giuseppe, additional

Published
2020
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8. Identification of novel BRCA1 large genomic rearrangements by a computational algorithm of amplicon-based Next-Generation Sequencing data

Author

Nicolussi, Arianna, primary, Belardinilli, Francesca, additional, Silvestri, Valentina, additional, Mahdavian, Yasaman, additional, Valentini, Virginia, additional, D’Inzeo, Sonia, additional, Petroni, Marialaura, additional, Zani, Massimo, additional, Ferraro, Sergio, additional, Di Giulio, Stefano, additional, Fabretti, Francesca, additional, Fratini, Beatrice, additional, Gradilone, Angela, additional, Ottini, Laura, additional, Giannini, Giuseppe, additional, Coppa, Anna, additional, and Capalbo, Carlo, additional

Published
2019
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11. Camping gas burns: our experience

Author

Farace, Francesco, primary, Gallo, Alessandro, additional, Lissia, Mario, additional, Di Giulio, Stefano, additional, Mele, Antonello, additional, and Rubino, Corrado, additional

Published
2007
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14. Enhancement by growth hormone of phorbol diester-stimulated respiratory burst in human polymorphonuclear leukocytes

Author

Spadoni, Gian Luigi, Spagnoli, Anna, Cianfarani, Stefano, Del Principe, Domenico, Menichelli, Adriana, Di Giulio, Stefano, and Boscherini, Brunetto

Abstract

The oxidative metabolic burst of mononuclear and polymorphonuclear phagocytes can be stimulated to produce free oxygen radicals. Several substances can enhance this respiratory burst activity by a priming action: recently growth hormone (rat and porcine) was demonstrated to act as a priming agent on rat peritoneal and on porcine alveolar macrophages. In our study we wanted to verify whether also human GH had a similar priming action on homologous cells, in particular on polymorphonuclear leukocytes. To determine the oxidative activity of polymorphonuclear leukocytes, after stimulation with phorbol myristate acetate, a flow-cytometric assay was employed which registered the intracellular formation of highly fluorescent products as indicators for the intracellular formation of hydrogen peroxide. The incubation of phorbol myristate acetate-stimulated polymorphonuclear leukocytes with GH resulted in a time-dependent and dose-dependent increase in fluorescence, thus demonstrating that human GH enhances in vitro the oxidative metabolic burst of these cells. The action of GH appeared to be significant after 30 min of incubation, was maximal at 60 min, and decreased after 90 min. After one hour of incubation, the first significant variation of fluorescence appeared with GH at a concentration of 50 μg/l. The maximum effect was seen at 100 μg/l with no further increase. Specificity of GH action was demonstrated by the inhibition of its effect by the addition of monoclonal antibodies to GH.

Published
1991
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17. MRE11 inhibition highlights a replication stress-dependent vulnerability of MYCN-driven tumors

Author

Lucia Di Marcotullio, Armando Bartolazzi, Stefano Di Giulio, Marialaura Petroni, Maria Sahùn Roncero, Francesca Belardinilli, Francesca Sardina, Carlo Capalbo, Anna Coppa, Giuseppe Giannini, Beatrice Cardinali, Francesca Fabretti, Paola Infante, Mauro Comes Franchini, Silvia Soddu, Alberto Gulino, Valeria Colicchia, Alessandra Tessitore, Erica Locatelli, Elena Petricci, Petroni, Marialaura, Sardina, Francesca, Infante, Paola, Bartolazzi, Armando, Locatelli, Erica, Fabretti, Francesca, Di Giulio, Stefano, Capalbo, Carlo, Cardinali, Beatrice, Coppa, Anna, Tessitore, Alessandra, Colicchia, Valeria, Sahùn Roncero, Maria, Belardinilli, Francesca, Di Marcotullio, Lucia, Soddu, Silvia, Comes Franchini, Mauro, Petricci, Elena, Gulino, Alberto, and Giannini, Giuseppe

Subjects
0301 basic medicine, Cancer Research, Apoptosis, Mice, Neuroblastoma, MYCN, MRE11 Homologue Protein, Mice, Inbred BALB C, N-Myc Proto-Oncogene Protein, Gene knockdown, lcsh:Cytology, MRE11, 3T3 Cells, Hep G2 Cells, Prognosis, Female, Programmed cell death, Cell Survival, DNA damage, Immunology, Mice, Nude, Pyrimidinones, Biology, Article, 03 medical and health sciences, Cellular and Molecular Neuroscience, Cell Line, Tumor, medicine, Animals, Humans, Progenitor cell, lcsh:QH573-671, neoplasms, Cell Proliferation, MRE11 inhibition, nanoparticles, mirin, neuroblastoma, nanocarrier, Cell Biology, DNA replication, Thiones, medicine.disease, Xenograft Model Antitumor Assays, enzymes and coenzymes (carbohydrates), HEK293 Cells, 030104 developmental biology, MRN complex, A549 Cells, Rad50, Cancer research, Tumor Suppressor Protein p53, DNA Damage
Abstract

MRE11 is a component of the MRE11/RAD50/NBS1 (MRN) complex, whose activity is essential to control faithful DNA replication and to prevent accumulation of deleterious DNA double-strand breaks. In humans, hypomorphic mutations in these genes lead to DNA damage response (DDR)-defective and cancer-prone syndromes. Moreover, MRN complex dysfunction dramatically affects the nervous system, where MRE11 is required to restrain MYCN-dependent replication stress, during the rapid expansion of progenitor cells. MYCN activation, often due to genetic amplification, represents the driving oncogenic event for a number of human tumors, conferring bad prognosis and predicting very poor responses even to the most aggressive therapeutic protocols. This is prototypically exemplified by neuroblastoma, where MYCN amplification occurs in about 25% of the cases. Intriguingly, MRE11 is highly expressed and predicts bad prognosis in MYCN-amplified neuroblastoma. Due to the lack of direct means to target MYCN, we explored the possibility to trigger intolerable levels of replication stress-dependent DNA damage, by inhibiting MRE11 in MYCN-amplified preclinical models. Indeed, either MRE11 knockdown or its pharmacological inhibitor mirin induce accumulation of replication stress and DNA damage biomarkers in MYCN-amplified cells. The consequent DDR recruits p53 and promotes a p53-dependent cell death, as indicated by p53 loss- and gain-of-function experiments. Encapsulation of mirin in nanoparticles allowed its use on MYCN-amplified neuroblastoma xenografts in vivo, which resulted in a sharp impairment of tumor growth, associated with DDR activation, p53 accumulation, and cell death. Therefore, we propose that MRE11 inhibition might be an effective strategy to treat MYCN-amplified and p53 wild-type neuroblastoma, and suggest that targeting replication stress with appropriate tools should be further exploited to tackle MYCN-driven tumors.

Published
2018
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