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13 results on '"Velletri, Tania"'

6. Single cell-derived spheroids capture the self-renewing subpopulations of metastatic ovarian cancer

Author

Velletri, Tania, primary, Villa, Carlo Emanuele, additional, Cilli, Domenica, additional, Barzaghi, Bianca, additional, Lo Riso, Pietro, additional, Lupia, Michela, additional, Luongo, Raffaele, additional, López-Tobón, Alejandro, additional, De Simone, Marco, additional, Bonnal, Raoul J. P., additional, Marelli, Luca, additional, Piccolo, Stefano, additional, Colombo, Nicoletta, additional, Pagani, Massimiliano, additional, Cavallaro, Ugo, additional, Minucci, Saverio, additional, and Testa, Giuseppe, additional

Published
2021
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8. Loss of p53 in mesenchymal stem cells promotes alteration of bone remodeling through negative regulation of osteoprotegerin

Author

Velletri, Tania, primary, Huang, Yin, additional, Wang, Yu, additional, Li, Qing, additional, Hu, Mingyuan, additional, Xie, Ningxia, additional, Yang, Qian, additional, Chen, Xiaodong, additional, Chen, Qing, additional, Shou, Peishun, additional, Gan, Yurun, additional, Candi, Eleonora, additional, Annicchiarico-Petruzzelli, Margherita, additional, Agostini, Massimiliano, additional, Yang, Huilin, additional, Melino, Gerry, additional, Shi, Yufang, additional, and Wang, Ying, additional

Published
2020
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10. Relative expression of TAp73 and ΔNp73 isoforms

Author

Conforti, Franco, primary, Yang, Ai Li, additional, Agostini, Massimiliano, additional, Rufini, Alessandro, additional, Tucci, Paola, additional, Nicklison-Chirou, Maria Victoria, additional, Grespi, Francesca, additional, Velletri, Tania, additional, Knight, Richard A., additional, Melino, Gerry, additional, and Sayan, Berna S., additional

Published
2012
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11. Erratum: Cellular senescence-like features of lung fibroblasts derived from idiopathic pulmonary fibrosis patients

Author

Conforti, Franco, primary, Yang, Ai Li, additional, Agostini, Massimiliano, additional, Rufini, Alessandro, additional, Tucci, Paola, additional, Nicklison-Chirou, Maria Victoria, additional, Grespi, Francesca, additional, Velletri, Tania, additional, Knight, Richard A., additional, Melino, Gerry, additional, and Sayan, Berna S., additional

Published
2012
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12. p73 in Cancer

Author

Rufini, Alessandro, Agostini, Massimiliano, Grespi, Francesca, Tomasini, Richard, Sayan, Berna S., Niklison-Chirou, Maria Victoria, Conforti, Franco, Velletri, Tania, Mastino, Antonio, Mak, Tak W., Melino, Gerry, and Knight, Richard A.

Abstract

p73 is a tumor suppressor belonging to the p53 family of transcription factors. Distinct isoforms are transcribed from the p73 locus. The use of 2 promoters at the N-terminus allows the expression of an isoform containing (TAp73) or not containing (?Np73) a complete N-terminal transactivation domain, with the latter isoform capable of a dominant negative effect over the former. In addition, both N-terminal variants are alternatively spliced at the C-terminus. TAp73 is a bona fide tumor suppressor, being able to induce cell death and cell cycle arrest; conversely, ?Np73 shows oncogenic properties, inhibiting TAp73 and p53 functions. Here, we discuss the latest findings linking p73 to cancer. The generation of isoform specific null mice has helped in dissecting the contribution of TA versus ?Np73 isoforms to tumorigenesis. The activity of both isoforms is regulated transcriptionally and by posttranslational modification. p73 dysfunction, particularly of TAp73, has been associated with mitotic abnormalities, which may lead to polyploidy and aneuploidy and thus contribute to tumorigenesis. Although p73 is only rarely mutated in cancer, the tumor suppressor actions of TAp73 are inhibited by mutant p53, a finding that has important implications for cancer therapy. Finally, we discuss the expression and role of p73 isoforms in human cancer, with a particular emphasis on the neuroblastoma cancer model. Broadly, the data support the hypothesis that the ratio between TAp73 and ?Np73 is crucial for tumor progression and therapeutic response.

Published
2011
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