B
Benedetta Peruzzi
Researcher at University of Florence
Publications - 44
Citations - 1898
Benedetta Peruzzi is an academic researcher from University of Florence. The author has contributed to research in topics: Medicine & Internal medicine. The author has an hindex of 17, co-authored 35 publications receiving 1582 citations. Previous affiliations of Benedetta Peruzzi include National Institutes of Health.
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Journal ArticleDOI
Impaired immune cell cytotoxicity in severe COVID-19 is IL-6 dependent.
Alessio Mazzoni,Lorenzo Salvati,Laura Maggi,Manuela Capone,Anna Vanni,Michele Spinicci,Jessica Mencarini,Roberto Caporale,Benedetta Peruzzi,Alberto Antonelli,Michele Trotta,Lorenzo Zammarchi,Luca Ciani,Leonardo Gori,Chiara Lazzeri,Andrea Matucci,Alessandra Vultaggio,Oliviero Rossi,Fabio Almerigogna,Paola Parronchi,Paolo Fontanari,Federico Lavorini,Adriano Peris,Gian Maria Rossolini,Alessandro Bartoloni,Sergio Romagnani,Francesco Liotta,Francesco Annunziato,Lorenzo Cosmi +28 more
TL;DR: The association between IL-6 serum levels and the impairment of cytotoxic activity suggests the possibility that targeting this cytokine may restore anti-viral mechanisms.
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Targeting the c-Met signaling pathway in cancer.
TL;DR: The present understanding of c-Met oncogenic signaling supports at least three avenues of pathway selective anticancer drug development: antagonism of ligand/receptor interaction, inhibition of TK catalytic activity, and blockade of intracellular receptor/effector interactions.
Journal ArticleDOI
Targeting the c-Met Signaling Pathway in Cancer
TL;DR: The present understanding of c-Met oncogenic signaling supports at least three avenues of pathway selective anticancer drug development: antagonism of ligand/receptor interaction, inhibition of TK catalytic activity, and blockade of intracellular receptor/effector interactions.
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Spleen endothelial cells from patients with myelofibrosis harbor the JAK2V617F mutation.
Vittorio Rosti,Laura Villani,Roberta Riboni,Valentina Poletto,Elisa Bonetti,Lorenzo Tozzi,Gaetano Bergamaschi,Paolo Catarsi,Elena Dallera,Francesca Novara,Margherita Massa,Rita Campanelli,Gabriela Fois,Benedetta Peruzzi,Marco Lucioni,Paola Guglielmelli,Alessandro Pancrazzi,Giacomo Fiandrino,Orsetta Zuffardi,Umberto Magrini,Marco Paulli,Alessandro M. Vannucchi,Giovanni Barosi +22 more
TL;DR: Evidence is provided that some ECs from the spleen and splenic veins of patients with MF bear the JAK2V617F mutation and it is suggested that splenic ECs are involved in the process of malignant transformation in MF.
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The von Hippel–Lindau tumor suppressor gene product represses oncogenic β-catenin signaling in renal carcinoma cells
TL;DR: It is concluded that, unlike many other cancers, where HGF pathway activation contributes to malignancy through the acquisition of autocrine signaling, receptor overexpression, or mutation, in RCC cells VHL loss enables HGF-driven oncogenic β-catenin signaling.