C
Carlo Santini
Researcher at University of Camerino
Publications - 155
Citations - 6413
Carlo Santini is an academic researcher from University of Camerino. The author has contributed to research in topics: Ligand & Copper. The author has an hindex of 35, co-authored 146 publications receiving 5560 citations. Previous affiliations of Carlo Santini include University of Milan & École Normale Supérieure.
Papers
More filters
Journal ArticleDOI
Advances in copper complexes as anticancer agents.
Carlo Santini,Maura Pellei,Valentina Gandin,Marina Porchia,Francesco Tisato,Cristina Marzano +5 more
Journal ArticleDOI
Copper complexes as anticancer agents
TL;DR: This overview, collecting the most significant strategies adopted in the last ten years to design promising anticancer copper(I,II) compounds, would be a help to the researchers working in this field.
Journal ArticleDOI
Copper in diseases and treatments, and copper-based anticancer strategies.
TL;DR: Investigations into the occurrence of mechanisms of action quite different from platinum drugs head toward the development of new anticancer metallodrugs with improved specificity and decreased toxic side effects.
Journal ArticleDOI
A novel copper complex induces paraptosis in colon cancer cells via the activation of ER stress signalling.
Valentina Gandin,Maura Pellei,Francesco Tisato,Marina Porchia,Carlo Santini,Cristina Marzano +5 more
TL;DR: Light is shed on the signaling pathways involved in paraptosis thus offering a new tool to overcome apoptosis‐resistance in colon cancer cells, and providing a mechanistic characterization of CP‐induced cancer cell death.
Journal ArticleDOI
In vitro antitumor activity of the water soluble copper(I) complexes bearing the tris(hydroxymethyl)phosphine ligand.
Cristina Marzano,Valentina Gandin,Maura Pellei,Davide Colavito,Grazia Papini,Giancarlo Gioia Lobbia,Elda Del Giudice,Marina Porchia,Francesco Tisato,Carlo Santini +9 more
TL;DR: Cytological stains and flow cytometric analyses indicated that the phosphine copper(I) complex is able to inhibit the growth of tumor cells via G2/M cell cycle arrest and paraptosis accompanied with the loss of mitochondrial transmembrane potential.