Ludovica Giancola
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Ludovica Giancola has a total of 6 co-authors. Here are the top co-authors by number of shared publications:
- Bruno Maras
Department of Biochemical Science, Sapienza University of Rome, Piazzale Aldo Moro 5, 00185 Rome, Italy
1 shared publication - Carmine Mancone
Department of Molecular Medicine, Sapienza University of Rome, 00161 Rome, Italy
1 shared publication - Giuseppina Mignogna
Department of Biochemical Science, Sapienza University of Rome, Piazzale Aldo Moro 5, 00185 Rome, Italy
1 shared publication - Luca Sallustio
Department of Molecular Medicine, Sapienza University of Rome, 00161 Rome, Italy
1 shared publication - Pietro Angelone
Department of Molecular Medicine, Sapienza University of Rome, 00161 Rome, Italy
1 shared publication - Veronica Porreca
Department of Molecular Medicine, Sapienza University of Rome, 00161 Rome, Italy
1 shared publication
Latest Publications
- Open Access
ERK1/2 Signaling in Intrahepatic Cholangiocarcinoma: From Preclinical Advances to Therapeutic Strategies
Extracellular signal-regulated kinase 1/2 (ERK1/2) is involved in the regulation of the key cellular processes that are essential for the proper functioning of the cell under physiological conditions. Notably, the hyperactivation of ERK1/2 is implicated in oncogenesis and metastatic dissemination across various tumor types, making it an attractive candidate for targeted therapy (TT) through functional inhibition. In intrahepatic cholangiocarcinoma (iCCA), sustained ERK1/2 activation represents one of the major events within the complex signaling network that drives tumor development and progression. In this review, we dissect the biological role of ERK1/2 signaling in iCCA and highlight recent preclinical advances involving selective small-molecule ERK1/2 inhibitors. In vitro and in vivo studies have demonstrated how these inhibitors present effective anti-tumorigenic properties. In particular, PD901 and U0126 effectively reduce iCCA cell proliferation and invasion. Furthermore, Ulixertinib has shown a favorable therapeutic index and encouraging activity in clinical trials involving advanced solid tumors, including iCCA, paving the way for a new therapeutic approach targeting ERK1/2. Nevertheless, the heterogeneous and dynamic molecular landscape of iCCA, often accompanied by drug resistance, presents significant therapeutic challenges. We underscore how targeting the ERK1/2 pathway could represent a cornerstone within a multifaceted therapeutic strategy, fostering the development of personalized treatment approaches and improving clinical outcomes in iCCA patients.
Open AccessERK1/2 Signaling in Intrahepatic Cholangiocarcinoma: From Preclinical Advances to Therapeutic Strategies
Extracellular signal-regulated kinase 1/2 (ERK1/2) is involved in the regulation of the key cellular processes that are essential for the proper functioning of the cell under physiological conditions. Notably, the hyperactivation of ERK1/2 is implicated in oncogenesis and metastatic dissemination across various tumor types, making it an attractive candidate for targeted therapy (TT) through functional inhibition. In intrahepatic cholangiocarcinoma (iCCA), sustained ERK1/2 activation represents one of the major events within the complex signaling network that drives tumor development and progression. In this review, we dissect the biological role of ERK1/2 signaling in iCCA and highlight recent preclinical advances involving selective small-molecule ERK1/2 inhibitors. In vitro and in vivo studies have demonstrated how these inhibitors present effective anti-tumorigenic properties. In particular, PD901 and U0126 effectively reduce iCCA cell proliferation and invasion. Furthermore, Ulixertinib has shown a favorable therapeutic index and encouraging activity in clinical trials involving advanced solid tumors, including iCCA, paving the way for a new therapeutic approach targeting ERK1/2. Nevertheless, the heterogeneous and dynamic molecular landscape of iCCA, often accompanied by drug resistance, presents significant therapeutic challenges. We underscore how targeting the ERK1/2 pathway could represent a cornerstone within a multifaceted therapeutic strategy, fostering the development of personalized treatment approaches and improving clinical outcomes in iCCA patients.