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16 results on '"Di Mauro, C"'

1. Inhibition of Hedgehog signalling by NVP-LDE225 (Erismodegib) interferes with growth and invasion of human renal cell carcinoma cells

Author

D’Amato, C, primary, Rosa, R, additional, Marciano, R, additional, D’Amato, V, additional, Formisano, L, additional, Nappi, L, additional, Raimondo, L, additional, Di Mauro, C, additional, Servetto, A, additional, Fulciniti, F, additional, Cipolletta, A, additional, Bianco, C, additional, Ciardiello, F, additional, Veneziani, B M, additional, De Placido, S, additional, and Bianco, R, additional

Published
2014
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16. The dual PI3K/mTOR inhibitor PKI-587 enhances sensitivity to cetuximab in EGFR-resistant human head and neck cancer models

Author

C. Di Mauro, Lucia Raimondo, Lucia Nappi, R. Marciano, Bianca Maria Veneziani, C Fusciello, Valentina D’Amato, C. D'Amato, Roberto Bianco, R. Rosa, S. De Placido, Alberto Servetto, Luigi Formisano, D'Amato, V, Rosa, R, D'Amato, C, Formisano, L, Marciano, R, Nappi, L, Raimondo, L, Di Mauro, C, Servetto, A, Fusciello, C, Veneziani, BIANCA MARIA, DE PLACIDO, Sabino, and Bianco, Roberto

Subjects
Cancer Research, Pathology, Cetuximab, Apoptosis, HNSCC, Mice, Antineoplastic Combined Chemotherapy Protocols, Neoplasm, Phosphoinositide-3 Kinase Inhibitors, Mice, Inbred BALB C, Caspase 3, Triazines, TOR Serine-Threonine Kinases, Cetuximab resistance, ErbB Receptors, Oncology, Head and Neck Neoplasms, Monoclonal, Carcinoma, Squamous Cell, medicine.drug, medicine.medical_specialty, Morpholines, PI3K-mTOR inhibitors, Mice, Nude, Antineoplastic Agents, Biology, Antibodies, Monoclonal, Humanized, Cell Line, Tumor, Autophagy, medicine, Carcinoma, Animals, Humans, neoplasms, PI3K/AKT/mTOR pathway, Cell Proliferation, cetuximab resistance, Squamous Cell Carcinoma of Head and Neck, target therapy, Cell growth, Cancer, medicine.disease, Xenograft Model Antitumor Assays, digestive system diseases, Drug Resistance, Neoplasm, PI3K7mTOR inhibitors, Cancer research, Translational Therapeutics
Abstract

Background:Cetuximab is the only targeted agent approved for the treatment of head and neck squamous cell carcinomas (HNSCC), but low response rates and disease progression are frequently reported. As the phosphoinositide 3-kinase (PI3K) and the mammalian target of rapamycin (mTOR) pathways have an important role in the pathogenesis of HNSCC, we investigated their involvement in cetuximab resistance.Methods:Different human squamous cancer cell lines sensitive or resistant to cetuximab were tested for the dual PI3K/mTOR inhibitor PF-05212384 (PKI-587), alone and in combination, both in vitro and in vivo.Results:Treatment with PKI-587 enhances sensitivity to cetuximab in vitro, even in the condition of epidermal growth factor receptor (EGFR) resistance. The combination of the two drugs inhibits cells survival, impairs the activation of signalling pathways and induces apoptosis. Interestingly, although significant inhibition of proliferation is observed in all cell lines treated with PKI-587 in combination with cetuximab, activation of apoptosis is evident in sensitive but not in resistant cell lines, in which autophagy is pre-eminent. In nude mice xenografted with resistant Kyse30 cells, the combined treatment significantly reduces tumour growth and prolongs mice survival.Conclusions:Phosphoinositide 3-kinase/mammalian target of rapamycin inhibition has an important role in the rescue of cetuximab resistance. Different mechanisms of cell death are induced by combined treatment depending on basal anti-EGFR responsiveness. © 2014 Cancer Research UK.

Published
2014
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