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2 results on '"Caroline Nebhan"'

1. 239 Efficacy and toxicity of single agent immune checkpoint inhibitors among adults with cancer aged ≥80 years: a multicenter international cohort study

Author

Abdul Rafeh Naqash, Shravanti Macherla, Alessio Cortellini, Melissa Bersanelli, Sebastiano Buti, Raffaele Giusti, Marco Filetti, Paolo Marchetti, Andrea Botticelli, Domenico Mallardo, Thomas Marron, Douglas Johnson, Christopher Hoimes, Vito Vanella, Toni Choueiri, Paolo Ascierto, Ella Daniels, Haocan Song, Fei Ye, Tamara Sussman, Domenico Galetta, Anwaar Saeed, Annamaria Catino, Carlo Genova, Pamela Pizzutilo, Giuseppe Lamberti, David Pinato, Rebecca Irlmeier, Caroline Nebhan, Weijie Ma, Teja Ganta, Neha Debnath, Maluki Radford, Asrar Alahmadi, Akiva Diamond, Nikhil Ramaiya, Carolyn Presley, Dwight Owen, Sarah Abou Alaiwi, Amin Nassar, Chiara Casartelli, Maria Giovanna Dal Bello, and Foteini Kalofonou

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Published
2021
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2. Acquired Resistance of EGFR-Mutant Lung Adenocarcinomas to Afatinib plus Cetuximab Is Associated with Activation of mTORC1

Author

Valentina Pirazzoli, Caroline Nebhan, Xiaoling Song, Anna Wurtz, Zenta Walther, Guoping Cai, Zhongming Zhao, Peilin Jia, Elisa de Stanchina, Erik M. Shapiro, Molly Gale, Ruonan Yin, Leora Horn, David P. Carbone, Philip J. Stephens, Vincent Miller, Scott Gettinger, William Pao, and Katerina Politi

Subjects
Biology (General), QH301-705.5
Abstract

Patients with EGFR-mutant lung adenocarcinomas (LUADs) who initially respond to first-generation tyrosine kinase inhibitors (TKIs) develop resistance to these drugs. A combination of the irreversible TKI afatinib and the EGFR antibody cetuximab can be used to overcome resistance to first-generation TKIs; however, resistance to this drug combination eventually emerges. We identified activation of the mTORC1 signaling pathway as a mechanism of resistance to dual inhibition of EGFR in mouse models. The addition of rapamycin reversed resistance in vivo. Analysis of afatinib-plus-cetuximab-resistant biopsy specimens revealed the presence of genomic alterations in genes that modulate mTORC1 signaling, including NF2 and TSC1. These findings pinpoint enhanced mTORC1 activation as a mechanism of resistance to afatinib plus cetuximab and identify genomic mechanisms that lead to activation of this pathway, revealing a potential therapeutic strategy for treating patients with resistance to these drugs.

Published
2014
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