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2 results on '"Carlo Capalbo"'

1. BRAF mutant colorectal cancer: ErbB2 expression levels as predictive factor for the response to combined BRAF/ErbB inhibitors

Author

Evelina Miele, Luana Abballe, Gian Paolo Spinelli, Zein Mersini Besharat, Giuseppina Catanzaro, Martina Chiacchiarini, Alessandra Vacca, Agnese Po, Carlo Capalbo, and Elisabetta Ferretti

Subjects
BRAFV600E mutation, Colon cancer, Molecular therapy, Afatinib, Vemurafenib, ErbB2, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background Colorectal cancer (CRC) is a heterogeneous disease with a complex biology and a wide number of altered genes such as BRAF, KRAS and PIK3CA. Advances with new-targeted therapies have been achieved and available treating options have prolonged patient’s survival. However, BRAF-mutated CRC patients remain unresponsive to available therapies with RAF inhibitors (RAFi) alone or combined with ErbB inhibitors (ErbBi). These unmet needs require further exploitation of oncogenic signaling in order to set up individualized treatments. Methods To this end, we tested the efficacy of single agent or combined treatments using the BRAFi, vemurafenib and two different ErbBi: panitumumab and afatinib in CRC cells characterized by different molecular phenotypes. Results Combination strategies with BRAFi and ErbBi achieved a better response in BRAFV600E mutated cells expressing high levels of ErbB2. Conclusions Our findings support the importance of ErbB2 evaluation in BRAF-mutated CRC patients and its role as a positive predictor factor of response to BRAFi/ErbBi combination.

Published
2020
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2. BRAF mutant colorectal cancer: ErbB2 expression levels as predictive factor for the response to combined BRAF/ErbB inhibitors

Author

Zein Mersini Besharat, Carlo Capalbo, Luana Abballe, Elisabetta Ferretti, Giuseppina Catanzaro, Alessandra Vacca, Agnese Po, Martina Chiacchiarini, Evelina Miele, and Gian Paolo Spinelli

Subjects
0301 basic medicine, Proto-Oncogene Proteins B-raf, Cancer Research, Molecular therapy, Colorectal cancer, Cell Survival, Receptor, ErbB-2, Afatinib, Disease, medicine.disease_cause, lcsh:RC254-282, 03 medical and health sciences, 0302 clinical medicine, BRAFV600E mutation, ErbB2, ErbB, Surgical oncology, Cell Line, Tumor, Antineoplastic Combined Chemotherapy Protocols, Genetics, medicine, Panitumumab, Humans, Molecular Targeted Therapy, Vemurafenib, neoplasms, Cell Proliferation, business.industry, medicine.disease, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, BRAFV, digestive system diseases, Colon cancer, 030104 developmental biology, Oncology, 600E, mutation, 030220 oncology & carcinogenesis, Mutation, Cancer research, KRAS, business, Colorectal Neoplasms, medicine.drug, Research Article, Signal Transduction
Abstract

Background Colorectal cancer (CRC) is a heterogeneous disease with a complex biology and a wide number of altered genes such as BRAF, KRAS and PIK3CA. Advances with new-targeted therapies have been achieved and available treating options have prolonged patient’s survival. However, BRAF-mutated CRC patients remain unresponsive to available therapies with RAF inhibitors (RAFi) alone or combined with ErbB inhibitors (ErbBi). These unmet needs require further exploitation of oncogenic signaling in order to set up individualized treatments. Methods To this end, we tested the efficacy of single agent or combined treatments using the BRAFi, vemurafenib and two different ErbBi: panitumumab and afatinib in CRC cells characterized by different molecular phenotypes. Results Combination strategies with BRAFi and ErbBi achieved a better response in BRAFV600E mutated cells expressing high levels of ErbB2. Conclusions Our findings support the importance of ErbB2 evaluation in BRAF-mutated CRC patients and its role as a positive predictor factor of response to BRAFi/ErbBi combination.

Published
2020

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