Aberrant activation of the MET receptor in cancer is sustained by genetic alterations or, more frequently, by transcriptional upregulations. A fraction of MET-amplified or mutated tumors are sensible to MET targeting agents, but their responsiveness is typically short-lasting, as secondary resistance eventually occurs. Since in the absence of genetic alterations MET is usually not a tumor driver, MET overexpressing tumors are not/poorly responsive to MET targeted therapies. Consequently, the vast majority of tumors exhibiting MET activation still represent an unmet medical need.

Efficacy of CAR-T immunotherapy in MET overexpressing tumors not eligible for anti-MET targeted therapy

Donini, Chiara;Cortese, Marco;Ughetto, Stefano;Modica, Chiara;Proment, Alessia;Vitali, Letizia;Comoglio, Paolo Maria;Giordano, Silvia;Sangiolo, Dario;Leuci, Valeria;Vigna, Elisa
2022-01-01

Abstract

Aberrant activation of the MET receptor in cancer is sustained by genetic alterations or, more frequently, by transcriptional upregulations. A fraction of MET-amplified or mutated tumors are sensible to MET targeting agents, but their responsiveness is typically short-lasting, as secondary resistance eventually occurs. Since in the absence of genetic alterations MET is usually not a tumor driver, MET overexpressing tumors are not/poorly responsive to MET targeted therapies. Consequently, the vast majority of tumors exhibiting MET activation still represent an unmet medical need.
2022
41
1
1
19
CAR; Gastric cancer; Immunotherapy; MET oncogene; Targeted therapy; Humans; Mice; Animals; Immunotherapy; T-Lymphocytes; Cell Line, Tumor; Heterografts; Xenograft Model Antitumor Assays; Receptors, Chimeric Antigen
Chiriaco, Cristina; Donini, Chiara; Cortese, Marco; Ughetto, Stefano; Modica, Chiara; Martinelli, Ilaria; Proment, Alessia; Vitali, Letizia; Fontani, ...espandi
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2318/1878036
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