KRAS oncogene mutations (MUTKRAS) drive resistance to EGFR inhibition by providing alternative signaling as demonstrated in colo-rectal cancer. In non-small cell lung cancer (NSCLC), the efficacy of treatment with EGFR tyrosine kinase inhibitors (EGFR-TKIs) depends on activating EGFR mutations (MUTEGFR). However, inhibition of EGFR may select resistant cells displaying alternative signaling, i.e., KRAS, or restoration of EGFR activity due to additional MUTEGFR, i.e., the c.2369C > T (p.T790MEGFR).

Contribution of KRAS mutations and c.2369C > T (p.T790M) EGFR to acquired resistance to EGFR-TKIs in EGFR mutant NSCLC: a study on circulating tumor DNA

DEL RE, MARZIA;PETRINI, IACOPO;LUCCHESI, MAURIZIO;Citi, Valentina;FALCONE, ALFREDO;DANESI, ROMANO
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Abstract

KRAS oncogene mutations (MUTKRAS) drive resistance to EGFR inhibition by providing alternative signaling as demonstrated in colo-rectal cancer. In non-small cell lung cancer (NSCLC), the efficacy of treatment with EGFR tyrosine kinase inhibitors (EGFR-TKIs) depends on activating EGFR mutations (MUTEGFR). However, inhibition of EGFR may select resistant cells displaying alternative signaling, i.e., KRAS, or restoration of EGFR activity due to additional MUTEGFR, i.e., the c.2369C > T (p.T790MEGFR).
In corso di stampa
DEL RE, Marzia; Tiseo, Marcello; Bordi, Paola; D'Incecco, Armida; Camerini, Andrea; Petrini, Iacopo; Lucchesi, Maurizio; Inno, Alessandro; Spada, Daniele; Vasile, Enrico; Citi, Valentina; Malpeli, Giorgio; Testa, Enrica; Gori, Stefania; Falcone, Alfredo; Amoroso, Domenico; Chella, Antonio; Cappuzzo, Federico; Ardizzoni, Andrea; Scarpa, Aldo; Danesi, Romano
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11568/771925
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