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; 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. - In: ONCOTARGET. - ISSN 1949-2553. - ELETTRONICO. - 8:8(2017), pp. 13611-13619. [10.18632/oncotarget.6957]
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
ARDIZZONI, ANDREA;
2017
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).I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
