Published in

Impact Journals, Oncotarget, 8(8), p. 13611-13619, 2016

DOI: 10.18632/oncotarget.6957

Links

Tools

Export citation

Search in Google Scholar

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

Journal article published in 2016 by Marzia Del Re ORCID, Marcello Tiseo, Paola Bordi, Armida D'Incecco, Armida D’Incecco, Andrea Camerini, Iacopo Petrini, Maurizio Lucchesi, Alessandro Inno, Daniele Spada, Enrico Vasile, Valentina Citi, Giorgio Malpeli, Enrica Testa, Stefania Gori and other authors.
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

Full text: Download

Red circle
Preprint: archiving forbidden
Red circle
Postprint: archiving forbidden
Green circle
Published version: archiving allowed
Upload
Policy details
Data provided by SHERPA/RoMEO

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).