title: Paracrine network: another step in the complexity of resistance to EGFR blockade?
abstract: Increased secretion of EGFR ligands amphiregulin and TGFα by limited KRAS-mutant clones is suggested as a paracrine resistance mechanism to anti-EGFR antibodies in colorectal cancer models. These findings are biologically sound but need to be replicated, including in the clinical setting, to foresee whether they are clinically relevant and therapeutically exploitable.
authors.affiliation: Department of Medical Oncology and Translational Research Laboratory, Catalan Institute of Oncology (ICO), Bellvitge Biomedical Research Institute (IDIBELL), L'Hospitalet de Llobregat, Barcelona, Spain.
authors.forename: Ramon
authors.initials: R
authors.lastname: Salazar
authors.affiliation: Hereditary Cancer Program and Translational Research Laboratory, Catalan Institute of Oncology (ICO), Bellvitge Biomedical Research Institute (IDIBELL), L'Hospitalet de Llobregat, Barcelona, Spain.
authors.forename: Gabriel
authors.initials: G
authors.lastname: Capellà
authors.affiliation: Medical Oncology Department, Vall d'Hebron University Hospital and Institute of Oncology (VHIO), Universitat Autònoma de Barcelona, Barcelona, Spain. jtabernero@vhio.net.
authors.forename: Josep
authors.initials: J
authors.lastname: Tabernero
mesh_terms: D066258:Amphiregulin / Q000378:metabolism*; D015179:Colorectal Neoplasms / Q000378:metabolism*; D019008:Drug Resistance, Neoplasm; D066246:ErbB Receptors / Q000037:antagonists & inhibitors*; D006801:Humans; D019899:Paracrine Communication; D016211:Transforming Growth Factor alpha / Q000378:metabolism*
chemical_list: D066258:Amphiregulin; D016211:Transforming Growth Factor alpha; D066246:ErbB Receptors