PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27507562-1 2017 BACKGROUND: The purpose of this study was to investigate the effects of combining the phosphotidylinositol-3-kinase (PI3K) inhibitor buparlisib (BKM)120 with the anti-epidermal growth factor receptor (EGFR) agent cetuximab and radiotherapy (RT) on an orthotopic model of head and neck squamous cell carcinoma (HNSCC). NVP-BKM120 133-143 epidermal growth factor receptor Homo sapiens 201-205 34178665-7 2021 An active EGFR pathway was predictive for the response to the PI3K inhibitor buparlisib (p = 6.36E-03) and an inactive EGFR and PI3K pathway was associated with efficacy of the B-cell lymphoma (BCL) inhibitor navitoclax (p = 9.26E-03). NVP-BKM120 77-87 epidermal growth factor receptor Homo sapiens 10-14 27121230-6 2016 Inhibition of the EGFR and KRAS downstream P13K pathway using BKM120 significantly inhibited the growth of NSCLC cell lines with either EGFR or KRAS mutations. NVP-BKM120 62-68 epidermal growth factor receptor Homo sapiens 136-140 27121230-5 2016 The present study aimed to elucidate the anticancer effects of PI3K (BKM120) and MEK (PD1056309) inhibitors on NSCLC cell lines with KRAS or EGFR mutations. NVP-BKM120 69-75 epidermal growth factor receptor Homo sapiens 141-145 27121230-6 2016 Inhibition of the EGFR and KRAS downstream P13K pathway using BKM120 significantly inhibited the growth of NSCLC cell lines with either EGFR or KRAS mutations. NVP-BKM120 62-68 epidermal growth factor receptor Homo sapiens 18-22