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dc.contributor.authorJohan F. Vansteenkisteen_US
dc.contributor.authorJean Luc Canonen_US
dc.contributor.authorFilippo De Brauden_US
dc.contributor.authorFrancesco Grossien_US
dc.contributor.authorTommaso De Pasen_US
dc.contributor.authorJhanelle E. Grayen_US
dc.contributor.authorWu Chou Suen_US
dc.contributor.authorEnriqueta Felipen_US
dc.contributor.authorHiroshige Yoshiokaen_US
dc.contributor.authorCesare Gridellien_US
dc.contributor.authorGrace K. Dyen_US
dc.contributor.authorSumitra Thongpraserten_US
dc.contributor.authorMartin Recken_US
dc.contributor.authorPaola Aimoneen_US
dc.contributor.authorGena Atalla Vidamen_US
dc.contributor.authorPantelia Roussouen_US
dc.contributor.authorYing A. Wangen_US
dc.contributor.authorEmmanuelle Di Tomasoen_US
dc.contributor.authorJean Charles Soriaen_US
dc.description.abstractCopyright © 2015 by the International Association for the Study of Lung Cancer. Introduction: The phosphatidylinositol 3-kinase (PI3K) pathway promotes tumor growth and treatment resistance in non-small cell lung cancer (NSCLC). The aim of the open-label, two-stage, Phase II study BASALT-1 (NCT01820325) was to investigate the pan-PI3K inhibitor buparlisib (BKM120) in patients with PI3K pathway-activated, relapsed NSCLC. Methods: After prescreening for PI3K pathway activation, patients with PI3K pathway-activated, metastatic, squamous or nonsquamous NSCLC, who had relapsed after prior systemic antineoplastic therapy, were enrolled. In Stage 1, patients received single-agent buparlisib (100 mg/day). A futility analysis was performed independently in each histology group, based on the 12-week progression-free survival rate for the first 30 patients treated in each group being less than 50%. Exploratory biomarker analyses were performed in archival tissue samples and circulating tumor DNA (ctDNA). Results: Of 1242 prescreened patients, 13.5% exhibited PI3K pathway activation. As of June 5, 2014, 63 patients (30 squamous and 33 nonsquamous) were treated in Stage 1. The 12-week progression-free survival rates were 23.3% (95% confidence interval: 9.9-42.3) and 20.0% (95% confidence interval: 7.7-38.6) in the squamous and nonsquamous groups, respectively. Stage 2 was therefore not initiated in either group. PI3K pathway mutations in ctDNA were more concordant with metastatic tissue than with primary biopsies. Conclusions: Despite preselecting patients for targeted treatment, BASALT-1 did not meet its primary objective during Stage 1. PI3K pathway activation can be detected using ctDNA, but may not be the main oncogenic driver in NSCLC. Combinations of PI3K inhibitors with other agents may demonstrate greater efficacy than monotherapy.en_US
dc.titleSafety and Efficacy of Buparlisib (BKM120) in Patients with PI3K Pathway-Activated Non-Small Cell Lung Cancer: Results from the Phase II BASALT-1 Studyen_US
article.title.sourcetitleJournal of Thoracic Oncologyen_US
article.volume10en_US Leuven– University Hospital Leuvenen_US Hôpital de Charleroien_US IRCCS Istituto Nazionale dei Tumori, Milanen_US Policlinico San Martinoen_US Europeo di Oncologiaen_US Cancer Centeren_US Cheng Kung University Hospitalen_US d`Hebron Institut de Oncologiaen_US Central Hospitalen_US Ospedaliera S.G. Moscatien_US Park Cancer Instituteen_US Mai Universityen_US of the German Center for Lung Researchen_US International AGen_US Pharmaceuticals Corporationen_US Institutes for BioMedical Research, Inc.en_US Paris-Sud XIen_US
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