PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 34210314-5 2021 H460 cells with K-RAS and PIK3CA mutation were most sensitive to MEK162 and BKM120 combinations. NVP-BKM120 76-82 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 26-32 31552290-0 2019 PIK3CA and MAP3K1 alterations imply luminal A status and are associated with clinical benefit from pan-PI3K inhibitor buparlisib and letrozole in ER+ metastatic breast cancer. NVP-BKM120 118-128 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 0-6 32352244-0 2020 Buparlisib in combination with tamoxifen in pretreated patients with hormone receptor-positive, HER2-negative advanced breast cancer molecularly stratified for PIK3CA mutations and loss of PTEN expression. NVP-BKM120 0-10 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 160-166 35457111-11 2022 Additionally, the presence of the PIK3CA c.1143C > G in KRAS-variant-carrying cell lines was observed to correlate with increased sensitivity to Buparlisib. NVP-BKM120 145-155 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 34-40 33376736-8 2020 From pairwise and network meta-analyses, buparlisib showed the most favorable ORR, as it was significantly different from fulvestrant in the PIK3CA-mutated patient group (2.80, 1.56 to 5.03). NVP-BKM120 41-51 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 141-147 33376736-12 2020 Conclusion: The PI3K inhibitors alpelisib and buparlisib appear to have superior efficacy and safety therapeutic choices for patients with BC, especially in PIK3CA-mutated patients. NVP-BKM120 46-56 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 157-163 31069145-5 2019 Using a humanized mouse model, we observed that BKM120, a pan-PI3K inhibitor, significantly inhibited the growth of a human bladder cancer cell line bearing a PIK3CA mutation, associated to increased immune cell infiltration (hCD45+). NVP-BKM120 48-54 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 159-165 30577988-11 2019 CONCLUSION: Buparlisib plus weekly paclitaxel might be a new treatment option for patients with metastatic MCB harboring a PIK3CA mutation. NVP-BKM120 12-22 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 123-129 31069145-7 2019 Moreover, the addition of BKM120 rendered PIK3CA-mutated tumors sensitive to PD-1 blockade. NVP-BKM120 26-32 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 42-48 30241001-9 2018 Median OS also trended in favour of buparlisib among patients with PIK3CA-mutant ctDNA (26.0 versus 24.8 months). NVP-BKM120 36-46 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 67-73 29223745-17 2018 Nonetheless, the efficacy of buparlisib supports the rationale for the use of PI3K inhibitors plus endocrine therapy in patients with PIK3CA mutations. NVP-BKM120 29-39 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 134-140 29472518-5 2018 Knockdown of NEK9 or MAP2K4 reduced both baseline and feedback MAPK/MEK signaling and showed synthetic lethality with buparlisib in vitro A complex in/del frameshift in PIK3CA decreased sensitivity to buparlisib via NEK9/MAP2K4-dependent mechanisms. NVP-BKM120 118-128 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 169-175 29472518-5 2018 Knockdown of NEK9 or MAP2K4 reduced both baseline and feedback MAPK/MEK signaling and showed synthetic lethality with buparlisib in vitro A complex in/del frameshift in PIK3CA decreased sensitivity to buparlisib via NEK9/MAP2K4-dependent mechanisms. NVP-BKM120 201-211 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 169-175 28725277-4 2017 PIK3CA mutation detected in circulating tumor DNA (ctDNA) was predictive for a buparlisib efficacy. NVP-BKM120 79-89 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 0-6 28036259-5 2017 Autophagy inhibition augmented the efficacy of BKM120 depending on PIK3CA-mutant cancer cell type. NVP-BKM120 47-53 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 67-73 28036259-8 2017 These data suggest that BKM120-induced nuclear translocation of FOXO3a might elicit autophagy and be a critical factor determining the synergistic activity of BKM120 and HCQ in PIK3CA-mutant cancer cells. NVP-BKM120 24-30 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 177-183 28036259-8 2017 These data suggest that BKM120-induced nuclear translocation of FOXO3a might elicit autophagy and be a critical factor determining the synergistic activity of BKM120 and HCQ in PIK3CA-mutant cancer cells. NVP-BKM120 159-165 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 177-183 27426307-3 2016 The aim of this study was to evaluate the therapeutic effect of PI3K inhibitor BKM120 and PARP inhibitor Olaparib on ovarian cancer cell lines bearing wild-type PIK3CA genes. NVP-BKM120 79-85 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 161-167 27426307-10 2016 CONCLUSIONS: The combined use of PI3K inhibitor BKM120 and PARP inhibitor Olaparib may be effective in ovarian cancers with a broader spectrum of cancer-associated genetic alterations but not limited to those with mutant PIK3CA or BRCA genes. NVP-BKM120 48-54 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 221-227 26715098-2 2016 BKM120 targets phosphatidylinositide-3-kinase (PIK3CA), but it is unknown whether BKM120 can reverse cetuximab resistance in KRAS mutant CRC. NVP-BKM120 0-6 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 47-53 26715098-5 2016 BKM120 only inhibited ERK phosphorylation in LoVo cells (PIK3CA wild type), but not in DLD1 or HCT116 cells at a concentration of 1 mumol/L. NVP-BKM120 0-6 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 57-63 26289070-6 2015 In contrast, PDX tumors harboring mutated PIK3CA demonstrated partial resistance to ASLAN002, which was overcome with addition of NVP-BKM120 to the treatment regimen. NVP-BKM120 134-140 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 42-48 25285632-1 2014 Recently, a new generation of PI3K-specific inhibitors, such as GDC0941 and BKM120, are being investigated in clinical trials for treatment against tumors harboring PIK3CA mutations. NVP-BKM120 76-82 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 165-171