PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33196586-27 2021 Moreover, in an in vivo assay, crizotinib, a ROS1 inhibitor, markedly inhibited the growth of MAN1A1-ROS1 rearrangement-induced transformed cells in a dose-dependent manner. Crizotinib 31-41 Ros1 proto-oncogene Mus musculus 101-105 34907086-4 2022 In addition, lorlatinib and repotrectinib are actively being explored in the setting of treatment naive or crizotinib-resistant ROS1 fusion driven NSCLC. Crizotinib 107-117 Ros1 proto-oncogene Mus musculus 128-132 33196586-27 2021 Moreover, in an in vivo assay, crizotinib, a ROS1 inhibitor, markedly inhibited the growth of MAN1A1-ROS1 rearrangement-induced transformed cells in a dose-dependent manner. Crizotinib 31-41 Ros1 proto-oncogene Mus musculus 45-49 33324391-4 2020 Ba/F3 cells expressing crizotinib sensitive ROS1 fusion and crizotinib resistant ROS1-G2032R mutation were used to explore the relationship between ROS1 fusion, ROS1-G2032R mutation and programmed death-ligand 1 (PD-L1) expression and the clinical potential of anti-PD-L1 ICI therapy. Crizotinib 23-33 Ros1 proto-oncogene Mus musculus 44-48 32923114-8 2020 We found PD-L1 expression was modulated by MEK-ERK pathway signaling in both parental and Crizotinib-resistant NSCLC cells with ROS1 fusion. Crizotinib 90-100 Ros1 proto-oncogene Mus musculus 128-132 32923114-9 2020 Conclusions: The correlation between ROS1-fusion and PD-L1 overexpression suggested that PD-L1/PD-1 blockade could be the second-line treatment option for the Crizotinib-resistant NSCLC with ROS1 rearrangement. Crizotinib 159-169 Ros1 proto-oncogene Mus musculus 37-41 32923114-9 2020 Conclusions: The correlation between ROS1-fusion and PD-L1 overexpression suggested that PD-L1/PD-1 blockade could be the second-line treatment option for the Crizotinib-resistant NSCLC with ROS1 rearrangement. Crizotinib 159-169 Ros1 proto-oncogene Mus musculus 191-195 31143519-1 2019 Crizotinib is a tyrosine kinase inhibitor (TKI) approved for the treatment of non-small cell lung cancers (NSLCL) and lymphomas expressing activating translocations or mutations of oncogenic tyrosine kinases (in particular ALK and ROS1). Crizotinib 0-10 Ros1 proto-oncogene Mus musculus 231-235 31260890-7 2019 Furthermore, molecular modeling disclosed that all the representative inhibitors could dock into the active site of ALK and ROS1, which gave a probable explanation of anti Crizotinib-resistant mutants. Crizotinib 172-182 Ros1 proto-oncogene Mus musculus 124-128 31260890-8 2019 These results indicated that our work has established a path forward for the generation of anti Crizotinib-resistant ALK/ROS1 dual inhibitors. Crizotinib 96-106 Ros1 proto-oncogene Mus musculus 121-125 31143519-2 2019 We recently observed that high-dose (final concentration in vivo: ~10 microM) crizotinib can induce immunogenic cell death (ICD) in cancer cells lacking ALK/ROS1 activation through off-target effects that require the inhibition of several other tyrosine kinases. Crizotinib 78-88 Ros1 proto-oncogene Mus musculus 157-161 25351743-0 2015 Cabozantinib overcomes crizotinib resistance in ROS1 fusion-positive cancer. Crizotinib 23-33 Ros1 proto-oncogene Mus musculus 48-52 28717217-2 2017 The ROS1 tyrosine kinase inhibitor (TKI) crizotinib has induced marked tumour shrinkage in ROS1-rearranged cancers. Crizotinib 41-51 Ros1 proto-oncogene Mus musculus 4-8 28717217-4 2017 Previous findings indicate that cabozantinib overcomes secondary mutation-mediated crizotinib-resistance in ROS1-fusion-positive cells. Crizotinib 83-93 Ros1 proto-oncogene Mus musculus 108-112 26964870-5 2016 Tumors developed progressively in the untreated TG mice of both lines, whereas those receiving oral administration of an ALK/MET/ROS1 inhibitor, crizotinib, and an ALK/ROS1 inhibitor, ASP3026, showed marked reduction in the tumor burden. Crizotinib 145-155 Ros1 proto-oncogene Mus musculus 129-133 25688157-9 2015 ROS1 G2032R and L2155S mutations conferred resistance to crizotinib in Ba/F3 cells. Crizotinib 57-67 Ros1 proto-oncogene Mus musculus 0-4 25351743-3 2015 Thus, understanding the crizotinib-resistance mechanisms in ROS1-rearranged NSCLC and identification of therapeutic strategies to overcome the resistance are required. Crizotinib 24-34 Ros1 proto-oncogene Mus musculus 60-64 25351743-8 2015 RESULTS: We identified multiple novel crizotinib-resistance mutations in the ROS1 kinase domain, including the G2032R mutation. Crizotinib 38-48 Ros1 proto-oncogene Mus musculus 77-81 23418494-9 2013 The ALK/MET/ROS1 kinase inhibitor, crizotinib, suppressed fusion-induced anchorage-independent growth of NIH3T3 cells. Crizotinib 35-45 Ros1 proto-oncogene Mus musculus 12-16