| 名稱 | SLC34A2-ROS1/BaF3 |
| 型號 | CBP73191 |
| 報價 |  |
| 特點 | SLC34A2-ROS1/BaF3,母細胞：BaF3，凍存條件：90% FBS+10% DMSO； |
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藥靶細胞株 > kinase激酶細胞株 > CBP73191SLC34A2-ROS1/BaF3
- 詳細內容
| CBP73191 | |
| I. Introduction | |
Cell Line Name： | SLC34A2-ROS1/BaF3 |
Host Cell: | Ba/F3 |
| Stability: | 16 passages (in-house test, that not means the cell line will be instable beyond the passages we tested.) |
Application: | Anti-proliferation assay and PD assay |
Freeze Medium: | 90% FBS+10% DMSO |
Complete Culture Medium: | RPMI-1640+10%FBS |
Mycoplasma Status: | Negative |
| II.Background | |
Approximately 2% of lung tumors harbor ROS1 fusions (Bergethon et al. 2012). Like ALK fusions, ROS1 fusions are more commonly found in light smokers (<10 pack years) and/or never-smokers. ROS1 fusions are also associated with younger age and adenocarcinomas (Bergethon et al. 2012). In preclinical models, ROS1 fusions are associated with sensitivity to tyrosine kinase inhibitors that have 'off-target' activity against ROS1, such as crizotinib (Bergethon et al. 2012; Davies et al. 2012). In addition, two patients—a previously treated metastatic NSCLC patient and a 65-year-old never smoker NSCLC patient—with tumors harboring ROS1 fusions have had partial responses to crizotinib (Bergethon et al. 2012; Davies et al. 2012). In an expansion cohort of a phase I study, 50 patients with ROS1-positive NSCLC demonstrated a 72% response rate and 19.2-month median progression-free survival interval when treated with crizotinib (Ou et al. 2013; Shaw et al. 2014). In a European case study, 32 ROS1-positive NSCLC cases treated with crizotinib were retrospectively reviewed, and an 80% response rate and a 9.1-month median progression-free survival interval was calculated in this cohort (Mazières et al. 2015). Several different ROS1 rearrangements have been described in NSCLC. These include SLC34A2-ROS1, CD74-ROS1, EZR-ROS1, TPM3-ROS1, and SDC4-ROS1 (Figure 1; Davies et al. 2012; Rikova et al. 2007; Takeuchi et al. 2012). Clinically, the presence of a ROS1 rearrangement is detected by fluorescence in situ hybridization (FISH) with a ROS1 breakapart probe. FISH testing is not able to discern which particular ROS1 fusion is found in a clinical sample. ROS1 rearrangements are non-overlapping with other oncogenic mutations found in NSCLC (e.g., EGFR mutations, KRAS mutations, ALK fusions, etc.; Bergethon et al. 2012). | |
| III. Representative Data | |
1. WB of SLC34A2-ROS1 expression | |
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2.Sanger Sequencing of SLC34A2-ROS1 Fusion
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2. Anti-proliferation assay | |
Figure 3. Anti-proliferation assay of two reference compounds on the SLC34A2-ROS1/BaF3 Stable Cell Line. | |
