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藥靶細(xì)胞株 > kinase激酶細(xì)胞株 > CBP73192SLC34A2-ROS1 G2032R/BaF3

SLC34A2-ROS1 G2032R/BaF3
名稱 SLC34A2-ROS1 G2032R/BaF3
型號(hào) CBP73192
報(bào)價(jià)
特點(diǎn) SLC34A2-ROS1 [G2032R]/BaF3,母細(xì)胞：BaF3，凍存條件：90% FBS+10% DMSO
  • 詳細(xì)內(nèi)容
CBP73192
I. Introduction

Cell Line Name：

SLC34A2-ROS1 [G2032R]/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 [G2032R]/BaF3expression

CBP73192 WB.png


Figure 1. Protein Expression of ROS1 detected by antibody


2.Sanger Sequencing of SLC34A2-ROS1 Fusion and G2032R mutation

CBP73192 sanger-1.png

Figure 2. SLC34A2-ROS1 Fusion

CBP73192 sanger2.png

Figure 3. ROS1 p.G2032R


3. Anti-proliferation assay

CBP73192 fig.png

Figure 4. Anti-proliferation assay of two reference compounds on the SLC34A2-ROS1 [G2032R]/BaF3 Stable Cell Line.



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