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科研细胞
药靶细胞
标准品
NGS靶向捕获探针
EGFR L858R-T790M-C797S/NCI-H1975
CBP73213 | |
I. Introduction | |
Cell Line Name: | EGFR L858R-T790M-C797S/NCI-H1975 |
Host Cell: | NCI-H1975 |
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 Cell-based kinase assay |
Freeze Medium: | 90% FBS+10% DMSO |
Complete Culture Medium: | RPMI-1640+10%FBS+2ug/ml puromycin |
Mycoplasma Status: | Negative |
II.Background | |
EGFR is widely recognized for its importance in cancer. Amplification and mutations have been shown to be driving events in many cancer types. Its role in non-small cell lung cancer, glioblastoma and basal-like breast cancers has spurred many research and drug development efforts. Tyrosine kinase inhibitors have shown efficacy in EGFR amplfied tumors, most notably gefitinib and erlotinib. Mutations in EGFR have been shown to confer resistance to these drugs, particularly the variant T790M, which has been functionally characterized as a resistance marker for both of these drugs. The later generation TKI's have seen some success in treating these resistant cases, and targeted sequencing of the EGFR locus has become a common practice in treatment of non-small cell lung cancer. Overproduction of ligands is another possible mechanism of activation of EGFR. ERBB ligands include EGF, TGF-a, AREG, EPG, BTC, HB-EGF, EPR and NRG1-4 (for detailed information please refer to the respective ligand section). In ligand-activated cancers, Cetuximab appears to be more effective than tyrosine-kinase inhibitors. | |
III. Representative Data | |
1.WB of EGFR L858R-T790M-C797S/NCI-H1975 |
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2.Sanger of EGFR L858R-T790M-C797S/NCI-H1975 Figure 2. EGFR L858R-T790M-C797S/NCI-H1975 T790M Figure 3. EGFR L858R-T790M-C797S/NCI-H1975 C797S
Figure 4. EGFR L858R-T790M-C797S/NCI-H1975 L858R |
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3.Anti-proliferation assay |
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Figure 5. Anti-proliferation assay of two reference compounds on the EGFR L858R-T790M-C797S/NCI-H1975 cells Line. |

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