Annotation Detail
Information
- Associated Genes
- ALK
- Associated Variants
- ALK EML4-ALK V1180L
- Associated Disease
- lung non-small cell carcinoma
- Source Database
- CIViC Evidence
- Description
- The V1180L mutation in the kinase domain of rearranged ALK was found in an alectinib resistant cell line named H3122 CHR-A1, which was derived from the alectinib sensitive EML4-ALK variant 1 containing NSCLC cell line H3122 by passaging into higher concentrations of alectinib. This cell line is a model for gain of alectinib resistance, and also shows resistance to crizotinib. On the other hand, the often used tool ALK inhibitor TAE684 was highly effective in killing H3122 CHR-A1, where H3122 cells were only slightly more sensitized to TAE684-induced cell death. Ectopic expression of EML4-ALK V1180L in Ba/F3 cells caused IL3 independent growth as well as marked sensitization to TAE684, to a level greater than that seen in EML4-ALK I1171T (alectinib resistance mutation) or EML4-ALK wt, and over 1000x greater sensitivity than unaltered Ba/F3 + IL3.
- Variant Origin
- somatic
- Variant Origin
- Somatic
- Evidence URL
- https://civic.genome.wustl.edu/links/evidence_items/1290
- Gene URL
- https://civic.genome.wustl.edu/links/genes/1
- Variant URL
- https://civic.genome.wustl.edu/links/variants/528
- Rating
- 3
- Evidence Type
- Predictive
- Disease
- Lung Non-small Cell Carcinoma
- Evidence Direction
- Supports
- Drug
- TAE684
- Evidence Level
- D
- Clinical Significance
- Sensitivity/Response
- Pubmed
- 25228534
Drugs
Drug Name | Sensitivity | Supported |
---|---|---|
TAE684 | Sensitivity | true |