Annotation Detail
Information
- Associated Genes
- ALK
- Associated Variants
- ALK EML4-ALK E6;A20
- Associated Disease
- lung non-small cell carcinoma
- Source Database
- CIViC Evidence
- Description
- Transduction of Ba/F3 cells with EML4-ALK variant 3a caused the cells to grow independently of IL3 addition. While incubation of Ba/F3 cells transduced with EML4-ALK variants 1 and 2 with Hsp90 inhibitor 17-DMAG caused cell death that was reversible with IL3 addition, Ba/F3 cells with variant 3a were not sensitized to 17-DMAG induced death, suggesting that 17-DMAG was effecting the EML4-ALK driver of IL3-independant proliferation. This in turn suggests that variant 3a may not rely on Hsp90 for stability in cancer cells to the extent of other variants.
- Variant Origin
- somatic
- Variant Origin
- Somatic
- Evidence URL
- https://civic.genome.wustl.edu/links/evidence_items/1205
- Gene URL
- https://civic.genome.wustl.edu/links/genes/1
- Variant URL
- https://civic.genome.wustl.edu/links/variants/503
- Rating
- 2
- Evidence Type
- Predictive
- Disease
- Lung Non-small Cell Carcinoma
- Evidence Direction
- Does Not Support
- Drug
- Alvespimycin
- Evidence Level
- D
- Clinical Significance
- Sensitivity/Response
- Pubmed
- 22912387
Drugs
Drug Name | Sensitivity | Supported |
---|---|---|
Alvespimycin | Sensitivity | false |