Gene defects and mutant ALK kinase in human solid tumors
US8288102B2 · kind B2 · utility
Assignee
Inventors
Key dates
| Filing date | Feb 27, 2010 |
| Grant date | Oct 16, 2012 |
| Priority date | — |
| Expiry date | Aug 30, 2030 |
Classification
- Technology area (CPC G)Physics
- CPC primaryG01N2333/9121
- WIPO fieldMeasurement
- WIPO sectorInstruments
Abstract
In accordance with the invention, novel gene deletions and translocations involving chromosome 2 resulting in fusion proteins combining part of Anaplastic Lymphoma Kinase (ALK) kinase with part of a secondary protein have now been identified in human solid tumors, e.g. non-small cell lung carcinoma (NSCLC). Secondary proteins include Echinoderm Microtubule-Associated Protein-Like 4 (EML-4) and TRK-Fusion Gene (TFG). The EML4-ALK fusion protein, which retains ALK tyrosine kinase activity, was confirmed to drive the proliferation and survival of NSCLC characterized by this mutation. The invention therefore provides, in part, isolated polynucleotides and vectors encoding the disclosed mutant ALK kinase polypeptides, probes for detecting it, isolated mutant polypeptides, recombinant polypeptides, and reagents for detecting the fusion and truncated polypeptides. The disclosed identification of this new fusion protein enables new methods for determining the presence of these mutant ALK kinase polypeptides in a biological sample, methods for screening for compounds that inhibit the proteins, and methods for inhibiting the progression of a cancer characterized by the mutant polynucleotides…
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