Understanding Anaplastic Lymphoma Kinase

Interesting article on Interpreting the Alk gene rearrangement:
http://www.mayomedicallaboratories.com/interpretive-guide/index.html?alpha=L&unit_code=60619

A youtube video explaining the FISH test for the Alk mutation in NSCLC.
http://www.youtube.com/watch?v=Bfsq5Vdr1OY&noredirect=1

ALKIn lung cancer, EML4-ALK is the most common 2p23 rearrangement associated with the ALK gene, which encodes anaplastic lymphoma kinase (ALK). EML4-ALK arises from fusion between the 5′ end of the EML4 gene and the 3′ end of the ALK gene. Patients with ALK rearrangements are younger than most patients with NSCLC.⁸ EML4-ALK rearrangements are more common in adenocarcinomas of never or light smokers whose tumors lack EGFR and KRAS mutations. Histology is typically characterized by mucin production and either a solid growth pattern containing signet-ring cells (more likely in Western patients) or acinar growth pattern (more likely in Asian patients).⁹

EML4-ALK and other 2p23 fusion products lead to the production of a constitutively activated kinase, which is likely to be sensitive to ALK inhibitors that have shown efficacy against ALK–rearranged lung tumors and cell lines. For example, in phase I testing, NSCLC harboring ALK rearrangements responded to PF-02341066 (crizotinib, Pfizer) treatment.¹⁰ Phase II and III clinical trials are underway. Patients who harbor ALK rearrangements do not benefit from treatment with the EGFR-specific TKIs and should be considered for ALK-targeted clinical trials.⁸

-More info on ALK
http://ghr.nlm.nih.gov/gene/ALK