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FLASH GENE

Symbol

ALK

contributors: mct/shn - updated : 14-11-2013

HGNC name	anaplastic lymphoma receptor tyrosine kinase
HGNC id	427

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

ASSOCIATED DISORDERS

corresponding disease(s)

IMT , ALCL , NBL2

Other morbid association(s)

Type Gene Modification Chromosome rearrangement Protein expression Protein Function tumoral fusion translocation     fused with SEC31L1, in a translocation t(2;4)(p23;q21), in an intraabdominal inflammatory myofibroblastic tumor tumoral   translocation     translocation t(2;5)(p23;q35),(see NPM1) in anaplastic nodal non Hodgkin lymphoma and B cell lymphoma tumoral   inversion     inv(2)(p23;q35)in anaplastic large-cell lymphoma tumoral fusion       with EML4 in non-small-cell lung cancer tumoral germinal mutation       in most hereditary neuroblastomas tumoral somatic mutation     gain of function activating mutations can be somatically acquired in neuroblastoma tumoral       gain of function in neuroblastoma

Susceptibility

Variant & Polymorphism

Candidate gene
Marker
Therapy target	represent a very attractive therapeutic target in this disease that is still frequently fatal with current treatments (ALK-specific kinase inhibitors might improve its clinical outcome)
	System Type Disorder Pubmed cancer lung   ALK inhibitors may provide a means to control NSCLC in the latter population of patients cancer     identification of the downstream effector pathways controlled by ALK should pave the way for the rational design of ALK-inhibition therapies for the treatment of a subset of human cancers that harbor ALK aberrations cancer brain glioma/neuroblstoma germline or acquired activation of this cell-surface kinase is a tractable therapeutic target for the neuroblastoma, lethal paediatric malignancy cancer     inhibition of ALK kinase activity results in anti-tumoural efficacy

ANIMAL & CELL MODELS

	Forced expression of wild-type ALK and Neuroblastoma-related constitutively active ALK mutants in cultures of proliferating immature sympathetic neurons results in a strong proliferation increase, whereas Alk knockdown and pharmacological inhibition of Alk activity decrease proliferation
	in vivo inhibition of Alk signaling by virus-mediated shRNA knockdown of Alk and Midkine leads to strongly reduced sympathetic neuron proliferation