Atlas of Genetics and Cytogenetics in Oncology and Haematology


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ALK (anaplastic lymphoma receptor tyrosine kinase)

Identity

Other namesanaplastic lymphoma kinase (Ki-1)
CD246
HGNC (Hugo) ALK
LocusID (NCBI) 238
Location 2p23.2
Location_base_pair Starts at 29415640 and ends at 30144477 bp from pter ( according to hg19-Feb_2009)  [Mapping]
 
  ALK (2p23) - Courtesy Mariano Rocchi, Resources for Molecular Cytogenetics.

DNA/RNA

Description The gene is composed of 29 exons spanning in a region of 728793 bp.
Transcription 6226 bp cDNA; coding sequence: 4.9 kb.

Protein

 
Description 1620 amino acids; 177 kDa; after glycosylation, produces a 200 kDa mature glycoprotein; type I transmembrane receptor; composed of an extracellular region (containing two MAM and one LDLa domains, and one glycin-rich region), a transmembrane, and an intracellular region (composed of a juxta-membrane domain, a tyrosine kinase domain (1122-1376), and a C-terminal domain; dimerization.
Expression Is tissue specific; mainly in: central and peripheral nervous system during development (less in adult), and testis; not in the lymphocytes.
Localisation Cell membrane.
Function ALK is a membrane associated tyrosine kinase receptor of the insulin receptor superfamily. The function of the full-length ALK receptor is poorly understood. It has a probable role in the central and peripheral nervous system development and maintenance. ALK is a dependence receptor, which may exert antagonist functions, proapoptotic or antiapoptotic, depending on the absence or presence of a ligand (Mourali et al., 2006). Dependence receptors have a potential role in cancer and development (Allouche, 2007). Ligands available for this demonstration were agonist anti-ALK antibodies (Motegi et al., 2004; Moog-Lutz et al., 2005). If a specific ALK ligand (jelly belly) has been clearly identified in Drosophila, it has no homologue in vertebrates (Palmer et al., 2009). ALK is still an orphan receptor, given the high level of controversy about pleiotrophin and midkine, which have been proposed as ligands by Stoica et al. (2001, 2002) (see review by Chiarle et al., 2008).
Homology Homologies with the insulin receptor super family: LTK (leucocyte tyrosine kinase), IGF1-R, IRb, TRKA, ROS (homolog of the drosophila Sevenless).

Implicated in

Entity ALK+ anaplastic large cell lymphoma (ALCL)
Disease ALCL are high grade non Hodgkin lymphomas. ALK+ ALCL are ALCL where ALK is involved in a fusion gene; systemic ALK+ ALCL (as opposed to cutaneous ALCL, which are usually ALK negative) represent 60 to 80 % of ALCL cases (they are CD30+, ALK+); 70 to 80% of ALK+ ALCL cases bear a t(2;5); the remaining ALK+ ALCL cases bear variant translocations "X-ALK", where X designates a partner gene.
Prognosis Although presenting as a high grade tumour, an 80% five year survival is associated with this anomaly, but recurrence is a concern.
Cytogenetics The prototype anomaly is the t(2;5)(p23;q35) generating the NPM1-ALK fusion.
Alternative anomalies involving the ALK gene in ALCL are described below as "cytoplasmic ALK+ ALCL" cases, among which the t(1;2) TPM3-ALK is found in 20% of ALK+ ALCL.
Complex karyotypes may also be found.
Hybrid/Mutated Gene 5' NPM1 - 3' ALK on the der(5).
Abnormal Protein 680 amino acids, 80 kDa; N-term 117 amino acids from NPM1 fused to the 563 C-term amino acids of ALK (i.e. composed of the oligomerization domain and the metal binding site of NPM1, and the entire cytoplasmic portion of ALK); no apparent expression of the ALK/NPM1 counterpart. Characteristic localisation in the cytoplasm, nucleus and nucleolus, due to heterooligomerization of NPM1-ALK and normal NPM1 whereas the normal NPM1 protein is confined to the nucleus and nucleolus; constitutive activation of the catalytic domain of ALK.
Oncogenesis Via the kinase function activated by oligomerization of NPM1-ALK mediated by the NPM1 part.
  
Entity Cytoplasmic ALK+ anaplasic large cell lymphoma (ALCL)
Prognosis Present a favourable prognosis comparable to the one found in t(2;5) ALK+ ALCL.
Cytogenetics Either t(X;2)(q11;p23), t(1;2)(q25;p23), inv(2)(p23q35), t(2;3)(p23;q21), t(2;17)(p23;q23), t(2;17)(p23;q25), t(2;19)(p23;p13.1) or t(2;22)(p23;q11.2).
Hybrid/Mutated Gene 5' MSN, TPM3, ATIC, TFG, CLTC, ALO17, TPM4 or MYH9 - 3' ALK.
Abnormal Protein N-term amino acids from the partner gene fused to the 563 C-term amino acids (in the great majority of cases) from ALK (i.e. the entire cytoplasmic portion of ALK with the tyrosine kinase domain); cytoplasmic/membraneous localisation only.
Oncogenesis The partner gene seems to provoke the dimerization of the fused X-ALK, which should lead to constitutive autophosphorylation and activation of the ALK tyrosine kinase, as for NPM1-ALK (see t(2;5)(p23;q35)).
  
Entity Inflammatory myofibroblastic tumours with 2p23 rearrangements
Disease Rare soft tissue tumour found in children and young adults about one third to half of inflammatory myofibroblastic tumour cases present with a 2p23 rearrangement involving ALK.
Prognosis Good prognosis.
Cytogenetics t(1;2)(q25;p23), t(2;2)(p23;q13) or inv(2)(p23;q11-13), inv(2)(p23;q35), t(2;4)(p23;q21), t(2;11)(p23;p15), t(2;17)(p23;q23), or t(2;19)(p23;p13.1) so far.
Hybrid/Mutated Gene 5' TPM3 in the t(1;2), RANBP2 in the t(2;2) or inv(2)(p23;q11-13), 5' ATIC in inv(2)(p23;q35), 5' SEC31L1 in t(2;4), 5' CARS in the t(2;11), 5' CLTC in the t(2;17), or 5' TPM4 in the t(2;19) - 3' ALK.
Abnormal Protein N-term amino acids from the partner gene fused to the 563 C-term amino acids from ALK (i.e. the entire cytoplasmic portion of ALK with the tyrosine kinase domain); homodimerization of the fusion protein is known or suspected.
Oncogenesis Fused-ALK is constitutively activated.
  
Entity ALK+ diffuse large B-cell lymphoma (DLBCL)
Disease Very rare form of DLBCL (40 cases described) expressing either ALK in fusion with CLTC (cytoplasmic granular localisation) associated to t(2;17)(p23;q23) (most frequently), or (rarely) NPM1-ALK in t(2;5)(p23;q35); tumours are EMA+, CD30- and CD20-negative.
Prognosis Poor prognosis: aggressive lymphoma with 25% five year survival.
Cytogenetics t(2;5)(p23;q35) or t(2;17)(p23;q23).
Hybrid/Mutated Gene 5' NPM1 or CLTC - 3' ALK.
Abnormal Protein N-term amino acids from the partner gene fused to the 563 C-term amino acids from ALK (i.e. the entire cytoplasmic portion of ALK with the tyrosine kinase domain); homodimerization of the fusion protein is known or suspected.
Oncogenesis Fused-ALK is constitutively activated.
  
Entity ALK+ non-small cell lung cancer (NSCLC)
Disease 1-6 % of all NSCLC present a rearrangement involving ALK fused to EML4 in an inv(2)(p21p23); studies on East Asian and American/European patients (Soda et al., 2007; Perner et al., 2008).
Prognosis 50% survival at 24 months, so far (first identification in 2007).
Cytogenetics inv(2)(p21;p23).
Hybrid/Mutated Gene 5' EML4 - 3' ALK; multiple variants of EML4-ALK noted depending on the breakpoint on the EML gene; ALK fusion starts at a portion encoded by exon 20.
Abnormal Protein N-term amino acids from the partner gene fused to the 563 C-term amino acids from ALK (i.e. the entire cytoplasmic portion of ALK with the tyrosine kinase domain); homodimerization of the fusion protein is known or suspected; protein is difficult to detect by classical immunohistochemistry methods (low expression).
Oncogenesis Fused-ALK is constitutively activated.
Note: in a European study, EML4-ALK fusion transcript has also been found in up to 9% non-tumour lung tissue from lung tumour patients. Interestingly, the EML4-ALK transcript was not detected in matching tumour samples from the same patients (Martelli et al., 2009).
  
Entity Familial neuroblastoma and sporadic neuroblastoma
Disease Neuroblastoma is a cancer of early childhood that arises from the developing autonomic nervous system, giving rise to peripheral tumours. It is the most common malignancy diagnosed in the first year of life and shows a wide range of clinical phenotypes, with a few patients having tumours that regress spontaneously, whereas most patients have aggressive metastatic disease. It can be transmitted in an autosomal dominant mode as a familial predisposition, or occur as a sporadic disease.
Prognosis Aggressive neuroblastoma cases have survival probabilities of less then 40% despite intensive chemoradiotherapy, and the disease continues to account for 15% of childhood cancer mortality.
Cytogenetics Gene amplifications or mutations of ALK;
Associated alterations: tumours from patients with an aggressive phenotype often show amplification of the MYCN oncogene, and/or deletions of chromosome arms 1p and 11q.
Hybrid/Mutated Gene Several point mutations located in the coding region of the receptor intracellular portion, mostly in the tyrosine kinase domain.
Abnormal Protein 54 ALK mutations reported, affecting 12 different residues (Caren et al., 2008; Chen et al., 2008; George et al., 2008; Janoueix-Lerosey et al., 2008; Mosse et al., 2008); two hotspots: F1174 and R1275.
Most frequent germline mutations (familial cases): G1128A, R1192P, R1275Q.
Most frequent somatic mutations (sporadic cases): F1174L/I, F1245C/V.
Oncogenesis Gene amplifications or point mutations both confer constitutive kinase activation.
  

Breakpoints

 
Note Most of the breakpoints occur in the same intron of ALK, whichever partner is involved in the fusion protein.

To be noted

ALK in fusion to several gene partners, is found implicated both in hematopoietic and non-hematopoietic solid tumours; this was a new concept in 2003, that several different types of tumour may result from the same chromosomal/genes rearrangement(s).

External links

Nomenclature
HGNC (Hugo)ALK   427
Cards
AtlasALK
Entrez_Gene (NCBI)ALK  238  anaplastic lymphoma receptor tyrosine kinase
GeneCards (Weizmann)ALK
Ensembl (Hinxton)ENSG00000171094 [Gene_View]  chr2:29415640-30144477 [Contig_View]  ALK [Vega]
AceView (NCBI)ALK
Genatlas (Paris)ALK
WikiGenes238
SOURCE (Princeton)NM_004304
Genomic and cartography
GoldenPath (UCSC)ALK  -  2p23.2   chr2:29415640-30144477 -  2p23   [Description]    (hg19-Feb_2009)
EnsemblALK - 2p23 [CytoView]
Mapping of homologs : NCBIALK [Mapview]
OMIM105590   256700   613014   
Gene and transcription
Genbank (Entrez)AB209477 AK296218 BC156207 BC157090 DA455128
RefSeq transcript (Entrez)NM_004304
RefSeq genomic (Entrez)AC_000134 NC_000002 NC_018913 NG_009445 NT_022184 NW_001838768 NW_004929300
Consensus coding sequences : CCDS (NCBI)ALK
Cluster EST : UnigeneHs.654469 [ NCBI ]
CGAP (NCI)Hs.654469
Alternative Splicing : Fast-db (Paris)GSHG0017525
Alternative Splicing GalleryENSG00000171094
Gene ExpressionALK [ NCBI-GEO ]     ALK [ SEEK ]   ALK [ MEM ]
Protein : pattern, domain, 3D structure
UniProt/SwissProtQ9UM73 (Uniprot)
NextProtQ9UM73  [Medical]
With graphics : InterProQ9UM73
Splice isoforms : SwissVarQ9UM73 (Swissvar)
Catalytic activity : Enzyme2.7.10.1 [ Enzyme-Expasy ]   2.7.10.12.7.10.1 [ IntEnz-EBI ]   2.7.10.1 [ BRENDA ]   2.7.10.1 [ KEGG ]   
Domaine pattern : Prosite (Expaxy)LDLRA_1 (PS01209)    LDLRA_2 (PS50068)    MAM_1 (PS00740)    MAM_2 (PS50060)    PROTEIN_KINASE_ATP (PS00107)    PROTEIN_KINASE_DOM (PS50011)    PROTEIN_KINASE_TYR (PS00109)    RECEPTOR_TYR_KIN_II (PS00239)   
Domains : Interpro (EBI)ALK    ConA-like_lec_gl_sf    Kinase-like_dom    LDrepeatLR_classA_rpt    MAM_dom    Prot_kinase_dom    Protein_kinase_ATP_BS    Ser-Thr/Tyr_kinase_cat_dom    Tyr_kinase_AS    Tyr_kinase_cat_dom    Tyr_kinase_rcpt_2_CS   
Related proteins : CluSTrQ9UM73
Domain families : Pfam (Sanger)MAM (PF00629)    Pkinase_Tyr (PF07714)   
Domain families : Pfam (NCBI)pfam00629    pfam07714   
Domain families : Smart (EMBL)LDLa (SM00192)  TyrKc (SM00219)  
DMDM Disease mutations238
Blocks (Seattle)Q9UM73
PDB (SRS)2KUP    2KUQ    2XB7    2XBA    2XP2    2YFX    2YHV    2YJR    2YJS    2YS5    2YT2    3AOX    3L9P    3LCS    3LCT    4ANL    4ANQ    4ANS    4DCE    4FNW    4FNX    4FNY    4FNZ    4FOB    4FOC    4FOD    4JOA   
PDB (PDBSum)2KUP    2KUQ    2XB7    2XBA    2XP2    2YFX    2YHV    2YJR    2YJS    2YS5    2YT2    3AOX    3L9P    3LCS    3LCT    4ANL    4ANQ    4ANS    4DCE    4FNW    4FNX    4FNY    4FNZ    4FOB    4FOC    4FOD    4JOA   
PDB (IMB)2KUP    2KUQ    2XB7    2XBA    2XP2    2YFX    2YHV    2YJR    2YJS    2YS5    2YT2    3AOX    3L9P    3LCS    3LCT    4ANL    4ANQ    4ANS    4DCE    4FNW    4FNX    4FNY    4FNZ    4FOB    4FOC    4FOD    4JOA   
PDB (RSDB)2KUP    2KUQ    2XB7    2XBA    2XP2    2YFX    2YHV    2YJR    2YJS    2YS5    2YT2    3AOX    3L9P    3LCS    3LCT    4ANL    4ANQ    4ANS    4DCE    4FNW    4FNX    4FNY    4FNZ    4FOB    4FOC    4FOD    4JOA   
Human Protein AtlasENSG00000171094
Peptide AtlasQ9UM73
HPRD00104
IPIIPI00395632   IPI00930494   IPI00910903   IPI00893651   
Protein Interaction databases
DIP (DOE-UCLA)Q9UM73
IntAct (EBI)Q9UM73
FunCoupENSG00000171094
BioGRIDALK
InParanoidQ9UM73
Interologous Interaction database Q9UM73
IntegromeDBALK
STRING (EMBL)ALK
Ontologies - Pathways
Ontology : AmiGOactivation of MAPK activity  NF-kappaB-inducing kinase activity  protein tyrosine kinase activity  transmembrane receptor protein tyrosine kinase activity  transmembrane receptor protein tyrosine kinase activity  protein binding  ATP binding  integral to plasma membrane  integral to plasma membrane  signal transduction  transmembrane receptor protein tyrosine kinase signaling pathway  cell proliferation  phosphorylation  phosphorylation  peptidyl-tyrosine phosphorylation  NIK/NF-kappaB cascade  regulation of apoptotic process  protein autophosphorylation  protein autophosphorylation  neuron development  positive regulation of NF-kappaB transcription factor activity  
Ontology : EGO-EBIactivation of MAPK activity  NF-kappaB-inducing kinase activity  protein tyrosine kinase activity  transmembrane receptor protein tyrosine kinase activity  transmembrane receptor protein tyrosine kinase activity  protein binding  ATP binding  integral to plasma membrane  integral to plasma membrane  signal transduction  transmembrane receptor protein tyrosine kinase signaling pathway  cell proliferation  phosphorylation  phosphorylation  peptidyl-tyrosine phosphorylation  NIK/NF-kappaB cascade  regulation of apoptotic process  protein autophosphorylation  protein autophosphorylation  neuron development  positive regulation of NF-kappaB transcription factor activity  
Pathways : KEGGNon-small cell lung cancer   
REACTOMEALK
Protein Interaction DatabaseALK
Wikipedia pathwaysALK
Gene fusion - rearrangments
Rearrangement : COSMICALK [2p23.2]  -  MSN [Xq12]
Rearrangement : COSMICATIC [2q35]  -  ALK [2p23.2]
Rearrangement : COSMICC2orf44 [2p23.3]  -  ALK [2p23.2]
Rearrangement : COSMICCARS [11p15.4]  -  ALK [2p23.2]
Rearrangement : COSMICCLTC [17q23.1]  -  ALK [2p23.2]
Rearrangement : COSMICEML4 [2p21]  -  ALK [2p23.2]
Rearrangement : COSMICFN1 [2q35]  -  ALK [2p23.2]
Rearrangement : COSMICKIF5B [10p11.22]  -  ALK [2p23.2]
Rearrangement : COSMICKLC1 [14q32.33]  -  ALK [2p23.2]
Rearrangement : COSMICMSN [Xq12]  -  ALK [2p23.2]
Rearrangement : COSMICNPM1 [5q35.1]  -  ALK [2p23.2]
Rearrangement : COSMICPPFIBP1 [12p11.23]  -  ALK [2p23.2]
Rearrangement : COSMICRANBP2 [2q12.3]  -  ALK [2p23.2]
Rearrangement : COSMICSEC31A [4q21.22]  -  ALK [2p23.2]
Rearrangement : COSMICSQSTM1 [5q35.3]  -  ALK [2p23.2]
Rearrangement : COSMICSTRN [2p22.2]  -  ALK [2p23.2]
Rearrangement : COSMICTFG [3q12.2]  -  ALK [2p23.2]
Rearrangement : COSMICTPM3 [1q21.3]  -  ALK [2p23.2]
Rearrangement : COSMICTPM4 [19p13.12]  -  ALK [2p23.2]
Rearrangement : COSMICVCL [10q22.2]  -  ALK [2p23.2]
Rearrangement : TICdbALK [2p23.2]  -  ALK [2p23.2]
Rearrangement : TICdbALK [2p23.2]  -  ALK [2p23.2]
Rearrangement : TICdbALK [2p23.2]  -  ATIC [2q35]
Rearrangement : TICdbALK [2p23.2]  -  C2orf44 [2p23.3]
Rearrangement : TICdbALK [2p23.2]  -  CARS [11p15.4]
Rearrangement : TICdbALK [2p23.2]  -  CLTC [17q23.1]
Rearrangement : TICdbALK [2p23.2]  -  EML4 [2p21]
Rearrangement : TICdbALK [2p23.2]  -  FN1 [2q35]
Rearrangement : TICdbALK [2p23.2]  -  KIF5B [10p11.22]
Rearrangement : TICdbALK [2p23.2]  -  KLC1 [14q32.33]
Rearrangement : TICdbALK [2p23.2]  -  MSN [Xq12]
Rearrangement : TICdbALK [2p23.2]  -  MYH9 [22q12.3]
Rearrangement : TICdbALK [2p23.2]  -  NPM1 [5q35.1]
Rearrangement : TICdbALK [2p23.2]  -  PPFIBP1 [12p11.23]
Rearrangement : TICdbALK [2p23.2]  -  PTPN3 [9q31.3]
Rearrangement : TICdbALK [2p23.2]  -  RANBP2 [2q12.3]
Rearrangement : TICdbALK [2p23.2]  -  RNF213 [17q25.3]
Rearrangement : TICdbALK [2p23.2]  -  SEC31A [4q21.22]
Rearrangement : TICdbALK [2p23.2]  -  SQSTM1 [5q35.3]
Rearrangement : TICdbALK [2p23.2]  -  STRN [2p22.2]
Rearrangement : TICdbALK [2p23.2]  -  TFG [3q12.2]
Rearrangement : TICdbALK [2p23.2]  -  TPM3 [1q21.3]
Rearrangement : TICdbALK [2p23.2]  -  TPM4 [19p13.12]
Rearrangement : TICdbALK [2p23.2]  -  VCL [10q22.2]
Rearrangement : TICdbATIC [2q35]  -  ALK [2p23.2]
Rearrangement : TICdbCARS [11p15.4]  -  ALK [2p23.2]
Rearrangement : TICdbCLTC [17q23.1]  -  ALK [2p23.2]
Rearrangement : TICdbEML4 [2p21]  -  ALK [2p23.2]
Rearrangement : TICdbKIF5B [10p11.22]  -  ALK [2p23.2]
Rearrangement : TICdbMSN [Xq12]  -  ALK [2p23.2]
Rearrangement : TICdbMYH9 [22q12.3]  -  ALK [2p23.2]
Rearrangement : TICdbNPM1 [5q35.1]  -  ALK [2p23.2]
Rearrangement : TICdbPTPN3 [9q31.3]  -  ALK [2p23.2]
Rearrangement : TICdbRANBP2 [2q12.3]  -  ALK [2p23.2]
Rearrangement : TICdbRNF213 [17q25.3]  -  ALK [2p23.2]
Rearrangement : TICdbSEC31A [4q21.22]  -  ALK [2p23.2]
Rearrangement : TICdbSQSTM1 [5q35.3]  -  ALK [2p23.2]
Rearrangement : TICdbTFG [3q12.2]  -  ALK [2p23.2]
Rearrangement : TICdbTPM3 [1q21.3]  -  ALK [2p23.2]
Rearrangement : TICdbTPM4 [19p13.12]  -  ALK [2p23.2]
Polymorphisms : SNP, mutations, diseases
SNP Single Nucleotide Polymorphism (NCBI)ALK
SNP (GeneSNP Utah)ALK
SNP : HGBaseALK
Genetic variants : HAPMAPALK
1000_GenomesALK 
ICGC programENSG00000171094 
Cancer Gene: CensusALK 
Somatic Mutations in Cancer : COSMICALK 
CONAN: Copy Number AnalysisALK 
Mutations and Diseases : HGMDALK
OMIM105590    256700    613014   
GENETestsALK
Disease Genetic AssociationALK
Huge Navigator ALK [HugePedia]  ALK [HugeCancerGEM]
Genomic VariantsALK  ALK [DGVbeta]
Exome VariantALK
dbVarALK
ClinVarALK
snp3D : Map Gene to Disease238
General knowledge
Homologs : HomoloGeneALK
Homology/Alignments : Family Browser (UCSC)ALK
Phylogenetic Trees/Animal Genes : TreeFamALK
Chemical/Protein Interactions : CTD238
Chemical/Pharm GKB GenePA24719
Clinical trialALK
Cancer Resource (Charite)ENSG00000171094
Other databases
Probes
Litterature
PubMed258 Pubmed reference(s) in Entrez
CoreMineALK
iHOPALK

Bibliography

Fusion of a kinase gene, ALK, to a nucleolar protein gene, NPM, in non-Hodgkin's lymphoma.
Morris SW, Kirstein MN, Valentine MB, Dittmer KG, Shapiro DN, Saltman DL, Look AT.
Science. 1994 Mar 4;263(5151):1281-4.
PMID 8122112
 
Anaplastic large cell lymphomas expressing the novel chimeric protein p80NPM/ALK: a distinct clinicopathologic entity.
Shiota M, Nakamura S, Ichinohasama R, Abe M, Akagi T, Takeshita M, Mori N, Fujimoto J, Miyauchi J, Mikata A, Nanba K, Takami T, Yamabe H, Takano Y, Izumo T, Nagatani T, Mohri N, Nasu K, Satoh H, Katano H, Fujimoto J, Yamamoto T, Mori S.
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PMID 7655022
 
High incidence of the t(2;5)(p23;q35) translocation in anaplastic large cell lymphoma and its lack of detection in Hodgkin's disease. Comparison of cytogenetic analysis, reverse transcriptase-polymerase chain reaction, and P-80 immunostaining.
Lamant L, Meggetto F, al Saati T, Brugieres L, de Paillerets BB, Dastugue N, Bernheim A, Rubie H, Terrier-Lacombe MJ, Robert A, Rigal F, Schlaifer D, Shiuta M, Mori S, Delsol G.
Blood. 1996 Jan 1;87(1):284-91.
PMID 8547653
 
Role of the nucleophosmin (NPM) portion of the non-Hodgkin's lymphoma-associated NPM-anaplastic lymphoma kinase fusion protein in oncogenesis.
Bischof D, Pulford K, Mason DY, Morris SW.
Mol Cell Biol. 1997 Apr;17(4):2312-25.
PMID 9121481
 
Molecular characterization of ALK, a receptor tyrosine kinase expressed specifically in the nervous system.
Iwahara T, Fujimoto J, Wen D, Cupples R, Bucay N, Arakawa T, Mori S, Ratzkin B, Yamamoto T.
Oncogene. 1997 Jan 30;14(4):439-49.
PMID 9053841
 
ALK, the chromosome 2 gene locus altered by the t(2;5) in non-Hodgkin's lymphoma, encodes a novel neural receptor tyrosine kinase that is highly related to leukocyte tyrosine kinase (LTK).
Morris SW, Naeve C, Mathew P, James PL, Kirstein MN, Cui X, Witte DP.
Oncogene. 1997 May 8;14(18):2175-88.
PMID 9174053
 
Detection of anaplastic lymphoma kinase (ALK) and nucleolar protein nucleophosmin (NPM)-ALK proteins in normal and neoplastic cells with the monoclonal antibody ALK1.
Pulford K, Lamant L, Morris SW, Butler LH, Wood KM, Stroud D, Delsol G, Mason DY.
Blood. 1997 Feb 15;89(4):1394-404.
PMID 9028963
 
Recurrent involvement of 2p23 in inflammatory myofibroblastic tumors.
Griffin CA, Hawkins AL, Dvorak C, Henkle C, Ellingham T, Perlman EJ.
Cancer Res. 1999 Jun 15;59(12):2776-80.
PMID 10383129
 
TRK-fused gene (TFG) is a new partner of ALK in anaplastic large cell lymphoma producing two structurally different TFG-ALK translocations.
Hernandez L, Pinyol M, Hernandez S, Bea S, Pulford K, Rosenwald A, Lamant L, Falini B, Ott G, Mason DY, Delsol G, Campo E.
Blood. 1999 Nov 1;94(9):3265-8.
PMID 10556217
 
A new fusion gene TPM3-ALK in anaplastic large cell lymphoma created by a (1;2)(q25;p23) translocation.
Lamant L, Dastugue N, Pulford K, Delsol G, Mariame B.
Blood. 1999 May 1;93(9):3088-95.
PMID 10216106
 
ATIC-ALK: A novel variant ALK gene fusion in anaplastic large cell lymphoma resulting from the recurrent cryptic chromosomal inversion, inv(2)(p23q35).
Colleoni GW, Bridge JA, Garicochea B, Liu J, Filippa DA, Ladanyi M.
Am J Pathol. 2000 Mar;156(3):781-9.
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Contributor(s)

Written09-1997Jean-Loup Huret
Genetics, Dept Medical Information, University of Poitiers, CHU Poitiers Hospital, F-86021 Poitiers, France
Updated08-2001Jean-Loup Huret
Genetics, Dept Medical Information, UMR 8125 CNRS, University of Poitiers, CHU Poitiers Hospital, F-86021 Poitiers, France
Updated08-2003Jean-Loup Huret, Sylvie Senon
Genetics, Dept Medical Information, UMR 8125 CNRS, University of Poitiers, CHU Poitiers Hospital, F-86021 Poitiers, France
Updated02-2010Michèle Allouche
INSERM U.563 CPTP, Bat. B, Pavillon Lefevre, CHU Purpan, BP 3028, 31024 Toulouse Cedex 3, France

Citation

This paper should be referenced as such :
Huret JL . ALK (anaplastic lymphoma receptor tyrosine kinase). Atlas Genet Cytogenet Oncol Haematol. September 1997 .
Huret JL . ALK (anaplastic lymphoma receptor tyrosine kinase). Atlas Genet Cytogenet Oncol Haematol. August 2001 .
Huret JL, Senon S . ALK (anaplastic lymphoma receptor tyrosine kinase). Atlas Genet Cytogenet Oncol Haematol. August 2003 .
Allouche M . ALK (anaplastic lymphoma receptor tyrosine kinase). Atlas Genet Cytogenet Oncol Haematol. February 2010 .
URL : http://AtlasGeneticsOncology.org/Genes/ALK.html

The various updated versions of this paper are referenced and archived by INIST as such :
http://documents.irevues.inist.fr/bitstream/handle/2042/32020/09-1997-ALK.pdf   [ Bibliographic record ]
http://documents.irevues.inist.fr/bitstream/2042/37775/1/08-2001-ALK.pdf   [ Bibliographic record ]
http://documents.irevues.inist.fr/bitstream/2042/38004/1/08-2003-ALK.pdf   [ Bibliographic record ]
http://documents.irevues.inist.fr/bitstream/2042/44894/1/02-2010-ALK.pdf   [ Bibliographic record ]

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