What have we learnt from mouse models of NPM-ALK-induced lymphomagenesis?

• Published in: Leukemia Vol. 19; no. 7; pp. 1128 - 1134
• Main Authors: TURNER, S. D, ALEXANDER, D. R
• Format: Journal Article
• Language: English
• Published: London Nature Publishing 01.07.2005; Nature Publishing Group
• Subjects: Animal models; Animals; Apoptosis; Biological and medical sciences; CD30 antigen; Cell activation; Chromosome aberrations; Disease Models, Animal; Fusion protein; Genotype & phenotype; Hematologic and hematopoietic diseases; Humans; Kinases; Leukemia; Lymphoma; Lymphoma - genetics; Lymphoma - immunology; Medical genetics; Medical sciences; Mice; Mice, Transgenic; Oncogene Proteins, Fusion - genetics; Oncogene Proteins, Fusion - immunology; Phosphorylation; Protein-tyrosine kinase; Protein-Tyrosine Kinases - genetics; Protein-Tyrosine Kinases - immunology; Proteins; Signal Transduction - genetics; Signal Transduction - immunology; Transgenic animals; Tumors; Tyrosine; Chromosomal aberration; Animal model; NPM-ALK; Hematology; Enzyme; Transferases; Rodentia; ALCL; oncogene; Carcinogenesis; Vertebrata; Mammalia; Abnormal chromosome B5; Mouse; Kinase; Abnormal chromosome A2; Abnormal chromosome; Onc gene; Hybrid gene; Chromosome translocation
• ISSN: 0887-6924; 1476-5551
• DOI: 10.1038/sj.leu.2403797

The nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) is generated as a t(2;5) chromosomal breakpoint product, typically in CD30(+) anaplastic large cell lymphomas. Activation of the NPM-ALK tyrosine kinase by NPM dimerisation causes autophosphorylation at multiple tyrosine residues and the consequent recruitment of a 'signalosome' that couples the fusion protein to pathways regulating mitogenesis and apoptosis. This review focuses on recent advances in our understanding of the transforming signals induced by this fusion protein in mouse models.