Access
To read this story in full you will need to login or make a payment (see right).
Article
Nature Medicine 11, 623 - 629 (2005)
Published online: 15 May 2005 | doi:10.1038/nm1249
Stat3 is required for ALK-mediated lymphomagenesis and provides a possible therapeutic target
Roberto Chiarle1,2, William J Simmons1, Honjying Cai1, Girish Dhall1,3, Alberto Zamo4, Regina Raz1, James G Karras5, David E Levy1 & Giorgio Inghirami1,2
Abstract
Anaplastic large cell lymphomas (ALCLs) are caused by chromosomal translocations that juxtapose the anaplastic lymphoma kinase (ALK) proto-oncogene to a dimerization partner, resulting in constitutive expression of ALK and ALK tyrosine kinase activity. One substrate of activated ALK in human ALCLs is the transcription factor Stat3, and its phosphorylation is accurately recapitulated in a new nucleophosmin (NPM)-ALK transgenic mouse model of lymphomagenesis. Here we show by gene targeting that Stat3 is required for the transformation of mouse embryonic fibroblasts in vitro, for the development of B-cell lymphoma in transgenic mice and for the growth and survival of both human and mouse NPM-ALK–transformed B and T cells. Ablation of Stat3 expression by antisense oligonucleotides significantly (P < 0.0001) impaired the growth of human and mouse NPM-ALK tumors in vivo. Pharmacological ablation of Stat3 represents a new candidate approach for the treatment of human lymphoma.
To read this story in full you will need to login or make a payment (see right).
MORE ARTICLES LIKE THIS
These links to content published by NPG are automatically generated.
RESEARCH
Dynamic programming of CD8 + T lymphocyte responsesNature Immunology Article (01 Apr 2003)
Plasma cell differentiation and the unfolded protein response intersect at the transcription factor XBP-1Nature Immunology Article (01 Apr 2003)
The anaplastic lymphoma kinase is an effective oncoantigen for lymphoma vaccinationNature Medicine Letter (01 Jun 2008)
See all 60 matches for Research