Activating mutations of STAT5B and STAT3 in lymphomas derived from γδ-T or NK cells View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2015-12

AUTHORS

Can Küçük, Bei Jiang, Xiaozhou Hu, Wenyan Zhang, John K C Chan, Wenming Xiao, Nathan Lack, Can Alkan, John C Williams, Kendra N Avery, Pınar Kavak, Anna Scuto, Emel Sen, Philippe Gaulard, Lou Staudt, Javeed Iqbal, Weiwei Zhang, Adam Cornish, Qiang Gong, Qunpei Yang, Hong Sun, Francesco d'Amore, Sirpa Leppä, Weiping Liu, Kai Fu, Laurence de Leval, Timothy McKeithan, Wing C Chan

ABSTRACT

Lymphomas arising from NK or γδ-T cells are very aggressive diseases and little is known regarding their pathogenesis. Here we report frequent activating mutations of STAT3 and STAT5B in NK/T-cell lymphomas (n=51), γδ-T-cell lymphomas (n=43) and their cell lines (n=9) through next generation and/or Sanger sequencing. STAT5B N642H is particularly frequent in all forms of γδ-T-cell lymphomas. STAT3 and STAT5B mutations are associated with increased phosphorylated protein and a growth advantage to transduced cell lines or normal NK cells. Growth-promoting activity of the mutants can be partially inhibited by a JAK1/2 inhibitor. Molecular modelling and surface plasmon resonance measurements of the N642H mutant indicate a marked increase in binding affinity of the phosphotyrosine-Y699 with the mutant histidine. This is associated with the prolonged persistence of the mutant phosphoSTAT5B and marked increase of binding to target sites. Our findings suggest that JAK-STAT pathway inhibition may represent a therapeutic strategy. More... »

PAGES

6025

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ncomms7025

DOI

http://dx.doi.org/10.1038/ncomms7025

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1043674607

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/25586472


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488 https://www.grid.ac/institutes/grid.417768.b schema:alternateName Center for Cancer Research
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