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

نویسندگان

  • 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
چکیده

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.

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عنوان ژورنال:
  • Nature communications

دوره 6  شماره 

صفحات  -

تاریخ انتشار 2015