Emergence of a STAT3 mutated NK clone in LGL leukemia

Yiyi Yan, Thomas L. Olson, Susan B. Nyland, David J. Feith, Thomas P. Loughran

Research output: Contribution to journalArticle

7 Scopus citations

Abstract

Large granular lymphocyte (LGL) leukemia is a chronic clonal lymphoproliferative disorder. Here, a T-LGL leukemia patient developed NK-LGL leukemia with residual leukemic T-LGL. TCRVβ usage and CDR3 sequence drifts were observed with disease progression. A STAT3 S614R mutation was identified in NK but not T-cells in the mixed leukemic stage. Multiple, non-dominant T-cell clones with distinct STAT3 mutations were present throughout. Our results suggest that T and NK-LGL leukemia may share common pathogenesis mechanisms and that STAT3 mutation alone is insufficient to bring about clonal expansion. Mutational and immunological monitoring may provide diagnostic and therapeutic significance in LGL leukemia.

Original languageEnglish (US)
Pages (from-to)4-7
Number of pages4
JournalLeukemia Research Reports
Volume4
Issue number1
DOIs
StatePublished - Jan 1 2015

Keywords

  • Classifications
  • Clonal evolution
  • Leukemia markers
  • Mutation detection
  • T cell receptor

ASJC Scopus subject areas

  • Hematology
  • Oncology

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    Yan, Y., Olson, T. L., Nyland, S. B., Feith, D. J., & Loughran, T. P. (2015). Emergence of a STAT3 mutated NK clone in LGL leukemia. Leukemia Research Reports, 4(1), 4-7. https://doi.org/10.1016/j.lrr.2014.12.001