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Leuk Res Rep. 2014 Dec 16;4(1):4-7. doi: 10.1016/j.lrr.2014.12.001. eCollection 2015.

Emergence of a STAT3 mutated NK clone in LGL leukemia.

Author information

1
Department of Medicine, York Hospital, York, PA, USA.
2
University of Virginia Cancer Center, P.O. Box 800334, Charlottesville, VA 22908-0334, USA.

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.

KEYWORDS:

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

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