Transformed aggressive γδ‐variant T‐cell large granular lymphocytic leukemia with acquired copy neutral loss of heterozygosity at 17q11.2q25.3 and additional aberrations |
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Authors: | Ling Zhang Radhakrishnan Ramchandren Peter Papenhausen Thomas P Loughran Lubomir Sokol |
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Institution: | 1. Department of Hematopathology and Laboratory Medicine, H Lee Moffitt Cancer Center and Research Institute, , Tampa, FL, USA;2. Department of Oncology, Barbara Ann Karmanos Cancer Center, Wayne State University, , Detroit, MI, USA;3. Department of Cytogenetics, Integrated Oncology‐Laboratory Corporation of America, , Winston‐Salem, NC, USA;4. Department of Medicine, University of Virginia Cancer Center, , Charlottesville, VA, USA;5. Department of Hematologic Malignancies, H Lee Moffitt Cancer Center and Research Institute, , Tampa, FL, USA |
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Abstract: | T‐cell large granular lymphocytic leukemia (T‐LGLL) is a rare indolent lymphoproliferative disorder characterized by cytopenias, splenomegaly, and various degrees of T‐cell lymphocytosis, due to a clonal expansion of CD8‐positive cytotoxic T‐cells. Phenotypic variants of T‐LGLL include CD4+/CD8? T‐cells, with dual CD4?/CD8?/γδ+ T‐cells being even rarer. Cytogenetic abnormalities in T‐LGLL have rarely been reported, and there is scientific debate regarding the existence of aggressive or transformed variants of T‐LGLL. We report a patient with T‐LGLL, γδ variant, with nearly 20‐year‐long duration of cytopenias before transformation to an unusual clinical scenario, manifesting with marked lymphocytosis >100 × 109/L and infiltration of lymph nodes, tonsils, and subcutaneous tissue. Single‐nucleotide polymorphism assays revealed acquired copy neutral loss of heterozygosity at 17q and deletion of 3p21.31, in addition to trisomy 5, monosomy X, and monosomy 21. These genetic abnormalities provided a better understanding of the molecular nature and the potentiality of disease transformation. |
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Keywords: | aggressive γ δ variant of T‐cell large granular lymphocytic leukemia profound lymphocytosis single‐nucleotide polymorphism cytogenetic abnormalities |
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