T-Cell Large Granular Lymphocytic Leukemia Presenting as Isolated Transfusion-Dependent Anemia Without Autoimmune Disease: A Case Report

Literature Review of All Cases of Aggressive T-Cell Large Granular Lymphocytic Leukemia Cases and Report of an Additional Case

Large Granular Lymphocyte Leukemia and Precapillary Pulmonary Hypertension

Ruxolitinib for refractory large granular lymphocyte leukemia.

Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL) Mediates and Sustains NF-κb Constitutive Activation in LGL Leukemia Cells

Retrospective Review of Patients with Large Granular Lymphocyte (LGL) Leukemia in a Single Institution over a Period of 11 Years

A Population-Based Study of Large Granular Lymphocyte Leukemia: Analysis of 978 Patients Using the SEER and NCDB Databases

Manifestation of Large Granular Lymphocyte Leukemia in Pediatric and Young Adult Population Is Distinct from Older Adult Cohorts

Introduction The typical clinical manifestations of T-cell large granular lymphocyte (T-LGL) leukemia are an increase in the number of large granular lymphocytes (LGLs) in the blood > 2000 cells/μL, neutropenia, and splenomegaly. In rare cases of so-called ‘aleukemic’ T-LGL leukemia, the number of LGLs is <400–500 cells/μL. In patients with rheumatoid arthritis (RA), distinguishing T-LGL leukemia with low tumor burden in the blood and bone marrow from Felty syndrome (FS) poses diagnostic challenges. Areas covered This review aimed to describe the basic characteristics and variants of aleukemic T-LGL leukemia, with a special focus on aleukemic T-LGL leukemia with massive splenomegaly (splenic variant of T-LGL leukemia) and differential diagnosis of such cases with hepatosplenic T-cell lymphoma. The significance of mutations in the signal transducer and activator of transcription 3 (STAT3) gene for distinguishing aleukemic RA-associated T-LGL leukemia from FS is discussed, along with the evolution of the T-LGL leukemia diagnostic criteria. PubMed database was used to search for the most relevant literature. Expert opinion Evaluation of STAT3 mutations in the blood and bone marrow using next-generation sequencing, as well as a comprehensive spleen study, may be necessary to establish a diagnosis of aleukemic RA-associated T-LGL leukemia.

Subset-Specific Recurrence of Mutations and Identification of Functional Modules Provides New Clues about the Pathogenesis of Large Granular Lymphocyte Leukemia

T Large Granular Lymphocyte (LGL) Leukemia Characterized by Expansion of Terminal CD3+/CD8+/CD62L−/CD45RA+ Effector Memory T Cells.

Hematologic malignancies of cytotoxic cells: Introduction

Large granular lymphocytic (LGL) leukemia is a chronic lymphoproliferative disease of cytotoxic T cells or NK cells with LGL morphology and frequently complicated cytopenia and/or different autoimmune diseases, which often require medical interventions, although LGL leukemia itself is seldom lethal. Immunologic dysregulations in LGL leukemia contribute to the development of complications, for example, neutropenia with the involvement of Fas ligand system and, in pure red cell aplasia, which is a common complication among the patients of East Asian origin, impairing erythroid developments by cytotoxic T cells. Rheumatoid arthritis (RA) is the most prevalent nonhematological consequence, and Felty syndrome, a rare form of RA, and T-LGL leukemia have a lot in common. When patients have LGL leukemia-associated complications, immunosuppressive medication is a mainstay of treatment. Characteristic mutational features in STAT3, STAT5B, CCL22, and other genes in specific subtypes of LGL leukemia have been detected, that would be associated with immunologically mediated molecular pathogenesis in LGL leukemia, and these new findings may help in creating optimal diagnostic approaches or novel therapies for LGL leukemia.

Chapter 12 - T-cell large granular lymphocytic leukemia in the setting of rheumatoid arthritis

An analysis of veterans diagnosed with large granular lymphocytic disorders at the national Veteran Affairs Healthcare System.

Blockade of Fas-dependent apoptosis by soluble Fas in LGL leukemia