Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

T-CUS and Low-Count T-LGLL: Diagnostic Uncertainties and the Unmet Need for Markers of Disease Progression.

International journal of laboratory hematology·2025
Same author

Belamaf: is renal toxicity an overlooked side effect?

Blood advances·2025
Same author

Diagnostic criteria for NK cell large granular lymphocyte leukemia: validation through a multicentric international study.

Blood advances·2025
Same author

Clinical and transcriptomic characterization of patients with chronic lymphocytic leukemia harboring t(14;19): an ERIC study.

Leukemia·2025
Same author

Correction: Mancuso et al. Forcing Ahead: Second-Line Treatment Options for Lenalidomide-Refractory Multiple Myeloma. <i>Cancers</i> 2025, <i>17</i>, 1168.

Cancers·2025
Same author

Transcriptomic landscape of CD8+ and CD4 + T-LGL leukemia revealed the distinct impact of STAT3 and STAT5B activating mutations.

Leukemia·2025

Related Experiment Video

Updated: Aug 28, 2025

Pre-clinical Evaluation of Tyrosine Kinase Inhibitors for Treatment of Acute Leukemia
10:49

Pre-clinical Evaluation of Tyrosine Kinase Inhibitors for Treatment of Acute Leukemia

Published on: September 18, 2013

18.2K

All that glitters is not LGL Leukemia.

Gianpietro Semenzato1,2, Antonella Teramo3,4, Giulia Calabretto3,4

  • 1University of Padova, Padova, Italy. g.semenzato@unipd.it.

Leukemia
|September 15, 2022
PubMed
Summary

Large granular lymphocyte (LGL) disorders are rare blood cancers. STAT gene mutations, particularly in STAT3 and STAT5b, are key to T-LGL leukemia development and diagnosis.

More Related Videos

Comprehensive Protocol to Sample and Process Bone Marrow for Measuring Measurable Residual Disease and Leukemic Stem Cells in Acute Myeloid Leukemia
09:57

Comprehensive Protocol to Sample and Process Bone Marrow for Measuring Measurable Residual Disease and Leukemic Stem Cells in Acute Myeloid Leukemia

Published on: March 5, 2018

29.6K
Isolating Malignant and Non-Malignant B Cells from lck:eGFP Zebrafish
08:32

Isolating Malignant and Non-Malignant B Cells from lck:eGFP Zebrafish

Published on: February 22, 2019

7.2K

Related Experiment Videos

Last Updated: Aug 28, 2025

Pre-clinical Evaluation of Tyrosine Kinase Inhibitors for Treatment of Acute Leukemia
10:49

Pre-clinical Evaluation of Tyrosine Kinase Inhibitors for Treatment of Acute Leukemia

Published on: September 18, 2013

18.2K
Comprehensive Protocol to Sample and Process Bone Marrow for Measuring Measurable Residual Disease and Leukemic Stem Cells in Acute Myeloid Leukemia
09:57

Comprehensive Protocol to Sample and Process Bone Marrow for Measuring Measurable Residual Disease and Leukemic Stem Cells in Acute Myeloid Leukemia

Published on: March 5, 2018

29.6K
Isolating Malignant and Non-Malignant B Cells from lck:eGFP Zebrafish
08:32

Isolating Malignant and Non-Malignant B Cells from lck:eGFP Zebrafish

Published on: February 22, 2019

7.2K

Area of Science:

  • Hematology
  • Molecular Genetics
  • Oncology

Background:

  • Large granular lymphocyte (LGL) disorders are rare hematological neoplasms characterized by significant heterogeneity.
  • Recent advancements have elucidated aberrant pathways in LGL leukemogenesis, with STAT signaling identified as critical for abnormal cell survival.

Purpose of the Study:

  • To review the role of clonality in T-LGL disorders.
  • To discuss strategies for distinguishing T-LGL leukemia from mimics like clonal hematopoiesis of indeterminate potential (CHIP).

Main Methods:

  • Review of current literature on LGL disorders, STAT signaling, and genetic mutations.
  • Analysis of diagnostic challenges and differential diagnoses in T-LGL leukemia.

Main Results:

  • STAT3 and STAT5b gain-of-function mutations are the most common genetic lesions in T-LGL leukemia, serving as hallmarks for subclassification.
  • The clinical distinction between T-LGL leukemia and overlapping conditions remains challenging due to incomplete understanding of their relationships.

Conclusions:

  • STAT gene mutations are crucial for understanding T-LGL leukemogenesis and refining classification.
  • Further research is needed to improve the accurate diagnosis of T-LGL leukemia and differentiate it from other clonal disorders.