ArticleBlood2014
Integrated genomic sequencing reveals mutational landscape of T-cell prolymphocytic leukemia.
Article in Blood, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 155 papers, 1 of them a synthesis that pooled it.
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Who cites it
155 citing papers in PubMed, 1 synthesis or guideline pooled it, 252 citations in OpenAlex.
- Advances and Perspectives in the Treatment of T-PLL.Current hematologic malignancy reports · 2020Pooled it
- Phase 1B pilot study of itacitinib with alemtuzumab in patients with T-cell prolymphocytic leukemia.Blood neoplasia · 2026Trial
- Trial
- Stat3 mutations impact on overall survival in large granular lymphocyte leukemia: a single-center experience of 205 patients.Leukemia · 2020Trial
- SAMHD1 is recurrently mutated in T-cell prolymphocytic leukemia.Blood cancer journal · 2018Trial
- Epigenetic therapy overcomes treatment resistance in T cell prolymphocytic leukemia.Science translational medicine · 2015Trial
- T cell lymphomas: cancers of aberrant immune synapse signalling.Nature reviews. Immunology · 2026Review
- Gene Expression, Non-Coding RNA, and Circular RNA Alterations in Patients with T-Prolymphocytic Leukemia.Cancers · 2026Article
- Disease-associated mutations in the STAT5B SH2 domain reprogram hepatic cholesterol and lipid metabolism.Endocrinology · 2026Article
- A case of T-prolymphocytic leukemia harboring RAS mutation.Annals of hematology · 2026Article
- Single-cell genomics highlight MYC-associated metabolic activation and altered cell interactions in T-prolymphocytic leukemia progression.Nature communications · 2026Article
- JAK Inhibitors in the Treatment of T-Cell Lymphomas: Current Evidence and Future Directions.Cancers · 2026Review
- Novel genetic variants identification and immune profiling in ataxia telangiectasia patients.Journal of translational medicine · 2026Article
- Combination of artesunate and ruxolitinib suppresses T cell leukemia/lymphoma proliferation via the JAK STAT pathway.Scientific reports · 2026Article
- Indolent natural killer-cell lymphoproliferative disorder of the gallbladder: a rare case report.Frontiers in oncology · 2026Article
- Impact of rare JAK/STAT germline mutations on vaccination-induced innate immune responses in a Tyrolian population.International journal of biological sciences · 2026Article
- Disease-associated mutations in the STAT5B SH2 domain reprogram hepatic cholesterol and lipid metabolism.bioRxiv : the preprint server for biology · 2025Article
- The Significance of the Microenvironment in T/Nk-Cell Neoplasms.International journal of molecular sciences · 2025Review
- Comparative preclinical drug response analyses of T-prolymphocytic leukemia reveal no differences between known gene expression subgroups.Biology direct · 2025Article
- The Mechanisms of Resistance to JAK Inhibitors in Lymphoid Leukemias: A Scoping Review of Evidence from Preclinical Models and Case Reports.International journal of molecular sciences · 2025Article
95 more citing papers are in PubMed but not listed here.
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Authors and funding
17 authors at 3 institutions in 2 countries.
Funding
Abstract
The comprehensive genetic alterations underlying the pathogenesis of T-cell prolymphocytic leukemia (T-PLL) are unknown. To address this, we performed whole-genome sequencing (WGS), whole-exome sequencing (WES), high-resolution copy-number analysis, and Sanger resequencing of a large cohort of T-PLL. WGS and WES identified novel mutations in recurrently altered genes not previously implicated in T-PLL including EZH2, FBXW10, and CHEK2. Strikingly, WGS and/or WES showed largely mutually exclusive mutations affecting IL2RG, JAK1, JAK3, or STAT5B in 38 of 50 T-PLL genomes (76.0%). Notably, gain-of-function IL2RG mutations are novel and have not been reported in any form of cancer. Further, high-frequency mutations in STAT5B have not been previously reported in T-PLL. Functionally, IL2RG-JAK1-JAK3-STAT5B mutations led to signal transducer and activator of transcription 5 (STAT5) hyperactivation, transformed Ba/F3 cells resulting in cytokine-independent growth, and/or enhanced colony formation in Jurkat T cells. Importantly, primary T-PLL cells exhibited constitutive activation of STAT5, and targeted pharmacologic inhibition of STAT5 with pimozide induced apoptosis in primary T-PLL cells. These results for the first time provide a portrait of the mutational landscape of T-PLL and implicate deregulation of DNA repair and epigenetic modulators as well as high-frequency mutational activation of the IL2RG-JAK1-JAK3-STAT5B axis in the pathogenesis of T-PLL. These findings offer opportunities for novel targeted therapies in this aggressive leukemia.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.