Compendium of Cancer Genome Aberrations

T-large granular lymphocytic leukaemia

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Haematolymphoid Tumours (WHO Classification, 5th ed.)

editContent Update To WHO 5th Edition Classification Is In Process; Content Below is Based on WHO 4th Edition Classification
This page was converted to the new template on 2023-12-07. The original page can be found at HAEM4:T-cell Large Granular Lymphocytic Leukemia.

(General Instructions – The focus of these pages is the clinically significant genetic alterations in each disease type. This is based on up-to-date knowledge from multiple resources such as PubMed and the WHO classification books. The CCGA is meant to be a supplemental resource to the WHO classification books; the CCGA captures in a continually updated wiki-stye manner the current genetics/genomics knowledge of each disease, which evolves more rapidly than books can be revised and published. If the same disease is described in multiple WHO classification books, the genetics-related information for that disease will be consolidated into a single main page that has this template (other pages would only contain a link to this main page). Use HUGO-approved gene names and symbols (italicized when appropriate), HGVS-based nomenclature for variants, as well as generic names of drugs and testing platforms or assays if applicable. Please complete tables whenever possible and do not delete them (add N/A if not applicable in the table and delete the examples); to add (or move) a row or column in a table, click nearby within the table and select the > symbol that appears. Please do not delete or alter the section headings. The use of bullet points alongside short blocks of text rather than only large paragraphs is encouraged. Additional instructions below in italicized blue text should not be included in the final page content. Please also see Author_Instructions and FAQs as well as contact your Associate Editor or Technical Support.)

Primary Author(s)* edit

  • Michelle Don, MD, MS
  • Nicolas LaScala, DO

WHO Classification of Disease edit

Structure Disease
Book Haematolymphoid Tumours (5th ed.)
Category T-cell and NK-cell lymphoid proliferations and lymphomas
Family Mature T-cell and NK-cell neoplasms
Type Mature T-cell and NK-cell leukaemias
Subtype(s) T-large granular lymphocytic leukaemia

Related Terminology edit

Acceptable T-cell lymphoproliferative disease of granular lymphocytes; T-cell large granular lymphocytic leukaemia
Not Recommended T-cell large granular lymphocytosis; T-gamma lymphoproliferative disease

Gene Rearrangements edit

No know chromosomal rearrangements. (Instructions: Details on clinical significance such as prognosis and other important information can be provided in the notes section. Please include references throughout the table. Do not delete the table.)

Driver Gene Fusion(s) and Common Partner Genes Molecular Pathogenesis Typical Chromosomal Alteration(s) Prevalence -Common >20%, Recurrent 5-20% or Rare <5% (Disease) Diagnostic, Prognostic, and Therapeutic Significance - D, P, T Established Clinical Significance Per Guidelines - Yes or No (Source) Clinical Relevance Details/Other Notes
N/A N/A N/A N/A N/A N/A N/A N/A
editv4:Chromosomal Rearrangements (Gene Fusions)
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editv4:Clinical Significance (Diagnosis, Prognosis and Therapeutic Implications).
Please incorporate this section into the relevant tables found in:
  • Chromosomal Rearrangements (Gene Fusions)
  • Individual Region Genomic Gain/Loss/LOH
  • Characteristic Chromosomal Patterns
  • Gene Mutations (SNV/INDEL)
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Individual Region Genomic Gain/Loss/LOH edit

No known recurrent copy number gain/loss/LOH, chromosomal abnormalities have been reported in a few cases.[1] (Instructions: Includes aberrations not involving gene rearrangements. Details on clinical significance such as prognosis and other important information can be provided in the notes section. Can refer to CGC workgroup tables as linked on the homepage if applicable. Please include references throughout the table. Do not delete the table.)

Chr # Gain, Loss, Amp, LOH Minimal Region Cytoband and/or Genomic Coordinates [Genome Build; Size] Relevant Gene(s) Diagnostic, Prognostic, and Therapeutic Significance - D, P, T Established Clinical Significance Per Guidelines - Yes or No (Source) Clinical Relevance Details/Other Notes
N/A N/A N/A N/A N/A N/A N/A
editv4:Genomic Gain/Loss/LOH
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Characteristic Chromosomal or Other Global Mutational Patterns edit

No characteristic chromosomal patterns have been identified. One reported case with unique cytogenetic findings of a γδ variant T-cell LGL include: interstitial deletion of 3p21.31, monosomy X, trisomy 5, monosomy 21, and CN-LOH, located at 17q.[2] (Instructions: Included in this category are alterations such as hyperdiploid; gain of odd number chromosomes including typically chromosome 1, 3, 5, 7, 11, and 17; co-deletion of 1p and 19q; complex karyotypes without characteristic genetic findings; chromothripsis; microsatellite instability; homologous recombination deficiency; mutational signature pattern; etc. Details on clinical significance such as prognosis and other important information can be provided in the notes section. Please include references throughout the table. Do not delete the table.)

Chromosomal Pattern Molecular Pathogenesis Prevalence -

Common >20%, Recurrent 5-20% or Rare <5% (Disease)

Diagnostic, Prognostic, and Therapeutic Significance - D, P, T Established Clinical Significance Per Guidelines - Yes or No (Source) Clinical Relevance Details/Other Notes
N/A N/A N/A N/A N/A N/A
editv4:Characteristic Chromosomal Aberrations / Patterns
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Gene Mutations (SNV/INDEL) edit

Somatic activating STAT3 and STAT5b mutations are the most common SNVs in T-LGL. (Instructions: This table is not meant to be an exhaustive list; please include only genes/alterations that are recurrent or common as well either disease defining and/or clinically significant. If a gene has multiple mechanisms depending on the type or site of the alteration, add multiple entries in the table. For clinical significance, denote associations with FDA-approved therapy (not an extensive list of applicable drugs) and NCCN or other national guidelines if applicable; Can also refer to CGC workgroup tables as linked on the homepage if applicable as well as any high impact papers or reviews of gene mutations in this entity. Details on clinical significance such as prognosis and other important information such as concomitant and mutually exclusive mutations can be provided in the notes section. Please include references throughout the table. Do not delete the table.)

Gene Genetic Alteration Tumor Suppressor Gene, Oncogene, Other Prevalence -

Common >20%, Recurrent 5-20% or Rare <5% (Disease)

Diagnostic, Prognostic, and Therapeutic Significance - D, P, T   Established Clinical Significance Per Guidelines - Yes or No (Source) Clinical Relevance Details/Other Notes
STAT3[3] Gain of function in src-like homologue 2 (SH2) domain of STAT 3, frequently affecting codons Y640 or D661[3]. Codons N647I[4],K658S[4], and K658F[5] are also affected Other [6] Common [7] D, P, T WHO, NCCN STAT3 mutation has been associated with statistically significant neutropenia, thrombocytopenia, and reduced numbers of most normal residual blood-leukocyte subsets[5]


STAT3 mutations are associated with a worse prognosis and reduced overall survival [3][8]



Patients with STAT 3 mutation required treatment more frequently when compared to patients with STAT3 wild type[9]



One prospective study showed a predictive response to methotrexate therapy in a small group of patients with STAT3 Y640F mutated genotype[10]



STAT3 mutation can also be seen in other T-cell lymphomas including hepatosplenic T-cell lymphoma[11]

17% of patients with STAT3 mutations, had multiple mutations in the STAT3 gene, solely in cytotoxic CD8+ or NK cells.[12]

STAT5B [3]
 Gain of function src-like homologue 2 (SH2) domain of STAT5.

Mutations include[13]:

N642H

Y665F

Q706L

S715F

T628S

P685R

V712E mutation of STAT5B is in the transactivation domain[13]

Mutations in the coiled-coil domain: CCD, Q220H [13]

Mutations in the DNA binding domain: DBD, E433G/K [13]

Mutations in the inter-domain region: P702A [13]

Other [14] Rare [1] D,P,T WHO, NCCN N642H mutation (associated with more aggressive disease)[15][16]

Clones can acquire multiple STAT5B mutations [13]

STAT5B mutations can also be seen in other T-cell lymphomas including hepatosplenic T-cell lymphoma[11]

N642H mutation is associated with CD3+/CD56+ phenotype[16]

STAT5B mutations are more common in CD4+ T-LGLL than in CD8+ T-LGLL [13][17]

TNFAIP3 [3] Loss of function

Somatic mutations:

Y353X

K354K

Q741

E630X

A717T

F127C [18]

Other [19] Recurrent [20] P,T WHO TNFAIP 3 mutation has been correlated with increased overall survival [21]

TNFAIP3 itself is a NF‐κB target gene[22]

In one study three of four of the patients with non‐synonymous TNFAIP3 alterations also harbored a STAT3 mutation (p  = 0.004)[4]

TET2 [3] Loss of function [23] Other [24] Common [20] N/A WHO Found to be the most prevalent mutation in myeloid neoplasm or myeloid clonal hematopoiesis coexisting with T-LGLL [25]
BCL11B [3] Missense H126R[26] Other[27] Rare[26] N/A WHO BCL11B is required for T-cell survival and overexpression could effectively increase T-cell activation and proliferation.[26]
FLT3[3] A high-impact Asp228Gly variant on JAK STAT has been demonstrated [28] Other[29] Rare[28] N/A WHO Connects STAT to the MAPK-Ras-ERK pathway and to IL-15[28]
PTPN23[3] R641Q[30] Other[31] Rare[30] N/A WHO Demonstrated in a patient with CD4+ T-LGLL without a STAT5B or STAT3 mutation[30]
KMT2D[23] Loss of function[23] Other[32] Recurrent[20] N/A None KMT2D has been linked to lymphomagenesis.[28]  


KMT2D has been how to exhibit significant co-occurrence with STAT3 mutation[23]

TRAF3 [25] c.650A>T p.E217V[25] Other[33] Rare[25] N/A None Mutated putative driver[25]
CLIP3[25] c.908A>T p.D303V


c.917A>T p.K306M[25]

Other[34] Rare[25] N/A None Mutated putative driver[25]
FBXW2[25] c.683C>G p.A228G [25] Other[35] Rare[25] N/A None Mutated putative driver[25]
CREBBP[25] c.1178A>G p.N393S


c.4306T>C p.C1436R[25]

Other[36] Rare[25] N/A None Mutated putative driver [25]
CCL2 [37] SNV, somatic Mutation  

P46R[37]

Other[38] Rare[37] N/A None CCL22 co-occurring with a STAT3 mutation in a CD8+ TCR αβ T-LGLL[37]

CCL22 co-occurring with a STAT3 mutation in a CD8+ TCR αβ T-LGLL[37]

Note: A more extensive list of mutations can be found in cBioportal, COSMIC, and/or other databases. When applicable, gene-specific pages within the CCGA site directly link to pertinent external content.

editv4:Gene Mutations (SNV/INDEL)
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Epigenomic Alterations edit

  • Epigenetic inactivation of JAK/STAT pathway inhibitors
    • SOCS3 has a crucial role in regulating STAT3 activation[39]
    • An epigenetic inhibition mechanism to SOCS3 gene is hypothesized[39]
    • KIR3DL1 has been shown to be down-modulated by hypermethylation of the promoter[39]
    • Mutations in KMT2D and TET2 have been found to significantly co-occur with STAT3 mutations[23]


Genes and Main Pathways Involved edit

(Instructions: Please include references throughout the table. Do not delete the table.)

Gene; Genetic Alteration Pathway Pathophysiologic Outcome
JAK/STAT[1] Constitutive activation Dysregulation of apoptosis
NK-kB[1] Pathway activation Preventing apoptosis
FAS and FASL[1] Resistance to FAS mediated apoptosis Activation of pro-survival pathways which is postulated to lead to neutropenia
RAS/RAF1/MEK1/ERK[1] Overactive RAS Constitutive activation of RAS and ERK
PI3K/AKT[1] Dysregulation Apoptosis inhibition
editv4:Genes and Main Pathways Involved
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Genetic Diagnostic Testing Methods edit

  • Morphologic assessment, flow cytometry and immunohistochemistry
  • PCR to assess for clonality, T-cell receptor (TCR) gene rearrangements
    • TCR gamma (TCRG) gene is rearranged in all cases, regardless of the type of TCR expressed, thus proves clonality[3]
    • Can be helpful in differentiating a reactive lymphocytosis from clonal T-LGL's
      • NK LGL proliferations do not express TCR, making assessment of clonality difficult[1]
      • Expression of activating isoforms of killer immunoglobulin-like receptors (KIR) can be used as a surrogate marker of clonality in NK LGL[1]
  • Myeloid neoplasms may present with clonal large granular lymphocyte expansion with STAT3/STAT5B mutations. Next generation sequencing can be diagnostically useful in these cases[40]

Familial Forms edit

  • No known familiar forms as of yet.

Additional Information edit

  • PI3K-Akt has been found to be upregulated in KLRG1- CD8+ T-LGLL. Studies are being conducted to examine treatment with linperlisib.[41]
  • Myleoid clonal hematopoiesis is associated with the presence of cytopenia in LGLL[25]

Links edit

References edit

(use the "Cite" icon at the top of the page) (Instructions: Add each reference into the text above by clicking where you want to insert the reference, selecting the “Cite” icon at the top of the wiki page, and using the “Automatic” tab option to search by PMID to select the reference to insert. If a PMID is not available, such as for a book, please use the “Cite” icon, select “Manual” and then “Basic Form”, and include the entire reference. To insert the same reference again later in the page, select the “Cite” icon and “Re-use” to find the reference; DO NOT insert the same reference twice using the “Automatic” tab as it will be treated as two separate references. The reference list in this section will be automatically generated and sorted.)

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 Lamy, Thierry; et al. (2017-03-02). "LGL leukemia: from pathogenesis to treatment". Blood. 129 (9): 1082–1094. doi:10.1182/blood-2016-08-692590. ISSN 0006-4971.
  2. ↑ Zhang, Ling; et al. (2014-09). "Transformed aggressive γδ‐variant T‐cell large granular lymphocytic leukemia with acquired copy neutral loss of heterozygosity at 17q11.2q25.3 and additional aberrations". European Journal of Haematology. 93 (3): 260–264. doi:10.1111/ejh.12313. ISSN 0902-4441. Check date values in: |date= (help)
  3. ↑ 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 "BlueBooksOnline".
  4. ↑ 4.0 4.1 4.2 Johansson, Patricia; et al. (2016-01-01). "Recurrent alterations of TNFAIP 3 (A20) in T-cell large granular lymphocytic leukemia: A20 mutations in T-LGL". International Journal of Cancer. 138 (1): 121–124. doi:10.1002/ijc.29697.
  5. ↑ 5.0 5.1 Muñoz-García, Noemí; et al. (2020-11-25). "STAT3 and STAT5B Mutations in T/NK-Cell Chronic Lymphoproliferative Disorders of Large Granular Lymphocytes (LGL): Association with Disease Features". Cancers. 12 (12): 3508. doi:10.3390/cancers12123508. ISSN 2072-6694. PMC 7760806 Check |pmc= value (help). PMID 33255665 Check |pmid= value (help).
  6. ↑ "STAT3 signal transducer and activator of transcription 3 [Homo sapiens (human)] - Gene - NCBI".
  7. ↑ Koskela, Hanna L.M.; et al. (2012-05-17). "Somatic STAT3 Mutations in Large Granular Lymphocytic Leukemia". New England Journal of Medicine. 366 (20): 1905–1913. doi:10.1056/NEJMoa1114885. ISSN 0028-4793.
  8. ↑ Barilà, Gregorio; et al. (2020-04). "Stat3 mutations impact on overall survival in large granular lymphocyte leukemia: a single-center experience of 205 patients". Leukemia. 34 (4): 1116–1124. doi:10.1038/s41375-019-0644-0. ISSN 0887-6924. Check date values in: |date= (help)
  9. ↑ Fei, Fei; et al. (2023-07-29). "Genomic landscape of T-large granular lymphocyte leukemia and chronic lymphoproliferative disorder of NK cells: a single institution experience". Leukemia & Lymphoma. 64 (9): 1536–1544. doi:10.1080/10428194.2023.2220450. ISSN 1042-8194.
  10. ↑ Loughran, T P; et al. (2015-04). "Immunosuppressive therapy of LGL leukemia: prospective multicenter phase II study by the Eastern Cooperative Oncology Group (E5998)". Leukemia. 29 (4): 886–894. doi:10.1038/leu.2014.298. ISSN 0887-6924. PMC 4377298. PMID 25306898. Check date values in: |date= (help)
  11. ↑ 11.0 11.1 Yabe, Mariko; et al. (2017-01). "Distinguishing Between Hepatosplenic T-cell Lymphoma and γδ T-cell Large Granular Lymphocytic Leukemia: A Clinicopathologic, Immunophenotypic, and Molecular Analysis". American Journal of Surgical Pathology. 41 (1): 82–93. doi:10.1097/PAS.0000000000000743. ISSN 0147-5185. Check date values in: |date= (help)
  12. ↑ Rajala HL, Olson T, Clemente MJ, Lagström S, Ellonen P, Lundan T, Hamm DE, Zaman SA, Marti JM, Andersson EI, Jerez A. The analysis of clonal diversity and therapy responses using STAT3 mutations as a molecular marker in large granular lymphocytic leukemia. haematologica. 2015 Jan 1;100(1):91-9.
  13. ↑ 13.0 13.1 13.2 13.3 13.4 13.5 13.6 Bhattacharya, Dipabarna; et al. (2022-02-24). "Identification of novel STAT5B mutations and characterization of TCRβ signatures in CD4+ T-cell large granular lymphocyte leukemia". Blood Cancer Journal. 12 (2): 31. doi:10.1038/s41408-022-00630-8. ISSN 2044-5385. PMC 8873566 Check |pmc= value (help). PMID 35210405 Check |pmid= value (help).
  14. ↑ "STAT5B signal transducer and activator of transcription 5B [Homo sapiens (human)] - Gene - NCBI".
  15. ↑ Rajala, Hanna L. M.; et al. (2013-05-30). "Discovery of somatic STAT5b mutations in large granular lymphocytic leukemia". Blood. 121 (22): 4541–4550. doi:10.1182/blood-2012-12-474577. ISSN 0006-4971. PMC 3668487. PMID 23596048.
  16. ↑ 16.0 16.1 Rajala, Hanna L. M.; et al. (2014-05-01). "Uncovering the pathogenesis of large granular lymphocytic leukemia—novel STAT3 and STAT5b mutations". Annals of Medicine. 46 (3): 114–122. doi:10.3109/07853890.2014.882105. ISSN 0785-3890.
  17. ↑ Andersson, Emma I.; et al. (2016-11-17). "High incidence of activating STAT5B mutations in CD4-positive T-cell large granular lymphocyte leukemia". Blood. 128 (20): 2465–2468. doi:10.1182/blood-2016-06-724856. ISSN 0006-4971. PMC 5114490. PMID 27697773.
  18. ↑ Johansson, Patricia; et al. (2016-01-01). "Recurrent alterations of TNFAIP 3 (A20) in T-cell large granular lymphocytic leukemia: A20 mutations in T-LGL". International Journal of Cancer. 138 (1): 121–124. doi:10.1002/ijc.29697.
  19. ↑ "TNFAIP3 TNF alpha induced protein 3 [Homo sapiens (human)] - Gene - NCBI".
  20. ↑ 20.0 20.1 20.2 Upadhyayula, Bhanu Surabi; et al. (2026-01). "Mutational Spectrum of T-Cell Large Granular Lymphocytic Leukemia: Insights From the AACR Project GENIE Consortium". Cancer Genomics - Proteomics. 23 (1): 135–143. doi:10.21873/cgp.20566. ISSN 1109-6535. PMC 12758657 Check |pmc= value (help). PMID 41482347 Check |pmid= value (help). Check date values in: |date= (help)
  21. ↑ Chen, Cunte; et al. (2021-09-15). "TNFAIP3 mutation may be associated with favorable overall survival for patients with T-cell lymphoma". Cancer Cell International. 21 (1): 490. doi:10.1186/s12935-021-02191-5. ISSN 1475-2867. PMC 8444556 Check |pmc= value (help). PMID 34526012 Check |pmid= value (help).
  22. ↑ Zhang, Ranran; et al. (2008-10-21). "Network model of survival signaling in large granular lymphocyte leukemia". Proceedings of the National Academy of Sciences. 105 (42): 16308–16313. doi:10.1073/pnas.0806447105. PMC 2571012. PMID 18852469.
  23. ↑ 23.0 23.1 23.2 23.3 23.4 Cheon, HeeJin; et al. (2022-05-19). "Genomic landscape of TCRαβ and TCRγδ T-large granular lymphocyte leukemia". Blood. 139 (20): 3058–3072. doi:10.1182/blood.2021013164. ISSN 0006-4971. PMC 9121841 Check |pmc= value (help). PMID 35015834 Check |pmid= value (help).
  24. ↑ "TET2 tet methylcytosine dioxygenase 2 [Homo sapiens (human)] - Gene - NCBI".
  25. ↑ 25.00 25.01 25.02 25.03 25.04 25.05 25.06 25.07 25.08 25.09 25.10 25.11 25.12 25.13 25.14 25.15 25.16 25.17 Kawashima, Naomi; et al. (2025-02). "Clonal hematopoiesis in large granular lymphocytic leukemia". Leukemia. 39 (2): 451–459. doi:10.1038/s41375-024-02460-y. ISSN 1476-5551. Check date values in: |date= (help)
  26. ↑ 26.0 26.1 26.2 Andersson, E. I.; et al. (2013-12). "Novel somatic mutations in large granular lymphocytic leukemia affecting the STAT-pathway and T-cell activation". Blood Cancer Journal. 3 (12): e168–e168. doi:10.1038/bcj.2013.65. ISSN 2044-5385. PMC 3877422. PMID 24317090. Check date values in: |date= (help)
  27. ↑ "BCL11 transcription factor B".
  28. ↑ 28.0 28.1 28.2 28.3 Coppe, A; et al. (2017-05). "Genomic landscape characterization of large granular lymphocyte leukemia with a systems genetics approach". Leukemia. 31 (5): 1243–1246. doi:10.1038/leu.2017.49. ISSN 0887-6924. PMC 5419584. PMID 28167832. Check date values in: |date= (help)
  29. ↑ "fms related receptor tyrosine kinase 3".
  30. ↑ 30.0 30.1 30.2 Andersson, Emma I.; et al. (2016-11-17). "High incidence of activating STAT5B mutations in CD4-positive T-cell large granular lymphocyte leukemia". Blood. 128 (20): 2465–2468. doi:10.1182/blood-2016-06-724856. ISSN 0006-4971. PMC 5114490. PMID 27697773.
  31. ↑ "protein tyrosine phosphatase non-receptor type 23".
  32. ↑ "KMT2D lysine methyltransferase 2D [Homo sapiens (human)] - Gene - NCBI".
  33. ↑ "TRAF3 TNF receptor associated factor 3 [Homo sapiens (human)] - Gene - NCBI".
  34. ↑ "TRAF3 TNF receptor associated factor 3 [Homo sapiens (human)] - Gene - NCBI".
  35. ↑ "F-box and WD repeat domain containing 2".
  36. ↑ "CREBBP CREB binding lysine acetyltransferase [Homo sapiens (human)] - Gene - NCBI".
  37. ↑ 37.0 37.1 37.2 37.3 37.4 Mizuno, Yuga; et al. (2024-05-30). "CCL22 mutations in large granular lymphocytic leukemia". Haematologica. doi:10.3324/haematol.2024.285404. ISSN 1592-8721. PMC 11367240 Check |pmc= value (help). PMID 38813714 Check |pmid= value (help).
  38. ↑ "C-C motif chemokine ligand 2".
  39. ↑ 39.0 39.1 39.2 Teramo, Antonella; et al. (2013-05-09). "Intrinsic and extrinsic mechanisms contribute to maintain the JAK/STAT pathway aberrantly activated in T-type large granular lymphocyte leukemia". Blood. 121 (19): 3843–3854, S1. doi:10.1182/blood-2012-07-441378. ISSN 1528-0020. PMID 23515927.
  40. ↑ Kavesh, Mark; et al. (2023-01-10). "Distinguishing STAT3/STAT5B -mutated large granular lymphocyte leukemia from myeloid neoplasms by genetic profiling". Blood Advances. 7 (1): 40–45. doi:10.1182/bloodadvances.2022008192. ISSN 2473-9529.
  41. ↑ Zhang, Lele; et al. (2025-04). "KLRG1 re-defines a leukemic clone of CD8 effector T cells sensitive to PI3K inhibitor in T cell large granular lymphocytic leukemia". Cell Reports Medicine. 6 (4): 102036. doi:10.1016/j.xcrm.2025.102036. PMC 12047471 Check |pmc= value (help). PMID 40147444 Check |pmid= value (help). Check date values in: |date= (help)


Notes edit

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*Citation of this Page: “T-large granular lymphocytic leukaemia”. Compendium of Cancer Genome Aberrations (CCGA), Cancer Genomics Consortium (CGC), updated 01/16/2026, https://ccga.io/index.php/HAEM5:T-large_granular_lymphocytic_leukaemia.

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