T-large granular lymphocytic leukaemia

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Haematolymphoid Tumours (WHO Classification, 5th ed.)

Primary Author(s)*

Nicolas LaScala, DO

Michelle Don, MD, MS

WHO Classification of Disease

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

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

No know chromosomal rearrangements.

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

Individual Region Genomic Gain/Loss/LOH

No known recurrent copy number gain/loss/LOH, chromosomal abnormalities have been reported in a few cases.[1]

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

Characteristic Chromosomal or Other Global Mutational Patterns

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]

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

Gene Mutations (SNV/INDEL)

Somatic activating STAT3 and STAT5b mutations are the most common SNVs in T-LGL.

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 Frequent co-occurrence of KMT2D and STAT3 mutations[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.

Epigenomic Alterations

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

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

Genetic Diagnostic Testing Methods

  • 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

No known familiar forms as of yet.

Additional Information

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

Hepatosplenic T-cell lymphoma

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 Lamy, Thierry; Moignet, Aline; Loughran, Thomas P. (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; Ramchandren, Radhakrishnan; Papenhausen, Peter; Loughran, Thomas P.; Sokol, Lubomir (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. {{cite journal}}: 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". {{cite journal}}: Cite journal requires |journal= (help)
  4. ↑ 4.0 4.1 4.2 Johansson, Patricia; Bergmann, Anke; Rahmann, Sven; Wohlers, Inken; Scholtysik, René; Przekopowitz, Martina; Seifert, Marc; Tschurtschenthaler, Gertraud; Webersinke, Gerald (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; Jara-Acevedo, María; Caldas, Carolina; Bárcena, Paloma; López, Antonio; Puig, Noemí; Alcoceba, Miguel; Fernández, Paula; Villamor, Neus (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. PMID 33255665.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  6. ↑ "STAT3 signal transducer and activator of transcription 3 [Homo sapiens (human)] - Gene - NCBI". {{cite journal}}: Cite journal requires |journal= (help)
  7. ↑ Koskela, Hanna L.M.; Eldfors, Samuli; Ellonen, Pekka; van Adrichem, Arjan J.; Kuusanmäki, Heikki; Andersson, Emma I.; Lagström, Sonja; Clemente, Michael J.; Olson, Thomas (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; Teramo, Antonella; Calabretto, Giulia; Vicenzetto, Cristina; Gasparini, Vanessa Rebecca; Pavan, Laura; Leoncin, Matteo; Vedovato, Susanna; Frigo, Anna Chiara (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. {{cite journal}}: Check date values in: |date= (help)
  9. ↑ Fei, Fei; Stehr, Henning; Zehnder, James L. (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; Zickl, L; Olson, T L; Wang, V; Zhang, D; Rajala, H L M; Hasanali, Z; Bennett, J M; Lazarus, H M (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. {{cite journal}}: Check date values in: |date= (help)
  11. ↑ 11.0 11.1 Yabe, Mariko; Medeiros, L. Jeffrey; Wang, Sa A.; Tang, Guilin; Bueso-Ramos, Carlos E.; Jorgensen, Jeffrey L.; Bhagat, Govind; Chen, Weina; Li, Shaoying (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. {{cite journal}}: 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; Teramo, Antonella; Gasparini, Vanessa Rebecca; Huuhtanen, Jani; Kim, Daehong; Theodoropoulos, Jason; Schiavoni, Gianluca; Barilà, Gregorio; Vicenzetto, Cristina (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. PMID 35210405.
  14. ↑ "STAT5B signal transducer and activator of transcription 5B [Homo sapiens (human)] - Gene - NCBI". {{cite journal}}: Cite journal requires |journal= (help)
  15. ↑ Rajala, Hanna L. M.; Eldfors, Samuli; Kuusanmäki, Heikki; van Adrichem, Arjan J.; Olson, Thomas; Lagström, Sonja; Andersson, Emma I.; Jerez, Andres; Clemente, Michael J. (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.; Porkka, Kimmo; Maciejewski, Jaroslaw P.; Loughran, Thomas P.; Mustjoki, Satu (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.; Tanahashi, Takahiro; Sekiguchi, Nodoka; Gasparini, Vanessa Rebecca; Bortoluzzi, Sabrina; Kawakami, Toru; Matsuda, Kazuyuki; Mitsui, Takeki; Eldfors, Samuli (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; Bergmann, Anke; Rahmann, Sven; Wohlers, Inken; Scholtysik, René; Przekopowitz, Martina; Seifert, Marc; Tschurtschenthaler, Gertraud; Webersinke, Gerald (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". {{cite journal}}: Cite journal requires |journal= (help)
  20. ↑ 20.0 20.1 20.2 Upadhyayula, Bhanu Surabi; Saglimbeni, Grace S.; Gobel, Edie; Gobel, Abbi; Morris, Tyson J.; Surendra, Akaash; Hsia, Beau; Sood, Akshat; Tauseef, Abubakar (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. PMID 41482347. {{cite journal}}: Check date values in: |date= (help)
  21. ↑ Chen, Cunte; Chen, Zheng; Huang, Ling; Zhou, Lingling; Zhu, Lihua; Liu, Sichu; Luo, Gengxin; Li, Wenyu; Zeng, Chengwu (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. PMID 34526012.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  22. ↑ Zhang, Ranran; Shah, Mithun Vinod; Yang, Jun; Nyland, Susan B.; Liu, Xin; Yun, Jong K.; Albert, Réka; Loughran, Thomas P. (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; Xing, Jeffrey C.; Moosic, Katharine B.; Ung, Johnson; Chan, Vivian W.; Chung, David S.; Toro, Mariella F.; Elghawy, Omar; Wang, John S. (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. PMID 35015834.
  24. ↑ "TET2 tet methylcytosine dioxygenase 2 [Homo sapiens (human)] - Gene - NCBI". {{cite journal}}: Cite journal requires |journal= (help)
  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; Gurnari, Carmelo; Bravo-Perez, Carlos; Kubota, Yasuo; Pagliuca, Simona; Guarnera, Luca; Williams, Nakisha D.; Durmaz, Arda; Ahmed, Arooj (2025-02). "Clonal hematopoiesis in large granular lymphocytic leukemia". Leukemia. 39 (2): 451–459. doi:10.1038/s41375-024-02460-y. ISSN 1476-5551. {{cite journal}}: Check date values in: |date= (help)
  26. ↑ 26.0 26.1 26.2 Andersson, E. I.; Rajala, H. L. M.; Eldfors, S.; Ellonen, P.; Olson, T.; Jerez, A.; Clemente, M. J.; Kallioniemi, O.; Porkka, K. (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. {{cite journal}}: Check date values in: |date= (help)
  27. ↑ "BCL11 transcription factor B". {{cite journal}}: Cite journal requires |journal= (help)
  28. ↑ 28.0 28.1 28.2 Coppe, A; Andersson, E I; Binatti, A; Gasparini, V R; Bortoluzzi, S; Clemente, M; Herling, M; Maciejewski, J; Mustjoki, S (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. {{cite journal}}: Check date values in: |date= (help)
  29. ↑ "fms related receptor tyrosine kinase 3". {{cite journal}}: Cite journal requires |journal= (help)
  30. ↑ 30.0 30.1 30.2 Andersson, Emma I.; Tanahashi, Takahiro; Sekiguchi, Nodoka; Gasparini, Vanessa Rebecca; Bortoluzzi, Sabrina; Kawakami, Toru; Matsuda, Kazuyuki; Mitsui, Takeki; Eldfors, Samuli (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". {{cite journal}}: Cite journal requires |journal= (help)
  32. ↑ "KMT2D lysine methyltransferase 2D [Homo sapiens (human)] - Gene - NCBI". {{cite journal}}: Cite journal requires |journal= (help)
  33. ↑ "TRAF3 TNF receptor associated factor 3 [Homo sapiens (human)] - Gene - NCBI". {{cite journal}}: Cite journal requires |journal= (help)
  34. ↑ "TRAF3 TNF receptor associated factor 3 [Homo sapiens (human)] - Gene - NCBI". {{cite journal}}: Cite journal requires |journal= (help)
  35. ↑ "F-box and WD repeat domain containing 2". {{cite journal}}: Cite journal requires |journal= (help)
  36. ↑ "CREBBP CREB binding lysine acetyltransferase [Homo sapiens (human)] - Gene - NCBI". {{cite journal}}: Cite journal requires |journal= (help)
  37. ↑ 37.0 37.1 37.2 37.3 37.4 Mizuno, Yuga; Kawakami, Toru; Higano, Daigo; Miyairi, Shotaro; Asakura, Ami; Kawakami, Fumihiro; Sato, Keijiro; Matsuzawa, Shuji; Nishina, Sayaka (2024-05-30). "CCL22 mutations in large granular lymphocytic leukemia". Haematologica. doi:10.3324/haematol.2024.285404. ISSN 1592-8721. PMC 11367240. PMID 38813714.
  38. ↑ "C-C motif chemokine ligand 2". {{cite journal}}: Cite journal requires |journal= (help)
  39. ↑ 39.0 39.1 39.2 Teramo, Antonella; Gattazzo, Cristina; Passeri, Francesca; Lico, Albana; Tasca, Giulia; Cabrelle, Anna; Martini, Veronica; Frezzato, Federica; Trimarco, Valentina (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; Mohebnasab, Maedeh; Angel, Marcela Riveros; Xie, Wei; Raess, Philipp W.; Cui, Wei; Press, Richard D.; Yang, Guang; Li, Peng (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; Qiu, Chen; Li, Ruonan; Shen, Yucan; Tian, Linzhu; Chang, Hong; Liang, Qian; Pan, Hong; Gao, Zhen (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. PMID 40147444. {{cite journal}}: Check date values in: |date= (help)CS1 maint: article number as page number (link)

Notes

*Citation of this Page: LaScala N, Don M“T-large granular lymphocytic leukaemia”. Compendium of Cancer Genome Aberrations (CCGA), Cancer Genomics Consortium (CGC), updated 02/17/2026, https://ccga.io/index.php/HAEM5:T-large_granular_lymphocytic_leukaemia.


*Primary authors will typically be those that initially create and complete the content of a page.  If a subsequent user modifies the content and feels the effort put forth is of high enough significance to warrant listing in the authorship section, please contact the Associate Editor or other CCGA representative.  When pages have a major update, the new author will be acknowledged at the beginning of the page, and those who contributed previously will be acknowledged below as a prior author.

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