EBV-positive nodal T- and NK-cell lymphoma
Haematolymphoid Tumours (WHO Classification, 5th ed.)
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Primary Author(s)*
FNU Monika, MBBS; Andrew Siref, MD
Creighton University, Omaha, NE
WHO Classification of Disease
(Will be autogenerated; Book will include name of specific book and have a link to the online WHO site)
| Structure | Disease |
|---|---|
| Book | |
| Category | |
| Family | |
| Type | |
| Subtype(s) |
WHO Essential and Desirable Genetic Diagnostic Criteria
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| WHO Essential Criteria (Genetics)* | |
| WHO Desirable Criteria (Genetics)* | |
| Other Classification |
*Note: These are only the genetic/genomic criteria. Additional diagnostic criteria can be found in the WHO Classification of Tumours.
Related Terminology
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| Acceptable | |
| Not Recommended |
Gene Rearrangements
Put your text here and fill in the table (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 |
|---|---|---|---|---|---|---|---|
| EXAMPLE: ABL1 | EXAMPLE: BCR::ABL1 | EXAMPLE: The pathogenic derivative is the der(22) resulting in fusion of 5’ BCR and 3’ABL1. | EXAMPLE: t(9;22)(q34;q11.2) | EXAMPLE: Common (CML) | EXAMPLE: D, P, T | EXAMPLE: Yes (WHO, NCCN) | EXAMPLE:
The t(9;22) is diagnostic of CML in the appropriate morphology and clinical context (add reference). This fusion is responsive to targeted therapy such as Imatinib (Gleevec) (add reference). BCR::ABL1 is generally favorable in CML (add reference). |
| EXAMPLE: CIC | EXAMPLE: CIC::DUX4 | EXAMPLE: Typically, the last exon of CIC is fused to DUX4. The fusion breakpoint in CIC is usually intra-exonic and removes an inhibitory sequence, upregulating PEA3 genes downstream of CIC including ETV1, ETV4, and ETV5. | EXAMPLE: t(4;19)(q25;q13) | EXAMPLE: Common (CIC-rearranged sarcoma) | EXAMPLE: D | EXAMPLE:
DUX4 has many homologous genes; an alternate translocation in a minority of cases is t(10;19), but this is usually indistinguishable from t(4;19) by short-read sequencing (add references). | |
| EXAMPLE: ALK | EXAMPLE: ELM4::ALK
|
EXAMPLE: Fusions result in constitutive activation of the ALK tyrosine kinase. The most common ALK fusion is EML4::ALK, with breakpoints in intron 19 of ALK. At the transcript level, a variable (5’) partner gene is fused to 3’ ALK at exon 20. Rarely, ALK fusions contain exon 19 due to breakpoints in intron 18. | EXAMPLE: N/A | EXAMPLE: Rare (Lung adenocarcinoma) | EXAMPLE: T | EXAMPLE:
Both balanced and unbalanced forms are observed by FISH (add references). | |
| EXAMPLE: ABL1 | EXAMPLE: N/A | EXAMPLE: Intragenic deletion of exons 2–7 in EGFR removes the ligand-binding domain, resulting in a constitutively active tyrosine kinase with downstream activation of multiple oncogenic pathways. | EXAMPLE: N/A | EXAMPLE: Recurrent (IDH-wildtype Glioblastoma) | EXAMPLE: D, P, T | ||
No chromosomal rearrangements are identified.
The combination of the 2 pieces of chromosome 9 formed the fusion of the promoter plus exon 1 of DOCK8 and exons 2-7 of PD-L1 (DOCK8/PD-L1 fusion). https://doi.org/10.1182/bloodadvances.2023012019
| Chromosomal Rearrangement | Genes in Fusion (5’ or 3’ Segments) | Pathogenic Derivative | Prevalence | Diagnostic Significance (Yes, No or Unknown) | Prognostic Significance (Yes, No or Unknown) | Therapeutic Significance (Yes, No or Unknown) | Notes |
|---|---|---|---|---|---|---|---|
| NA | NA | NA | NA | NA | NA | NA | NA |
Individual Region Genomic Gain/Loss/LOH
Put your text here and fill in the table (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 |
|---|---|---|---|---|---|---|
| EXAMPLE:
7 |
EXAMPLE: Loss | EXAMPLE:
chr7 |
EXAMPLE:
Unknown |
EXAMPLE: D, P | EXAMPLE: No | EXAMPLE:
Presence of monosomy 7 (or 7q deletion) is sufficient for a diagnosis of AML with MDS-related changes when there is ≥20% blasts and no prior therapy (add reference). Monosomy 7/7q deletion is associated with a poor prognosis in AML (add references). |
| EXAMPLE:
8 |
EXAMPLE: Gain | EXAMPLE:
chr8 |
EXAMPLE:
Unknown |
EXAMPLE: D, P | EXAMPLE:
Common recurrent secondary finding for t(8;21) (add references). | |
| EXAMPLE:
17 |
EXAMPLE: Amp | EXAMPLE:
17q12; chr17:39,700,064-39,728,658 [hg38; 28.6 kb] |
EXAMPLE:
ERBB2 |
EXAMPLE: D, P, T | EXAMPLE:
Amplification of ERBB2 is associated with HER2 overexpression in HER2 positive breast cancer (add references). Add criteria for how amplification is defined. | |
Put your text here and fill in the table (Instructions: Includes aberrations not involving gene fusions. Can include references in the table. Can refer to CGC workgroup tables as linked on the homepage if applicable. Do not delete table.)
| Chr # | Gain / Loss / Amp / LOH | Minimal Region Genomic Coordinates [Genome Build] | Minimal Region Cytoband | Diagnostic Significance (Yes, No or Unknown) | Prognostic Significance (Yes, No or Unknown) | Therapeutic Significance (Yes, No or Unknown) | Notes |
|---|---|---|---|---|---|---|---|
| 3[1] | Loss | 3q26.1 | 3q26.1 | No | No | No | |
| 22[1] | Loss | 22q11.23 | 22q11.23 | No | No | No | |
| 14[1] | Loss | 14q11.2 | 14q11.2 | May be | No | No | Loss of chr14q11.2 is the most frequent CNA, consistent with this aberration as a marker of T-cell lineage.[1] |
| 3[2] | Gain | 3p14.1 | 3p14.1 | No | No | No | Gain of 3p14.1 is found in 14.3% cases compared to 5.9% and 76.0% of ENKTL and PTCL-NOS cases, respectively |
| 6[2] | Gain | 6p22.3 | 6p22.3 | No | No | No | Gain of 6p22.3 is found more frequently in ENKTL (20.6%) and PTCL-NOS (58.6%) than in PTCL-EBV (7.1%) (P=0.005). |
| 6[2] | Gain | 6p22.1 | 6p22.1 | No | No | No | Gain of 6p22.1 is seen more in 21.4% of PTCL-EBV cases compared to 8.8% of ENKTL and 58.6% of PTCL-NOS cases |
| 17[2] | Gain | 17q21.33 | 17q21.33 | No | No | No |
Characteristic Chromosomal or Other Global Mutational Patterns
No specific characteristic chromosomal patterns have been described in EBV-positive nodal T- and NK-cell lymphoma.
| 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 |
|---|---|---|---|---|---|
Gene Mutations (SNV/INDEL)
Put your text here and fill in the table (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 |
|---|---|---|---|---|---|---|
| EXAMPLE:EGFR
|
EXAMPLE: Exon 18-21 activating mutations | EXAMPLE: Oncogene | EXAMPLE: Common (lung cancer) | EXAMPLE: T | EXAMPLE: Yes (NCCN) | EXAMPLE: Exons 18, 19, and 21 mutations are targetable for therapy. Exon 20 T790M variants cause resistance to first generation TKI therapy and are targetable by second and third generation TKIs (add references). |
| EXAMPLE: TP53; Variable LOF mutations
|
EXAMPLE: Variable LOF mutations | EXAMPLE: Tumor Supressor Gene | EXAMPLE: Common (breast cancer) | EXAMPLE: P | EXAMPLE: >90% are somatic; rare germline alterations associated with Li-Fraumeni syndrome (add reference). Denotes a poor prognosis in breast cancer. | |
| EXAMPLE: BRAF; Activating mutations | EXAMPLE: Activating mutations | EXAMPLE: Oncogene | EXAMPLE: Common (melanoma) | EXAMPLE: T | ||
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.
Based on the recent published literature, the most commonly mutated genes in EBV-positive nodal T- and NK-cell lymphoma identified in the Asian population are given below:
| Gene; Genetic Alteration | Presumed Mechanism (Tumor Suppressor Gene [TSG] / Oncogene / Other) | Prevalence (COSMIC / TCGA / Other) | Concomitant Mutations | Mutually Exclusive Mutations | Diagnostic Significance (Yes, No or Unknown) | Prognostic Significance (Yes, No or Unknown) | Therapeutic Significance (Yes, No or Unknown) | Notes |
|---|---|---|---|---|---|---|---|---|
| TET2 | TSG | 64%- 68%[2][3] | DNMT3A[3] | NA | NA | Yes | No | Both gene mutations are associated with clonal hematopoiesis and were found to have an overall poor survival in cohort of patients with concurrent mutations[3] |
| DNMT3A | TSG | 32%[3] | TET2[3] | NA | NA | Yes | No | Same as above |
| PIK3CD | 33%[2] | NA | NA | NA | NA | NA | ||
| STAT3 | Oncogene | 19%[2] | NA | NA | NA | NA | NA | |
| DDX3X | TSG | 20%[2] | NA | NA | NA | NA | NA | |
| PTPRD | 18%[2] | NA | NA | NA | NA | NA | ||
| SETD2 | 8%[4] | NA | NA | NA | NA | NA |
Epigenomic Alterations
Genes and Main Pathways Involved
Recent studies have demonstrated that EBV-positive nodal T- and NK-cell lymphoma is characterized by low genomic instability, upregulation of immune pathways (NFκB and check point protein PD-L1) that promote immune evasion, downregulation of EBV miRNAS and T-cell receptor (TCR) clonality. Furthermore, gene expression profiling analysis has identified enriched expression of genes related to cytotoxic activation, IL-6/JAK/STAT3 signaling, cell cycle and genomic instability, immune-related pathways, and interferon-α/γ response. NF-κB pathway–associated genes and proteins (BIRC3, NFKB1, and CD27) are upregulated. PDL1 (CD274) is also upregulated and is thought to be correlated with IFN-γ, IL-6/JAK/STAT3, and NF-κB pathways upregulation, although there is no gain of 9p24.1. Some of these pathways may be considered as potential therapeutic targets for EBV-positive nodal T- and NK-cell lymphoma as drugs targeting JAK-STAT, NFκB, STAT3, IFNγ, PD1/PD-L1 are either approved by FDA for different cancers or are being evaluated in clinical trials for lymphomas.[2]
| Gene; Genetic Alteration | Pathway | Pathophysiologic Outcome |
|---|---|---|
| TET2; point mutations[3] | DNA demethylation; epigenetic modifier | |
| DNMT3 | DNA methylation; epigenetic modifier | |
| STAT3; gain-of-function mutation | JAK-STAT Pathway | Cell proliferation, migration and apoptosis |
| PIK3CD | IL-9 Signaling Pathways; Immune response | |
| DDX3X | Innate Immune System and Toll-like receptor signaling pathway | |
| PTPRD | Protein-protein interactions at synapses and Transmission across Chemical Synapses | Cell growth, differentiation, mitotic cycle, and oncogenic transformation |
| SETD2 | Key regulator of DNA mismatch repair in G1 and early S phase |
Genetic Diagnostic Testing Methods
Diagnosis of EBV-positive nodal T- and NK-cell lymphoma requires a combination of clinical evaluation, laboratory tests, imaging studies, and genetic testing to identify diagnostic criteria.
T-cell clonality can be confirmed by PCR, NGS, or flow cytometry. Cytogenetics, FISH and NGS can be helpful in differentiating this lymphoma from other types of EBV-T/NK cell lymphoproliferative disorders.
Familial Forms
None.
Additional Information
This disease is defined/characterized as detailed below:
- EBV-positive nodal T- and NK-cell lymphoma is a rare EBV-positive lymphoma of cytotoxic T- or NK-cell lineage, primarily involving lymph nodes in adults.[5]
- Is a distinct entity in the 5th Edition of the WHO classification and as a provisional entity in the International Consensus Classification 2022.[6][7]
The epidemiology/prevalence of this disease is detailed below:
- Rare lymphoma
- Occurs mostly in eastern Asia
- Affects mainly older adults (median age: 61–64 years) although cases in younger adults have been reported
- The M:F ratio is 1.5–3.8:1 [5][8]
The clinical features of this disease are detailed below:
Signs and symptoms[5][9][10][11] - Lymphadenopathy; Advanced clinical stage III/IV disease at diagnosis (86–88% of cases); B symptoms (72–80%); High or high/intermediate International Prognostic Index (IPI) score (64–87%)
Laboratory findings - Anemia; Leukopenia; Thrombocytopenia; Elevated serum lactate dehydrogenase
The sites of involvement of this disease are detailed below:
- Primarily lymph nodes (most commonly cervical, inguinal, and axillary), although limited extranodal involvement can be seen[5]
- Liver and/or bone marrow (24–60% of cases); other extranodal sites, such as the skin and gastrointestinal tract, are less commonly involved[9][10][12]
- No nasal involvement has been reported[5]
The morphologic features of this disease are detailed below:
- Architectural effacement of lymph node by a diffuse infiltrate of monotonous medium-sized to large lymphoid cells
- The neoplastic cells have centroblastic appearance with vesicular chromatin
- Less frequently, the neoplastic cells display large pleomorphic or mixed-cell morphology with abundant histiocytes and small lymphocytes in the background[5][13]
- Lacks classic morphological findings of angioinvasion and necrosis seen in extranodal EBV+ T- and NK-cell lymphomas[9]
The immunophenotype of this disease is detailed below:
Positive (universal) - CD3, CD2, CD56 (7–22%), cytotoxic molecules (TIA1, granzyme B, and perforin), EBER (ISH)
CD4/CD8[5][8][9][10][12] - CD4-/CD8- (21%), CD4+/CD8- (8%), CD4-/CD8+ (63-72%)
TCR[5][8][9][10][12] - TCRβ (+, 43–64%), TCRγ (+, 0–13%), TCRβ and TCRγ (-, 25%)
Positive (subset) - CD30[6]
Negative (universal) – CD5
Links
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References
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Notes
*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 CCGA coordinators (contact information provided on the homepage). Additional global feedback or concerns are also welcome.
- ↑ 1.0 1.1 1.2 1.3 Ng, Siok-Bian; et al. (2018-02-01). "Epstein-Barr virus-associated primary nodal T/NK-cell lymphoma shows a distinct molecular signature and copy number changes". Haematologica. 103 (2): 278–287. doi:10.3324/haematol.2017.180430. ISSN 1592-8721. PMC 5792272. PMID 29097495.CS1 maint: PMC format (link)
- ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 Wai, Cho Mar Myint; et al. (2022-01-13). "Immune pathway upregulation and lower genomic instability distinguish EBV-positive nodal T/NK-cell lymphoma from ENKTL and PTCL-NOS". Haematologica. 107 (8): 1864–1879. doi:10.3324/haematol.2021.280003. ISSN 1592-8721. PMC PMC9335103 Check
|pmc=value (help). PMID 35021606 Check|pmid=value (help).CS1 maint: PMC format (link) - ↑ 3.0 3.1 3.2 3.3 3.4 3.5 Kato, Seiichi; et al. (2024-05-14). "EBV+ nodal T/NK-cell lymphoma associated with clonal hematopoiesis and structural variations of the viral genome". Blood Advances. 8 (9): 2138–2147. doi:10.1182/bloodadvances.2023012019. ISSN 2473-9529. PMC PMC11068532 Check
|pmc=value (help). PMID 38429084 Check|pmid=value (help).CS1 maint: PMC format (link) - ↑ Climent, Fina; et al. (2023-09-01). "Cytotoxic peripheral T-cell lymphomas and EBV-positive T/NK-cell lymphoproliferative diseases: emerging concepts, recent advances, and the putative role of clonal hematopoiesis. A report of the 2022 EA4HP/SH lymphoma workshop". Virchows Archiv. 483 (3): 333–348. doi:10.1007/s00428-023-03616-4. ISSN 1432-2307. PMC PMC10542298 Check
|pmc=value (help). PMID 37646869 Check|pmid=value (help).CS1 maint: PMC format (link) - ↑ 5.0 5.1 5.2 5.3 5.4 5.5 5.6 5.7 Siok-Bian Ng, et al. EBV-positive nodal T- and NK-cell lymphoma. In: WHO Classification of Tumours Editorial Board. Haematolymphoid tumours [Internet]. Lyon (France): International Agency for Research on Cancer; 2024 [cited 2024 Oct 6]. (WHO classification of tumors series, 5th ed.; vol. 11). Available from: BlueBooksOnline (who.int)
- ↑ 6.0 6.1 Yu, Fang; et al. (2024-04). "EBV-positive Nodal T-Cell and NK-Cell Lymphoma: A Study of 26 Cases Including a Subset With Strong CD30 Expression Mimicking Anaplastic Large Cell Lymphoma". American Journal of Surgical Pathology. 48 (4): 406–416. doi:10.1097/PAS.0000000000002184. ISSN 0147-5185. Check date values in:
|date=(help) - ↑ Kato, Seiichi; et al. (2024-05-14). "EBV+ nodal T/NK-cell lymphoma associated with clonal hematopoiesis and structural variations of the viral genome". Blood Advances. 8 (9): 2138–2147. doi:10.1182/bloodadvances.2023012019. ISSN 2473-9529. PMC PMC11068532 Check
|pmc=value (help). PMID 38429084 Check|pmid=value (help).CS1 maint: PMC format (link) - ↑ 8.0 8.1 8.2 Ha, Sang Yun; et al. (2013-07-01). "Epstein–Barr virus-positive nodal peripheral T cell lymphomas: Clinicopathologic and gene expression profiling study". Pathology - Research and Practice. 209 (7): 448–454. doi:10.1016/j.prp.2013.04.013. ISSN 0344-0338.
- ↑ 9.0 9.1 9.2 9.3 9.4 Jeon, Yoon Kyung; et al. (2015-07). "Epstein-Barr virus–positive nodal T/NK-cell lymphoma: an analysis of 15 cases with distinct clinicopathological features". Human Pathology. 46 (7): 981–990. doi:10.1016/j.humpath.2015.03.002. Check date values in:
|date=(help) - ↑ 10.0 10.1 10.2 10.3 Kato, Seiichi; et al. (2015-04). "T-cell Receptor (TCR) Phenotype of Nodal Epstein-Barr Virus (EBV)-positive Cytotoxic T-cell Lymphoma (CTL): A Clinicopathologic Study of 39 Cases". American Journal of Surgical Pathology. 39 (4): 462–471. doi:10.1097/PAS.0000000000000323. ISSN 0147-5185. Check date values in:
|date=(help) - ↑ Yu, Fang; et al. (2024-04). "EBV-positive Nodal T-Cell and NK-Cell Lymphoma: A Study of 26 Cases Including a Subset With Strong CD30 Expression Mimicking Anaplastic Large Cell Lymphoma". American Journal of Surgical Pathology. 48 (4): 406–416. doi:10.1097/PAS.0000000000002184. ISSN 0147-5185. Check date values in:
|date=(help) - ↑ 12.0 12.1 12.2 Yamashita, Daisuke; et al. (2018-08). "Reappraisal of nodal Epstein‐Barr Virus‐negative cytotoxic T‐cell lymphoma: Identification of indolent CD 5 + diseases". Cancer Science. 109 (8): 2599–2610. doi:10.1111/cas.13652. ISSN 1347-9032. PMC 6113510. PMID 29845715. Check date values in:
|date=(help)CS1 maint: PMC format (link) - ↑ Attygalle, Ayoma D; et al. (2014-01). "Peripheral T‐cell and NK ‐cell lymphomas and their mimics; taking a step forward – report on the lymphoma workshop of the XVI th meeting of the European Association for Haematopathology and the Society for Hematopathology". Histopathology. 64 (2): 171–199. doi:10.1111/his.12251. ISSN 0309-0167. PMC 6364972. PMID 24128129. Check date values in:
|date=(help)CS1 maint: PMC format (link)