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Primary large B-cell lymphoma of immune-privileged sites

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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:Diffuse Large B-cell Lymphoma, Not Otherwise Specified.

Another relevent page is: HAEM4:Primary Diffuse Large B-cell Lymphoma of the CNS

(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 | edit source]

Ashwini Yenamandra, PhD FACMG, Vanderbilt University Medical Center, Laveniya Satgunaseelan MBBS BMedSc FRCPA, Royal Prince Alfred Hospital

WHO Classification of Disease[edit | edit source]

Structure Disease
Book Haematolymphoid Tumours (5th ed.)
Category B-cell lymphoid proliferations and lymphomas
Family Mature B-cell neoplasms
Type Large B-cell lymphomas
Subtype(s) Primary large B-cell lymphoma of immune-privileged sites

Related Terminology[edit | edit source]

Acceptable Primary diffuse large B-cell lymphoma of the CNS; primary diffuse large B-cell lymphoma of the vitreoretina; primary diffuse large B-cell lymphoma of the testis
Not Recommended Primary CNS lymphoma; primary intraocular lymphoma; primary testicular lymphoma

Gene Rearrangements[edit | edit source]

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 5’BCL6 / 3’IGH Overexpression of Bcl6 and impairment of IGH immunoglobulin due to translocation is thought to be a contributor to CNS-DLNCL pathogenesis[1]. t(3;14)(q27;q32) 17%-20%[2][3] D, P 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 5’IGH / 3’BCL2 Uncommon translocation in CNS-DLBCL; can be found in CNS-DLBCL involving meninges, or secondary involvement by extra-CNS DLBCL[4]. t(14;18)(q31;q21) 6.7%[3] 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 5’MYC / 3’IGH Rare translocation in CNS-DLBCL[5]. t(8;14)(q24;q32) 3%[6] D EXAMPLE:

Both balanced and unbalanced forms are observed by FISH (add references).

EXAMPLE: ABL1 5’ ETV6 / 3’IGH Novel surrogate fusion in CNS-DLBCL indicating favorable prognosis[7]. t(12;14)(p13;q32) 18%[8] D,P
5’PD-L2 / 3’IGL Translocations involving PD-L1 and PD-L2 are potentially the basis of immune evasion in CNS-DLBCL[9]. t(9;22)(p24;q11) 13%[2] D
5’PD-L1 / 3’BCNP1 Translocations involving PD-L1 and PD-L2 are potentially the basis of immune evasion in CNS-DLBCL[10]. t(9;19)(p24;p13) 13%[2] D


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)

Prognosis: Diagnosis this disease may allow appropriate prophylactic measures, including H1 and H2 blockers, proton pump inhibitors and steroids, to be initiated to minimize its protean complications.


Therapeutic Implications:

End of V4 Section

Individual Region Genomic Gain/Loss/LOH[edit | edit source]

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
18 Gain chr18: 45,900,000-61,300,000 [hg38] BCL2 Common recurrent gain (43%) involving BCL2 gene[11].
19 Gain chr19:55,800,001-58,617,616 [hg38] ZNF genes Common recurrent gain (47%) involving ZNF cluster[12].
19 Gain chr19:42,900,001-44,700,000 [hg38] ZNF genes Recurrent gain (37%) involving ZNF cluster[13].
12 Gain chr12: 1-133,275,309 [hg38] STAT6 and CD27 Recurrent gain (26%) involving STAT6 and CD27[14].
6 Loss chr6:105,000,001-114,200,000 [hg38] PRDM1 Common recurrent loss (52%) involving PRDM1[15].
6 Loss chr6:32,100,001-33,500,000 [hg38] MHC genes Loss affecting 74% of CNS-DLBCL cases overall, with region harboring MHC genes including HLA-DRB, HLA-DQA and HLA-DQB (37% homozygous deletion and 37% uniparental disomy)[16].
8 Loss chr8:54,600,001-60,600,001 [hg38] TOX, CA8 and RAB2A Common recurrent loss (32%) involving TOX, CA8 and RAB2A[17].
9 Loss chr9:19,900,001-25,600,000 [hg38] CDKN2A/B Common recurrent loss (48%) involving CDKN2A/B (32% homozygous deletion; 16% partial uniparental disomy)[18].
editv4:Genomic Gain/Loss/LOH
The content below was from the old template. Please incorporate above.

AMPLIFICATION: BCL2, REL, CD274, PDCD1LG2, JAK2, KRAs, TBL1XR1, RB1

DELETION: CDKN2A, TNFAIP3, CDKN2B, TNFRSF14, CD70, CD58, PTEN

Chromosome Number Gain/Loss/Amp/LOH Region
EXAMPLE: 8 EXAMPLE: Gain EXAMPLE: chr8:0-1000000
EXAMPLE: 7 EXAMPLE: Loss EXAMPLE: chr7:0-1000000
End of V4 Section

Characteristic Chromosomal or Other Global Mutational Patterns[edit | edit source]

Put your text here and fill in the table (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
EXAMPLE:

Co-deletion of 1p and 18q

EXAMPLE: See chromosomal rearrangements table as this pattern is due to an unbalanced derivative translocation associated with oligodendroglioma (add reference). EXAMPLE: Common (Oligodendroglioma) EXAMPLE: D, P
EXAMPLE:

Microsatellite instability - hypermutated

EXAMPLE: Common (Endometrial carcinoma) EXAMPLE: P, T
editv4:Characteristic Chromosomal Aberrations / Patterns
The content below was from the old template. Please incorporate above.

Due to the clinicopathologic, biological and genetic diversity, DLBCL is sub divided into morphological variants and molecular subtypes. Initial workup and evaluation of DLBCL has become increasingly complex partly due to the genetic abnormalities that are targets for specific therapy and play an important role in monitoring residual disease. Genomic studies help in clinical management, risk stratification, enrolling patients onto treatment protocols, clinical trials, and detection of therapeutic targets. GS, If IHC is positive for GCB like DLBCL, FISH and Cytogenetics for MYC, BCL2 or BCL6 gene rearrangement are recommended to rule out double and triple hit lymphoma.

End of V4 Section

Gene Mutations (SNV/INDEL)[edit | edit source]

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
MYD88;

GOF mutation

EXAMPLE: Exon 18-21 activating mutations Oncogene 50% to 76%[19][20] D EXAMPLE: Yes (NCCN) Common missense mutation is MYD88 L265P. Affects NF-kB pathway synergistically with CARD11 (occurring in 29%[21]).
CD79B; GOF mutation EXAMPLE: Variable LOF mutations Oncogene 83%[20] D Both CD79B and MYD88 lead to constitutive action of NF-kB pathway[22].
SHIP;

Loss of function

EXAMPLE: Activating mutations Tumor suppressor gene 25%[23] Component of B-cell receptor signaling cascade altered by point mutation in SHIP[24].

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)
The content below was from the old template. Please incorporate above.

SNV : MLL2, TP53, MYD88, B2M, CREBBP, TNFAIP3, PIM1, BCL2, EZH2, TNFRSF14, CD79B

Gene Mutation Oncogene/Tumor Suppressor/Other Presumed Mechanism (LOF/GOF/Other; Driver/Passenger) Prevalence (COSMIC/TCGA/Other)
EXAMPLE: TP53 EXAMPLE: R273H EXAMPLE: Tumor Suppressor EXAMPLE: LOF EXAMPLE: 20%

Other Mutations[edit | edit source]

Type Gene/Region/Other
Concomitant Mutations EXAMPLE: IDH1 R123H
Secondary Mutations EXAMPLE: Trisomy 7
Mutually Exclusive EXAMPLE: EGFR Amplification
End of V4 Section

Epigenomic Alterations[edit | edit source]

Promoter hypermethylation of genes has been established as a potential pathogenetic mechanism in CNS-DLBCL[25]. Genes affected include DAPK (84% of CNS-DLBCL cases), CDKN2A/B (75%), TSP1 (68%), MGMT (52%) and RFC (30%)[25][26]). RFC promoter hypermethylation may have a theranostic role in those treated with high-dose methotrexate regimens.

Genes and Main Pathways Involved[edit | edit source]

Genetic alterations observed in CNS-DLBCL converge on the NF-kB pathway, leading to its constitutive activation. The gene pathways upstream of the NF-kB complex are affected in CNS-DLBCL. These include the B-cell receptor pathway (SHIP, CD79B), its target pathway, the BCM complex (CARD11, MALT1) and toll-like receptor pathway (MYD88)[27][28].

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

Gene; Genetic Alteration Pathway Pathophysiologic Outcome
EXAMPLE: BRAF and MAP2K1; Activating mutations EXAMPLE: MAPK signaling EXAMPLE: Increased cell growth and proliferation
EXAMPLE: CDKN2A; Inactivating mutations EXAMPLE: Cell cycle regulation EXAMPLE: Unregulated cell division
EXAMPLE: KMT2C and ARID1A; Inactivating mutations EXAMPLE: Histone modification, chromatin remodeling EXAMPLE: Abnormal gene expression program
editv4:Genes and Main Pathways Involved
The content below was from the old template. Please incorporate above.

B-Cell differentiation, TP53 pathway, NF-kB pathway, Apoptosis, Cell migration, Immune response,BCR-MYD88 signaling, PI3K-AKT-mTCR pathway

End of V4 Section

Genetic Diagnostic Testing Methods[edit | edit source]

NGS, If IHC is positive for GCB like DLBCL, FISH and Cytogenetics for MYC, BCL2 or BCL6 gene rearrangement are recommended to rule out double and triple hit lymphoma.Diagnostic testing methods include karyotyping, fluorescent in situ hybridization, RT-PCR and next generation sequencing techniques (whole genome/whole exome sequencing).

Familial Forms[edit | edit source]

Not applicable

Additional Information[edit | edit source]

Not applicable

Links[edit | edit source]

Put a link here or anywhere appropriate in this page (Instructions: Highlight the text to which you want to add a link in this section or elsewhere, select the "Link" icon at the top of the wiki page, and search the name of the internal page to which you want to link this text, or enter an external internet address by including the "http://www." portion.)

References[edit | edit source]

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  1. ↑ Zorofchian, Soheil; et al. (2018-12). "Characterization of genomic alterations in primary central nervous system lymphomas". Journal of Neuro-Oncology. 140 (3): 509–517. doi:10.1007/s11060-018-2990-6. ISSN 1573-7373. PMID 30171453. Check date values in: |date= (help)
  2. ↑ 2.0 2.1 2.2 Chapuy, Bjoern; et al. (2016-02-18). "Targetable genetic features of primary testicular and primary central nervous system lymphomas". Blood. 127 (7): 869–881. doi:10.1182/blood-2015-10-673236. ISSN 1528-0020. PMC 4760091. PMID 26702065.
  3. ↑ 3.0 3.1 Zorofchian, Soheil; et al. (2018-12). "Characterization of genomic alterations in primary central nervous system lymphomas". Journal of Neuro-Oncology. 140 (3): 509–517. doi:10.1007/s11060-018-2990-6. ISSN 1573-7373. PMID 30171453. Check date values in: |date= (help)
  4. ↑ Zorofchian, Soheil; et al. (2018-12). "Characterization of genomic alterations in primary central nervous system lymphomas". Journal of Neuro-Oncology. 140 (3): 509–517. doi:10.1007/s11060-018-2990-6. ISSN 1573-7373. PMID 30171453. Check date values in: |date= (help)
  5. ↑ Montesinos-Rongen, Manuel; et al. (2002-10). "Interphase cytogenetic analysis of lymphoma-associated chromosomal breakpoints in primary diffuse large B-cell lymphomas of the central nervous system". Journal of Neuropathology and Experimental Neurology. 61 (10): 926–933. doi:10.1093/jnen/61.10.926. ISSN 0022-3069. PMID 12387458. Check date values in: |date= (help)
  6. ↑ Cady, Francois M.; et al. (2008-10-10). "Del(6)(q22) and BCL6 rearrangements in primary CNS lymphoma are indicators of an aggressive clinical course". Journal of Clinical Oncology: Official Journal of the American Society of Clinical Oncology. 26 (29): 4814–4819. doi:10.1200/JCO.2008.16.1455. ISSN 1527-7755. PMC 2653136. PMID 18645192.
  7. ↑ Bruno, Aurélie; et al. (2018-07-05). "Identification of novel recurrent ETV6-IgH fusions in primary central nervous system lymphoma". Neuro-Oncology. 20 (8): 1092–1100. doi:10.1093/neuonc/noy019. ISSN 1523-5866. PMC 6280140. PMID 29432597.
  8. ↑ Bruno, Aurélie; et al. (2018-07-05). "Identification of novel recurrent ETV6-IgH fusions in primary central nervous system lymphoma". Neuro-Oncology. 20 (8): 1092–1100. doi:10.1093/neuonc/noy019. ISSN 1523-5866. PMC 6280140. PMID 29432597.
  9. ↑ Chapuy, Bjoern; et al. (2016-02-18). "Targetable genetic features of primary testicular and primary central nervous system lymphomas". Blood. 127 (7): 869–881. doi:10.1182/blood-2015-10-673236. ISSN 1528-0020. PMC 4760091. PMID 26702065.
  10. ↑ Chapuy, Bjoern; et al. (2016-02-18). "Targetable genetic features of primary testicular and primary central nervous system lymphomas". Blood. 127 (7): 869–881. doi:10.1182/blood-2015-10-673236. ISSN 1528-0020. PMC 4760091. PMID 26702065.
  11. ↑ Schwindt, H.; et al. (2009-10). "Chromosomal imbalances and partial uniparental disomies in primary central nervous system lymphoma". Leukemia. 23 (10): 1875–1884. doi:10.1038/leu.2009.120. ISSN 1476-5551. PMID 19494841. Check date values in: |date= (help)
  12. ↑ Schwindt, H.; et al. (2009-10). "Chromosomal imbalances and partial uniparental disomies in primary central nervous system lymphoma". Leukemia. 23 (10): 1875–1884. doi:10.1038/leu.2009.120. ISSN 1476-5551. PMID 19494841. Check date values in: |date= (help)
  13. ↑ Schwindt, H.; et al. (2009-10). "Chromosomal imbalances and partial uniparental disomies in primary central nervous system lymphoma". Leukemia. 23 (10): 1875–1884. doi:10.1038/leu.2009.120. ISSN 1476-5551. PMID 19494841. Check date values in: |date= (help)
  14. ↑ Schwindt, H.; et al. (2009-10). "Chromosomal imbalances and partial uniparental disomies in primary central nervous system lymphoma". Leukemia. 23 (10): 1875–1884. doi:10.1038/leu.2009.120. ISSN 1476-5551. PMID 19494841. Check date values in: |date= (help)
  15. ↑ Schwindt, H.; et al. (2009-10). "Chromosomal imbalances and partial uniparental disomies in primary central nervous system lymphoma". Leukemia. 23 (10): 1875–1884. doi:10.1038/leu.2009.120. ISSN 1476-5551. PMID 19494841. Check date values in: |date= (help)
  16. ↑ Schwindt, H.; et al. (2009-10). "Chromosomal imbalances and partial uniparental disomies in primary central nervous system lymphoma". Leukemia. 23 (10): 1875–1884. doi:10.1038/leu.2009.120. ISSN 1476-5551. PMID 19494841. Check date values in: |date= (help)
  17. ↑ Schwindt, H.; et al. (2009-10). "Chromosomal imbalances and partial uniparental disomies in primary central nervous system lymphoma". Leukemia. 23 (10): 1875–1884. doi:10.1038/leu.2009.120. ISSN 1476-5551. PMID 19494841. Check date values in: |date= (help)
  18. ↑ Schwindt, H.; et al. (2009-10). "Chromosomal imbalances and partial uniparental disomies in primary central nervous system lymphoma". Leukemia. 23 (10): 1875–1884. doi:10.1038/leu.2009.120. ISSN 1476-5551. PMID 19494841. Check date values in: |date= (help)
  19. ↑ Montesinos-Rongen, Manuel; et al. (2011-12). "Activating L265P mutations of the MYD88 gene are common in primary central nervous system lymphoma". Acta Neuropathologica. 122 (6): 791–792. doi:10.1007/s00401-011-0891-2. ISSN 1432-0533. PMID 22020631. Check date values in: |date= (help)
  20. ↑ 20.0 20.1 Nakamura, T.; et al. (2016-04). "Recurrent mutations of CD79B and MYD88 are the hallmark of primary central nervous system lymphomas". Neuropathology and Applied Neurobiology. 42 (3): 279–290. doi:10.1111/nan.12259. ISSN 1365-2990. PMID 26111727. Check date values in: |date= (help)
  21. ↑ Chapuy, Bjoern; et al. (2016-02-18). "Targetable genetic features of primary testicular and primary central nervous system lymphomas". Blood. 127 (7): 869–881. doi:10.1182/blood-2015-10-673236. ISSN 1528-0020. PMC 4760091. PMID 26702065.
  22. ↑ Nakamura, T.; et al. (2016-04). "Recurrent mutations of CD79B and MYD88 are the hallmark of primary central nervous system lymphomas". Neuropathology and Applied Neurobiology. 42 (3): 279–290. doi:10.1111/nan.12259. ISSN 1365-2990. PMID 26111727. Check date values in: |date= (help)
  23. ↑ Deckert, Martina; et al. (2014-02). "Systems biology of primary CNS lymphoma: from genetic aberrations to modeling in mice". Acta Neuropathologica. 127 (2): 175–188. doi:10.1007/s00401-013-1202-x. ISSN 1432-0533. PMID 24240734. Check date values in: |date= (help)
  24. ↑ Deckert, Martina; et al. (2014-02). "Systems biology of primary CNS lymphoma: from genetic aberrations to modeling in mice". Acta Neuropathologica. 127 (2): 175–188. doi:10.1007/s00401-013-1202-x. ISSN 1432-0533. PMID 24240734. Check date values in: |date= (help)
  25. ↑ 25.0 25.1 Chu, Linda C.; et al. (2006-11-15). "Epigenetic silencing of multiple genes in primary CNS lymphoma". International Journal of Cancer. 119 (10): 2487–2491. doi:10.1002/ijc.22124. ISSN 0020-7136. PMID 16858686.
  26. ↑ Ferreri, Andrés J. M.; et al. (2004-09). "Aberrant methylation in the promoter region of the reduced folate carrier gene is a potential mechanism of resistance to methotrexate in primary central nervous system lymphomas". British Journal of Haematology. 126 (5): 657–664. doi:10.1111/j.1365-2141.2004.05109.x. ISSN 0007-1048. PMID 15327516. Check date values in: |date= (help)
  27. ↑ Deckert, Martina; et al. (2014-02). "Systems biology of primary CNS lymphoma: from genetic aberrations to modeling in mice". Acta Neuropathologica. 127 (2): 175–188. doi:10.1007/s00401-013-1202-x. ISSN 1432-0533. PMID 24240734. Check date values in: |date= (help)
  28. ↑ Vater, I.; et al. (2015-03). "The mutational pattern of primary lymphoma of the central nervous system determined by whole-exome sequencing". Leukemia. 29 (3): 677–685. doi:10.1038/leu.2014.264. ISSN 1476-5551. PMID 25189415. Check date values in: |date= (help)


Notes[edit | edit source]

*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.

Prior Author(s):


*Citation of this Page: “Primary large B-cell lymphoma of immune-privileged sites”. Compendium of Cancer Genome Aberrations (CCGA), Cancer Genomics Consortium (CGC), updated 07/3/2025, https://ccga.io/index.php/HAEM5:Primary_large_B-cell_lymphoma_of_immune-privileged_sites.

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