Splenic marginal zone lymphoma

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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:Splenic Marginal Zone Lymphoma.

(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)*

  • Snehal Patel, MD, PhD

WHO Classification of Disease

Structure Disease
Book Haematolymphoid Tumours (5th ed.)
Category B-cell lymphoid proliferations and lymphomas
Family Mature B-cell neoplasms
Type Splenic B-cell lymphomas and leukaemias
Subtype(s) Splenic marginal zone lymphoma

WHO Essential and Desirable Genetic Diagnostic Criteria

(Instructions: The table will have the diagnostic criteria from the WHO book autocompleted; remove any non-genetics related criteria. If applicable, add text about other classification systems that define this entity and specify how the genetics-related criteria differ.)

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

(Instructions: The table will have the related terminology from the WHO autocompleted.)

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


Other fusion partners include KIF5B, NPM1, STRN, TFG, TPM3, CLTC, KLC1

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
editv4:Chromosomal Rearrangements (Gene Fusions)
The content below was from the old template. Please incorporate above.
  • Rare but (some) recurrent translocations/gene fusions:
    • t(8;14)(q24;q32)/IGH-MYC[1][2]
    • KMT2A fusion in large cell transformation of SMZL[3]
    • t(2;7)(p11.2;q21.2/IGK-CDK6[4][5]
      • Also reported in CD5-negative monoclonal B-cell lymphocytosis[6]
    • t(14;18)(q32;q21)/IGH-BCL2[7]
    • t(5;7)(p15.33;p11)/TERT fusion[8]
    • t(9;14)(p13;q32)/IGH-PAX5[9][10][11]
End of V4 Section


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)
Alteration Clinical Significance Note
BRAF mutations Diagnostic (exclusion) Present in hairy cell leukemia (HCL) and absent in SMZL[12]
MYD88 mutations Diagnostic (exclusion) Present in lymphoplasmacytic lymphoma (LPL) and rare but not absent in SMZL
t(11;14)(q13;q32)/IGH-CCND1* Diagnostic (exclusion) Present in mantle cell lymphoma (MCL) and absent in SMZL
t(14;18)(q32;q21)/IGH-BCL2 Diagnostic (exclusion) Present in follicular lymphoma (FL) and rare but not absent in SMZL[7]
t(11;18)(q21;q21)/BIRC3-MALT1 Diagnostic (exclusion) Present in MALT lymphoma and absent in SMZL
t(14;18)(q32;q21)/IGH-MALT1 Diagnostic (exclusion) Present in MALT lymphoma and absent in SMZL[13]
t(1;14)(p22;q32)/IGH-BCL10 Diagnostic (exclusion) Present in MALT lymphoma and absent in SMZL

*Cases previously reported as SMZL with IGH-CCND1 fusion should now be classified as MCL

End of V4 Section

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.

editv4:Genomic Gain/Loss/LOH
The content below was from the old template. Please incorporate above.
Chromosome Number Gain/Loss/Amp/LOH Significance Prevalence
7q31-32 Loss (heterozygous) Unknown; possible haploinsufficiency of IRF5 tumor suppressor[14] 26–45%[15][16][17]
3/3q Gain (trisomy) Unknown 15%[15][17][16]
End of V4 Section

Characteristic Chromosomal or Other Global Mutational Patterns

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.
  • Ig gene rearrangements
End of V4 Section

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.

editv4:Gene Mutations (SNV/INDEL)
The content below was from the old template. Please incorporate above.
Gene* Oncogene/Tumor Suppressor/Other Presumed Mechanism (LOF/GOF/Other) Prevalence (COSMIC)
NOTCH2 Oncogene or Tumor Suppressor[18] Other 21%
MYD88 Oncogene GOF 7%
KLF2 Likely tumor suppressor in most contexts[19] LOF 20%[20]
TNFAIP3 Tumor Suppressor LOF 8%
TP53 Tumor Suppressor LOF 7%
BIRC3 Oncogene or Tumor Suppressor[21] Other 5%
CARD11 Oncogene GOF 4%
IKBKB Oncogene GOF 4%
SPEN Tumor Suppressor LOF 6%
NOTCH1 Oncogene or Tumor Suppressor[18] Other 11%
TBL1XR1 Oncogene or Tumor Suppressor[22] Other 7%
NFKBIE Tumor Suppressor LOF 2%

*Specific mutations in these genes may be found in cBioPortal or COSMIC.

End of V4 Section

Epigenomic Alterations

  • Epigenetic dysregulation expected on basis of genetic alterations in histone modifying and chromatin remodeling factors:
    • TBL1XR1 is a member of nuclear receptor corepressor (N-CoR) and histone deacetylase 3 (HDAC3) complexes
    • CREBBP is a histone acetyltransferase
    • ARID1A is a member of SWI-SNF complexes
    • EP300 is a histone acetyltransferase
    • DNMT3A is a DNA methyltransferase
  • Promoter methylation and gene expression study revealed two clusters of SMZL[23]
    • high methylation group compared to low methylation group showed
      • Methylated/repressed tumor suppressor genes and unmethylated/overexpressed prosurvival genes
      • Association with NOTCH2 mutations, 7q31-32 loss, and histologic transformation
      • Reduced overall survival
      • Reduced proliferation and reversion of phenotype in response to demethylating agents in vitro

Genes and Main Pathways Involved

Put your text here and fill in the table (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.
Molecular Feature Pathway Pathophysiologic outcome
NOTCH2, NOTCH1, DTX, and SPEN mutations NOTCH signaling[24] Increased proliferation and survival
MYD88, TNFAIP3, BIRC3, CARD11, IKBKB, NFKBIE, and TRAF3 mutations NF-κB signaling[25][26][27] Lymphocyte development
TP53 mutations TP53 pathway Dysregulation of genomic stability and apoptosis
TBL1XR1, CREBBP, ARID1A, EP300, and DNMT3A mutations Histone modification and chromatin remodeling[24] Abnormal gene expression program
End of V4 Section

Genetic Diagnostic Testing Methods

  • Clinical, morphologic, and immunophenotypic findings and exclusion of other low-grade B-cell lymphomas are generally sufficient for diagnosis
  • No established specific diagnostic test currently exists
  • Molecular testing may help exclude other entities in some cases (see below)

Familial Forms

  • None

Additional Information

  • None

Links

References

(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. Shi, Xiaofeng; et al. (2018). "A rare case of B-lymphoproliferative disorder with villous lymphocytes harboring t(8;14)(q24;q32) translocation". Frontiers of Medicine. 12 (3): 324–329. doi:10.1007/s11684-017-0558-z. ISSN 2095-0217.
  2. Scapinello, Greta; et al. (2018). "Splenic marginal zone lymphoma with a de novo t(8;14)(q24;q32) and a prolymphocytoid evolution responsive to rituximab-bendamustine". Annals of Hematology. 97 (10): 2001–2003. doi:10.1007/s00277-018-3351-4. ISSN 0939-5555.
  3. Gindin, Tatyana; et al. (2015). "MLL / KMT2A translocations in diffuse large B-cell lymphomas: MLL / KMT2A translocations in diffuse large B-cell lymphomas". Hematological Oncology. 33 (4): 239–246. doi:10.1002/hon.2158.
  4. Remstein, E D; et al. (2008). "The prevalence of IG translocations and 7q32 deletions in splenic marginal zone lymphoma". Leukemia. 22 (6): 1268–1272. doi:10.1038/sj.leu.2405027. ISSN 0887-6924.
  5. Corcoran, M M; et al. (1999). "Dysregulation of cyclin dependent kinase 6 expression in splenic marginal zone lymphoma through chromosome 7q translocations". Oncogene. 18 (46): 6271–6277. doi:10.1038/sj.onc.1203033. ISSN 0950-9232.
  6. Parker, Edward; et al. (2011). "Molecular characterization of a t(2;7) translocation linking CDK6 to the IGK locus in CD5− monoclonal B-cell lymphocytosis". Cancer Genetics. 204 (5): 260–264. doi:10.1016/j.cancergen.2011.03.004.
  7. 7.0 7.1 Baseggio, Lucile; et al. (2012). "In non-follicular lymphoproliferative disorders, IGH/BCL2-fusion is not restricted to chronic lymphocytic leukaemia". British Journal of Haematology. 158 (4): 489–498. doi:10.1111/j.1365-2141.2012.09178.x.
  8. Nagel, Inga; et al. (2010). "Deregulation of the telomerase reverse transcriptase (TERT) gene by chromosomal translocations in B-cell malignancies". Blood. 116 (8): 1317–1320. doi:10.1182/blood-2009-09-240440. ISSN 0006-4971.
  9. Kelly, Richard J.; et al. (2007). "The t(9;14)(p13;q32) is a recurrent but rare abnormality in splenic marginal zone lymphoma". Leukemia & Lymphoma. 48 (8): 1636–1637. doi:10.1080/10428190701474415. ISSN 1042-8194.
  10. Sole, F.; et al. (2006). "Translocation t(9;14)(p13;q32) in cases of splenic marginal zone lymphoma". Haematologica. 91 (9): 1289–1291. ISSN 0390-6078. PMID 16956840.
  11. K, Kawakami; et al. (1998). "A Case of Primary Splenic Large Cell Lymphoma With a t(9;14)(p13;q32)". PMID 9631587.
  12. Naseem, Shano; et al. (2020). "BRAF V600E mutation detection in hairy cell leukemia-utility of archival DNA from bone marrow aspirate/imprint smear and amplification refractory mutation system". Molecular Biology Reports. doi:10.1007/s11033-020-05509-0. ISSN 0301-4851.
  13. Streubel, Berthold; et al. (2003). "T(14;18)(q32;q21) involving IGH andMALT1 is a frequent chromosomal aberration in MALT lymphoma". Blood. 101 (6): 2335–2339. doi:10.1182/blood-2002-09-2963. ISSN 1528-0020.
  14. Fresquet, Vicente; et al. (2012). "High-throughput sequencing analysis of the chromosome 7q32 deletion reveals IRF5 as a potential tumour suppressor in splenic marginal-zone lymphoma". British Journal of Haematology. 158 (6): 712–726. doi:10.1111/j.1365-2141.2012.09226.x.
  15. 15.0 15.1 Salido, Marta; et al. (2010). "Cytogenetic aberrations and their prognostic value in a series of 330 splenic marginal zone B-cell lymphomas: a multicenter study of the Splenic B-Cell Lymphoma Group". Blood. 116 (9): 1479–1488. doi:10.1182/blood-2010-02-267476. ISSN 0006-4971.
  16. 16.0 16.1 Baró, Cristina; et al. (2008). "New chromosomal alterations in a series of 23 splenic marginal zone lymphoma patients revealed by Spectral Karyotyping (SKY)". Leukemia Research. 32 (5): 727–736. doi:10.1016/j.leukres.2007.09.012.
  17. 17.0 17.1 Gruszka-Westwood, Alicja M.; et al. (2003). "Deletion mapping on the long arm of chromosome 7 in splenic lymphoma with villous lymphocytes". Genes, Chromosomes and Cancer. 36 (1): 57–69. doi:10.1002/gcc.10142. ISSN 1045-2257.
  18. 18.0 18.1 Lobry, Camille; et al. (2011). "Oncogenic and tumor suppressor functions of Notch in cancer: it's NOTCH what you think". The Journal of Experimental Medicine. 208 (10): 1931–1935. doi:10.1084/jem.20111855. ISSN 1540-9538. PMC 3182047. PMID 21948802.CS1 maint: PMC format (link)
  19. Wang, Chunmei; et al. (2017). "Krüppel-like factor 2 suppresses human gastric tumorigenesis through inhibiting PTEN/AKT signaling". Oncotarget. 8 (59): 100358–100370. doi:10.18632/oncotarget.22229. ISSN 1949-2553. PMC 5725026. PMID 29245984.CS1 maint: PMC format (link)
  20. Jaramillo Oquendo, Carolina; et al. (2019). "Systematic Review of Somatic Mutations in Splenic Marginal Zone Lymphoma". Scientific Reports. 9 (1). doi:10.1038/s41598-019-46906-1. ISSN 2045-2322. PMC 6639539. PMID 31320741.CS1 maint: PMC format (link)
  21. Yamato, Azusa; et al. (2015). "Oncogenic activity of BIRC2 and BIRC3 mutants independent of nuclear factor-κB-activating potential". Cancer Science. 106 (9): 1137–1142. doi:10.1111/cas.12726. PMC 4582982. PMID 26094954.CS1 maint: PMC format (link)
  22. Cao, Qinghua; et al. (2018). "TBL1XR1 promotes migration and invasion in osteosarcoma cells and is negatively regulated by miR-186-5p". American Journal of Cancer Research. 8 (12): 2481–2493. ISSN 2156-6976. PMC 6325474. PMID 30662805.
  23. Arribas, Alberto J.; et al. (2015). "DNA methylation profiling identifies two splenic marginal zone lymphoma subgroups with different clinical and genetic features". Blood. 125 (12): 1922–1931. doi:10.1182/blood-2014-08-596247. ISSN 0006-4971. PMC 4416938. PMID 25612624.CS1 maint: PMC format (link)
  24. 24.0 24.1 Rossi, Davide; et al. (2012). "The coding genome of splenic marginal zone lymphoma: activation of NOTCH2 and other pathways regulating marginal zone development". The Journal of Experimental Medicine. 209 (9): 1537–1551. doi:10.1084/jem.20120904. ISSN 1540-9538. PMC 3428941. PMID 22891273.CS1 maint: PMC format (link)
  25. Spina, Valeria; et al. (2016). "NF-κB deregulation in splenic marginal zone lymphoma". Seminars in Cancer Biology. 39: 61–67. doi:10.1016/j.semcancer.2016.08.002.
  26. Yan, Q.; et al. (2012). "BCR and TLR signaling pathways are recurrently targeted by genetic changes in splenic marginal zone lymphomas". Haematologica. 97 (4): 595–598. doi:10.3324/haematol.2011.054080. ISSN 0390-6078. PMC 3347666. PMID 22102703.CS1 maint: PMC format (link)
  27. Rossi, Davide; et al. (2011). "Alteration of BIRC3 and multiple other NF-κB pathway genes in splenic marginal zone lymphoma". Blood. 118 (18): 4930–4934. doi:10.1182/blood-2011-06-359166. ISSN 0006-4971.


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 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: “Splenic marginal zone lymphoma”. Compendium of Cancer Genome Aberrations (CCGA), Cancer Genomics Consortium (CGC), updated 02/11/2025, https://ccga.io/index.php/HAEM5:Splenic_marginal_zone_lymphoma.