Compendium of Cancer Genome Aberrations

HAEM5:In situ follicular B-cell neoplasm: Difference between revisions

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<blockquote class='blockedit'>{{Box-round|title=Content 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:In Situ Follicular Neoplasia]].
<blockquote class="blockedit">{{Box-round|title=Content 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:In Situ Follicular Neoplasia]].
}}</blockquote>
}}</blockquote>


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Rachel D. Burnside, PhD, MBA, FACMGG
Rachel D. Burnside, PhD, MBA, FACMGG
__TOC__
==WHO Classification of Disease==
==WHO Classification of Disease==


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|}
|}


==Definition / Description of Disease==
==Related Terminology==
 
''In situ'' FL is a proliferation of abnormal B-cells within the germinal center or follicles of secondary lymphoid tissues. The neoplastic cells do not infiltrate beyond the follicular dendritic cell barrier and remain confined to the follicles.
 
==Synonyms / Terminology==
 
Intrafollicular neoplasia, ''in situ'' follicular neoplasia (ISFN), FL ''in situ'' (FLIS), lymphoma-like B-cells of uncertain/undetermined significance, FL B-cells of undetermined significance, ''in situ'' localization of FL, incipient FL, FL of compartmentalized follicular center cells<ref>{{Cite journal|last=Carbone|first=Antonino|last2=Gloghini|first2=Annunziata|date=2014-03|title=Emerging issues after the recognition of in situ follicular lymphoma|url=http://www.tandfonline.com/doi/full/10.3109/10428194.2013.807926|journal=Leukemia & Lymphoma|language=en|volume=55|issue=3|pages=482–490|doi=10.3109/10428194.2013.807926|issn=1042-8194}}</ref>
 
==Epidemiology / Prevalence==
 
The prevalence of in situ FL is unknown but is found in 2-3% of reactive lymph nodes. Fewer than 5% of cases progress to overt FL.<ref>{{Cite journal|last=Tamber|first=Gurdip S|last2=Chévarie‐Davis|first2=Myriam|last3=Warner|first3=Margaret|last4=Séguin|first4=Chantal|last5=Caron|first5=Carole|last6=Michel|first6=René P|date=2021-12|title=In‐situ follicular neoplasia: a clinicopathological spectrum|url=https://onlinelibrary.wiley.com/doi/10.1111/his.14535|journal=Histopathology|language=en|volume=79|issue=6|pages=1072–1086|doi=10.1111/his.14535|issn=0309-0167}}</ref>
 
==Clinical Features==
 
Put your text here and fill in the table <span style="color:#0070C0">(''Instruction: Can include references in the table. Do not delete table.'') </span>
{| class="wikitable"
|'''Signs and Symptoms'''
|<span class="blue-text">EXAMPLE:</span> Asymptomatic (incidental finding on complete blood counts)
 
<span class="blue-text">EXAMPLE:</span> B-symptoms (weight loss, fever, night sweats)
 
<span class="blue-text">EXAMPLE:</span> Fatigue
 
<span class="blue-text">EXAMPLE:</span> Lymphadenopathy (uncommon)
|-
|'''Laboratory Findings'''
|<span class="blue-text">EXAMPLE:</span> Cytopenias
 
<span class="blue-text">EXAMPLE:</span> Lymphocytosis (low level)
|}
 
==Sites of Involvement==
 
Abnormal B-cells are confined to the germinal centers in otherwise reactive lymph nodes and do not infiltrate the interfollucular regions.
 
==Morphologic Features==
 
Morphology is insufficient to diagnose ''in situ'' FL; immunhistochemistry and genetic testing for t(14;18) are necessary. GCs show monotonous morphology and lack tingible body macrophages. By IHC, cells show strong and uniform staining for BCL2 and CD10 and a low Ki67 index.<ref>{{Cite journal|last=Vogelsberg|first=Antonio|last2=Steinhilber|first2=Julia|last3=Mankel|first3=Barbara|last4=Federmann|first4=Birgit|last5=Schmidt|first5=Janine|last6=Montes-Mojarro|first6=Ivonne A.|last7=Hüttl|first7=Katrin|last8=Rodriguez-Pinilla|first8=Maria|last9=Baskaran|first9=Praveen|date=2021|title=Genetic evolution of in situ follicular neoplasia to aggressive B-cell lymphoma of germinal center subtype|url=https://haematologica.org/article/view/9914|journal=Haematologica|language=en|volume=106|issue=10|pages=2673–2681|doi=10.3324/haematol.2020.254854|issn=1592-8721|pmc=PMC8485666|pmid=32855278}}</ref>
 
The following description of ISFN is derived from Jegalian et al<ref>{{Cite journal|url=https://ashpublications.org/blood/article/118/11/2976/28482/Follicular-lymphoma-in-situ-clinical-implications|doi=10.1182/blood-2011-05-355255|pmc=PMC3175777|pmid=21768298}}</ref>:
 
*Unlike early-stage or partial involvement of FL, ''in situ'' FL retains follicular architecture with normal-sized follicles;
*Involved follicles are dispersed throughout the lymph node, as opposed to being clustered together;
*There is an intact cuff with distinct edges to the GC;
*Very strong and uniform expression of BCL2 and CD10 within the follicle;
*Atypical cells are confined to the GC and are almost completely [https://www.sciencedirect.com/topics/immunology-and-microbiology/centrocyte centrocytes] (B-cells which have undergone somatic hypermutation of the B-cell receptor but not yet undergone anitbody affinity maturation)
 
<br />
 
==Immunophenotype==
 
Low Ki67 index
 
{| class="wikitable sortable"
|-
!Finding!!Marker
|-
|Positive (universal)||BCL2+ (strong)
|-
|Positive (universal)||CD10+ (strong)
|-
|Negative (universal)||IGD-
|-
|Negative (universal)||CD3-
|}


==WHO Essential and Desirable Genetic Diagnostic Criteria==
<span style="color:#0070C0">(''Instructions: The table will have the diagnostic criteria from the WHO book <u>autocompleted</u>; remove any <u>non</u>-genetics related criteria. If applicable, add text about other classification'' ''systems that define this entity and specify how the genetics-related criteria differ.'')</span>
{| class="wikitable"
|+
|WHO Essential Criteria (Genetics)*
|
|-
|WHO Desirable Criteria (Genetics)*
|
|-
|Other Classification
|
|}
<nowiki>*</nowiki>Note: These are only the genetic/genomic criteria. Additional diagnostic criteria can be found in the [https://tumourclassification.iarc.who.int/home <u>WHO Classification of Tumours</u>].
==Related Terminology==
<span style="color:#0070C0">(''Instructions: The table will have the related terminology from the WHO <u>autocompleted</u>.)''</span>
{| class="wikitable"
{| class="wikitable"
|+
|+
|Acceptable
|Acceptable
|
|In situ follicular neoplasia
|-
|-
|Not Recommended
|Not Recommended
|
|Follicular lymphoma in situ
|}
|}


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|No
|No
|No
|No
|The translocation results in the juxtaposition of the BCL2 major or minor breakpoint cluster with the VDJ region of IGH during erroneous VDJ recombination<ref>{{Cite journal|url=https://ashpublications.org/blood/article/118/11/2976/28482/Follicular-lymphoma-in-situ-clinical-implications|doi=10.1182/blood-2011-05-355255|pmc=PMC3175777|pmid=21768298}}</ref><ref>{{Cite journal|last=Sotomayor|first=Edgar A.|last2=Shah|first2=Inangati M.|last3=Sanger|first3=Warren G.|last4=Mark|first4=Hon Fong L.|date=2007-10-01|title=In situ follicular lymphoma with a 14;18 translocation diagnosed by a multimodal approach|url=https://www.sciencedirect.com/science/article/pii/S001448000700038X|journal=Experimental and Molecular Pathology|volume=83|issue=2|pages=254–258|doi=10.1016/j.yexmp.2007.03.001|issn=0014-4800}}</ref>
|The translocation results in the juxtaposition of the BCL2 major or minor breakpoint cluster with the VDJ region of IGH during erroneous VDJ recombination<ref name=":1">{{Cite journal|last=Jegalian|first=Armin G.|last2=Eberle|first2=Franziska C.|last3=Pack|first3=Svetlana D.|last4=Mirvis|first4=Mariya|last5=Raffeld|first5=Mark|last6=Pittaluga|first6=Stefania|last7=Jaffe|first7=Elaine S.|date=2011-09-15|title=Follicular lymphoma in situ: clinical implications and comparisons with partial involvement by follicular lymphoma|url=https://pubmed.ncbi.nlm.nih.gov/21768298|journal=Blood|volume=118|issue=11|pages=2976–2984|doi=10.1182/blood-2011-05-355255|issn=1528-0020|pmc=3175777|pmid=21768298}}</ref><ref>{{Cite journal|last=Sotomayor|first=Edgar A.|last2=Shah|first2=Inangati M.|last3=Sanger|first3=Warren G.|last4=Mark|first4=Hon Fong L.|date=2007-10-01|title=In situ follicular lymphoma with a 14;18 translocation diagnosed by a multimodal approach|url=https://www.sciencedirect.com/science/article/pii/S001448000700038X|journal=Experimental and Molecular Pathology|volume=83|issue=2|pages=254–258|doi=10.1016/j.yexmp.2007.03.001|issn=0014-4800}}</ref>
|}
|}


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{| class="wikitable sortable"
{| class="wikitable sortable"
|-
|-
!Chr #!!'''Gain, Loss, Amp, LOH'''!!'''Minimal Region Cytoband and/or Genomic Coordinates [Genome Build; Size]'''!!'''Relevant Gene(s)'''
!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'''
!Diagnostic, Prognostic, and Therapeutic Significance - D, P, T
!'''Established Clinical Significance Per Guidelines - Yes or No (Source)'''
!Established Clinical Significance Per Guidelines - Yes or No (Source)
!'''Clinical Relevance Details/Other Notes'''
!Clinical Relevance Details/Other Notes
|-
|-
|<span class="blue-text">EXAMPLE:</span>
|<span class="blue-text">EXAMPLE:</span>
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!Chromosomal Pattern
!Chromosomal Pattern
!Molecular Pathogenesis
!Molecular Pathogenesis
!'''Prevalence -'''
!Prevalence -  
'''Common >20%, Recurrent 5-20% or Rare <5% (Disease)'''
Common >20%, Recurrent 5-20% or Rare <5% (Disease)
!'''Diagnostic, Prognostic, and Therapeutic Significance - D, P, T'''
!Diagnostic, Prognostic, and Therapeutic Significance - D, P, T
!'''Established Clinical Significance Per Guidelines - Yes or No (Source)'''
!Established Clinical Significance Per Guidelines - Yes or No (Source)
!'''Clinical Relevance Details/Other Notes'''
!Clinical Relevance Details/Other Notes
|-
|-
|<span class="blue-text">EXAMPLE:</span>
|<span class="blue-text">EXAMPLE:</span>
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|}
|}
==Gene Mutations (SNV/INDEL)==
==Gene Mutations (SNV/INDEL)==
Put your text here and fill in the table <span style="color:#0070C0">(''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.'') </span>
{| class="wikitable sortable"
|-
!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
|-
|<span class="blue-text">EXAMPLE:</span>''EGFR''
<br />
|<span class="blue-text">EXAMPLE:</span> Exon 18-21 activating mutations
|<span class="blue-text">EXAMPLE:</span> Oncogene
|<span class="blue-text">EXAMPLE:</span> Common (lung cancer)
|<span class="blue-text">EXAMPLE:</span> T
|<span class="blue-text">EXAMPLE:</span> Yes (NCCN)
|<span class="blue-text">EXAMPLE:</span> 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).
|-
|<span class="blue-text">EXAMPLE:</span> ''TP53''; Variable LOF mutations
<br />
|<span class="blue-text">EXAMPLE:</span> Variable LOF mutations
|<span class="blue-text">EXAMPLE:</span> Tumor Supressor Gene
|<span class="blue-text">EXAMPLE:</span> Common (breast cancer)
|<span class="blue-text">EXAMPLE:</span> P
|
|<span class="blue-text">EXAMPLE:</span> >90% are somatic; rare germline alterations associated with Li-Fraumeni syndrome (add reference). Denotes a poor prognosis in breast cancer.
|-
|<span class="blue-text">EXAMPLE:</span> ''BRAF''; Activating mutations
|<span class="blue-text">EXAMPLE:</span> Activating mutations
|<span class="blue-text">EXAMPLE:</span> Oncogene
|<span class="blue-text">EXAMPLE:</span> Common (melanoma)
|<span class="blue-text">EXAMPLE:</span> T
|
|
|-
|
|
|
|
|
|
|
|}Note: A more extensive list of mutations can be found in [https://www.cbioportal.org/ <u>cBioportal</u>], [https://cancer.sanger.ac.uk/cosmic <u>COSMIC</u>], and/or other databases. When applicable, gene-specific pages within the CCGA site directly link to pertinent external content.


Put your text here and fill in the table
Put your text here and fill in the table
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{| class="wikitable sortable"
{| class="wikitable sortable"
|-
|-
!Gene; Genetic Alteration!!'''Presumed Mechanism (Tumor Suppressor Gene [TSG] / Oncogene / Other)'''!!'''Prevalence (COSMIC /  TCGA / Other)'''!!'''Concomitant Mutations'''!!'''Mutually Exclusive Mutations'''
!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)'''
!Diagnostic Significance (Yes, No or Unknown)
!Prognostic Significance (Yes, No or Unknown)
!Prognostic Significance (Yes, No or Unknown)
!Therapeutic Significance (Yes, No or Unknown)
!Therapeutic Significance (Yes, No or Unknown)
!Notes
!Notes
|-
|-
|'''''CREBBP''''' inactivating missense variants (various); mutation hotspots in exons 24-28 and exon 30.
|''CREBBP'' inactivating missense variants (various); mutation hotspots in exons 24-28 and exon 30.
|TSG
|TSG
|32.6%<ref name=":0">{{Cite journal|last=Pasqualucci|first=Laura|last2=Dominguez-Sola|first2=David|last3=Chiarenza|first3=Annalisa|last4=Fabbri|first4=Giulia|last5=Grunn|first5=Adina|last6=Trifonov|first6=Vladimir|last7=Kasper|first7=Lawryn H.|last8=Lerach|first8=Stephanie|last9=Tang|first9=Hongyan|date=2011-03|title=Inactivating mutations of acetyltransferase genes in B-cell lymphoma|url=https://www.nature.com/articles/nature09730|journal=Nature|language=en|volume=471|issue=7337|pages=189–195|doi=10.1038/nature09730|issn=1476-4687}}</ref>
|32.6%<ref name=":0">{{Cite journal|last=Pasqualucci|first=Laura|last2=Dominguez-Sola|first2=David|last3=Chiarenza|first3=Annalisa|last4=Fabbri|first4=Giulia|last5=Grunn|first5=Adina|last6=Trifonov|first6=Vladimir|last7=Kasper|first7=Lawryn H.|last8=Lerach|first8=Stephanie|last9=Tang|first9=Hongyan|date=2011-03|title=Inactivating mutations of acetyltransferase genes in B-cell lymphoma|url=https://www.nature.com/articles/nature09730|journal=Nature|language=en|volume=471|issue=7337|pages=189–195|doi=10.1038/nature09730|issn=1476-4687}}</ref>
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|
|
|
|
|Inactivating mutations prevent acetylation of the protein and creates an environment permissive for accumulation of mutations<ref>{{Cite journal|last=Schmidt|first=Janine|last2=Ramis-Zaldivar|first2=Joan Enric|last3=Bonzheim|first3=Irina|last4=Steinhilber|first4=Julia|last5=Müller|first5=Inga|last6=Haake|first6=Andrea|last7=Yu|first7=Shan Chi|last8=Raffeld|first8=Mark|last9=Fend|first9=Falko|date=2018-12-20|title=CREBBP gene mutations are frequently detected in in situ follicular neoplasia|url=https://www.sciencedirect.com/science/article/pii/S0006497120429210|journal=Blood|volume=132|issue=25|pages=2687–2690|doi=10.1182/blood-2018-03-837039|issn=0006-4971}}</ref>. Mutations in ''CREBBP'' are thought to be early driver mutations and possibly necessary for transformation to FL, as they have been found in ISFN and paired FL samples<ref>{{Cite journal|last=Schmidt|first=Janine|last2=Ramis-Zaldivar|first2=Joan Enric|last3=Bonzheim|first3=Irina|last4=Steinhilber|first4=Julia|last5=Müller|first5=Inga|last6=Haake|first6=Andrea|last7=Yu|first7=Shan Chi|last8=Raffeld|first8=Mark|last9=Fend|first9=Falko|date=2018-12-20|title=CREBBP gene mutations are frequently detected in in situ follicular neoplasia|url=https://www.sciencedirect.com/science/article/pii/S0006497120429210|journal=Blood|volume=132|issue=25|pages=2687–2690|doi=10.1182/blood-2018-03-837039|issn=0006-4971}}</ref>.
|Inactivating mutations prevent acetylation of the protein and creates an environment permissive for accumulation of mutations<ref name=":2">{{Cite journal|last=Schmidt|first=Janine|last2=Ramis-Zaldivar|first2=Joan Enric|last3=Bonzheim|first3=Irina|last4=Steinhilber|first4=Julia|last5=Müller|first5=Inga|last6=Haake|first6=Andrea|last7=Yu|first7=Shan Chi|last8=Raffeld|first8=Mark|last9=Fend|first9=Falko|date=2018-12-20|title=CREBBP gene mutations are frequently detected in in situ follicular neoplasia|url=https://pubmed.ncbi.nlm.nih.gov/30401710|journal=Blood|volume=132|issue=25|pages=2687–2690|doi=10.1182/blood-2018-03-837039|issn=1528-0020|pmc=6302496|pmid=30401710}}</ref>. Mutations in ''CREBBP'' are thought to be early driver mutations and possibly necessary for transformation to FL, as they have been found in ISFN and paired FL samples<ref name=":2" />.
<br />
<br />
|-
|-
|'''''EZH2'''''
|''EZH2''
p.Y646, p.A682G, p.A692V
p.Y646, p.A682G, p.A692V
Gain of function variants. Y646 may have multiple amino acid replacements
Gain of function variants. Y646 may have multiple amino acid replacements
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==Additional Information==
==Additional Information==


Put your text here
This disease is <u>defined/characterized</u> as detailed below:
 
* ''In situ'' FL is a proliferation of abnormal B-cells within the germinal center or follicles of secondary lymphoid tissues. The neoplastic cells do not infiltrate beyond the follicular dendritic cell barrier and remain confined to the follicles.<ref>{{Cite journal|last=Carbone|first=Antonino|last2=Gloghini|first2=Annunziata|date=2014-03|title=Emerging issues after the recognition of in situ follicular lymphoma|url=http://www.tandfonline.com/doi/full/10.3109/10428194.2013.807926|journal=Leukemia & Lymphoma|language=en|volume=55|issue=3|pages=482–490|doi=10.3109/10428194.2013.807926|issn=1042-8194}}</ref>
 
The <u>epidemiology/prevalence</u> of this disease is detailed below:
 
* The prevalence of in situ FL is unknown but is found in 2-3% of reactive lymph nodes. Fewer than 5% of cases progress to overt FL.<ref>{{Cite journal|last=Tamber|first=Gurdip S|last2=Chévarie‐Davis|first2=Myriam|last3=Warner|first3=Margaret|last4=Séguin|first4=Chantal|last5=Caron|first5=Carole|last6=Michel|first6=René P|date=2021-12|title=In‐situ follicular neoplasia: a clinicopathological spectrum|url=https://onlinelibrary.wiley.com/doi/10.1111/his.14535|journal=Histopathology|language=en|volume=79|issue=6|pages=1072–1086|doi=10.1111/his.14535|issn=0309-0167}}</ref>
 
The <u>sites of involvement</u> of this disease are detailed below:
 
* Abnormal B-cells are confined to the germinal centers in otherwise reactive lymph nodes and do not infiltrate the interfollucular regions.
 
The <u>morphologic features</u> of this disease are detailed below:
 
* Morphology is insufficient to diagnose ''in situ'' FL; immunhistochemistry and genetic testing for t(14;18) are necessary. GCs show monotonous morphology and lack tingible body macrophages. By IHC, cells show strong and uniform staining for BCL2 and CD10 and a low Ki67 index.<ref>{{Cite journal|last=Vogelsberg|first=Antonio|last2=Steinhilber|first2=Julia|last3=Mankel|first3=Barbara|last4=Federmann|first4=Birgit|last5=Schmidt|first5=Janine|last6=Montes-Mojarro|first6=Ivonne A.|last7=Hüttl|first7=Katrin|last8=Rodriguez-Pinilla|first8=Maria|last9=Baskaran|first9=Praveen|date=2021|title=Genetic evolution of in situ follicular neoplasia to aggressive B-cell lymphoma of germinal center subtype|url=https://haematologica.org/article/view/9914|journal=Haematologica|language=en|volume=106|issue=10|pages=2673–2681|doi=10.3324/haematol.2020.254854|issn=1592-8721|pmc=PMC8485666|pmid=32855278}}</ref>
* The following description of ISFN is derived from Jegalian et al<ref name=":1" />:
**Unlike early-stage or partial involvement of FL, ''in situ'' FL retains follicular architecture with normal-sized follicles;
**Involved follicles are dispersed throughout the lymph node, as opposed to being clustered together;
**There is an intact cuff with distinct edges to the GC;
**Very strong and uniform expression of BCL2 and CD10 within the follicle;
**Atypical cells are confined to the GC and are almost completely [https://www.sciencedirect.com/topics/immunology-and-microbiology/centrocyte centrocytes] (B-cells which have undergone somatic hypermutation of the B-cell receptor but not yet undergone anitbody affinity maturation)
 
The <u>immunophenotype</u> of this disease is detailed below:
 
* Low Ki67 index
 
* Positive (universal) - BCL2+ (strong), CD10+ (strong)
 
* Negative (universal) - IGD-, CD3-


==Links==
==Links==
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<nowiki>*</nowiki>''Citation of this Page'': “In situ follicular B-cell neoplasm”. Compendium of Cancer Genome Aberrations (CCGA), Cancer Genomics Consortium (CGC), updated {{REVISIONMONTH}}/{{REVISIONDAY}}/{{REVISIONYEAR}}, <nowiki>https://ccga.io/index.php/HAEM5:In_situ_follicular_B-cell_neoplasm</nowiki>.
<nowiki>*</nowiki>''Citation of this Page'': “In situ follicular B-cell neoplasm”. Compendium of Cancer Genome Aberrations (CCGA), Cancer Genomics Consortium (CGC), updated {{REVISIONMONTH}}/{{REVISIONDAY}}/{{REVISIONYEAR}}, <nowiki>https://ccga.io/index.php/HAEM5:In_situ_follicular_B-cell_neoplasm</nowiki>.
[[Category:HAEM5]][[Category:DISEASE]][[Category:Diseases I]]
[[Category:HAEM5]]
[[Category:DISEASE]]
[[Category:Diseases I]]
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