@@ Line 1: / Line 1: @@
-{{DISPLAYTITLE:B lymphoblastic leukaemia/lymphoma with TCF3::PBX1 fusion}}
+{{DISPLAYTITLE:B lymphoblastic leukaemia/lymphoma with TCF3::PBX1 fusion}}[[HAEM5:Table_of_Contents|Haematolymphoid Tumours (WHO Classification, 5th ed.)]]
-[[HAEM5:Table_of_Contents|Haematolymphoid Tumours (WHO Classification, 5th ed.)]]
-{{Under Construction}}
-<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:B-Lymphoblastic Leukemia/Lymphoma with t(1;19)(q23;p13.3); TCF3-PBX1]].
-}}</blockquote>
-<span style="color:#0070C0">(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 [https://www.genenames.org/ <u>HUGO-approved gene names and symbols</u>] (italicized when appropriate), [https://varnomen.hgvs.org/ <u>HGVS-based nomenclature for variants</u>], 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 </span><u>[[Author_Instructions]]</u><span style="color:#0070C0"> and [[Frequently Asked Questions (FAQs)|<u>FAQs</u>]] as well as contact your [[Leadership|<u>Associate Editor</u>]] or [mailto:CCGA@cancergenomics.org <u>Technical Support</u>].)</span>
 ==Primary Author(s)*==
@@ Line 37: / Line 28: @@
 {| class="wikitable"
-|+
 |Acceptable
 |N/A
@@ Line 47: / Line 37: @@
 ==Gene Rearrangements==
-Put your text here and fill in the table <span style="color:#0070C0">(''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.'')</span>
 {| class="wikitable sortable"
 |-
@@ Line 58: / Line 46: @@
 |-
 |''TCF3::PBX1'' fusion protein||''TCF3::PBX1''||The ''TCF3''::''PBX1'' fusion results in the production of a fusion protein that has an oncogenic role as a transcriptional activator; it also probably interferes with the normal function of the transcription factors encoded by ''TCF3'' and ''PBX1''<ref>{{Cite journal|last=LeBrun|first=David P.|date=2003-05-01|title=E2A basic helix-loop-helix transcription factors in human leukemia|url=https://pubmed.ncbi.nlm.nih.gov/12700034|journal=Frontiers in Bioscience: A Journal and Virtual Library|volume=8|pages=s206–222|doi=10.2741/1030|issn=1093-9946|pmid=12700034}}</ref>. Oligomerization and/or direct interaction with HOX proteins through the PBX1 moiety may play a role in ''TCF3-PBX1'' leukemogenesis<ref>{{Cite journal|last=Lin|first=Chiou-Hong|last2=Wang|first2=Zhong|last3=Duque-Afonso|first3=Jesús|last4=Wong|first4=Stephen Hon-Kit|last5=Demeter|first5=Janos|last6=Loktev|first6=Alexander V.|last7=Somervaille|first7=Tim C. P.|last8=Jackson|first8=Peter K.|last9=Cleary|first9=Michael L.|date=2019-03-20|title=Oligomeric self-association contributes to E2A-PBX1-mediated oncogenesis|url=https://pubmed.ncbi.nlm.nih.gov/30894657|journal=Scientific Reports|volume=9|issue=1|pages=4915|doi=10.1038/s41598-019-41393-w|issn=2045-2322|pmc=6426973|pmid=30894657}}</ref>.||t(1;19)(q23;q13.3)
-|Common
+|Ubiquitous
 |D: Requires demonstration of ''TCF3''::''PBX1'' rearrangement
 P: Associated with intermediate to relatively favorable clinical outcomes<ref>{{Cite journal|last=Burmeister|first=Thomas|last2=Gökbuget|first2=Nicola|last3=Schwartz|first3=Stefan|last4=Fischer|first4=Lars|last5=Hubert|first5=Daniela|last6=Sindram|first6=Annette|last7=Hoelzer|first7=Dieter|last8=Thiel|first8=Eckhard|date=2010-02|title=Clinical features and prognostic implications of TCF3-PBX1 and ETV6-RUNX1 in adult acute lymphoblastic leukemia|url=https://pubmed.ncbi.nlm.nih.gov/19713226|journal=Haematologica|volume=95|issue=2|pages=241–246|doi=10.3324/haematol.2009.011346|issn=1592-8721|pmc=2817026|pmid=19713226}}</ref><ref>{{Cite journal|last=Felice|first=María S.|last2=Gallego|first2=Marta S.|last3=Alonso|first3=Cristina N.|last4=Alfaro|first4=Elizabeth M.|last5=Guitter|first5=Myriam R.|last6=Bernasconi|first6=Andrea R.|last7=Rubio|first7=Patricia L.|last8=Zubizarreta|first8=Pedro A.|last9=Rossi|first9=Jorge G.|date=2011-07|title=Prognostic impact of t(1;19)/ TCF3-PBX1 in childhood acute lymphoblastic leukemia in the context of Berlin-Frankfurt-Münster-based protocols|url=https://pubmed.ncbi.nlm.nih.gov/21534874|journal=Leukemia & Lymphoma|volume=52|issue=7|pages=1215–1221|doi=10.3109/10428194.2011.565436|issn=1029-2403|pmid=21534874}}</ref><ref>{{Cite journal|last=Lin|first=Anna|last2=Cheng|first2=Frankie W. T.|last3=Chiang|first3=Alan K. S.|last4=Luk|first4=Chung-Wing|last5=Li|first5=Rever C. H.|last6=Ling|first6=Alvin S. C.|last7=Cheuk|first7=Daniel K. L.|last8=Chang|first8=Kai-On|last9=Ku|first9=Dennis|date=2018-12|title=Excellent outcome of acute lymphoblastic leukaemia with TCF3-PBX1 rearrangement in Hong Kong|url=https://pubmed.ncbi.nlm.nih.gov/30051646|journal=Pediatric Blood & Cancer|volume=65|issue=12|pages=e27346|doi=10.1002/pbc.27346|issn=1545-5017|pmid=30051646}}</ref><ref>{{Cite journal|last=Yilmaz|first=Musa|last2=Kantarjian|first2=Hagop M.|last3=Toruner|first3=Gokce|last4=Yin|first4=C. Cameron|last5=Kanagal-Shamanna|first5=Rashmi|last6=Cortes|first6=Jorge E.|last7=Issa|first7=Ghayyas|last8=Short|first8=Nicholas J.|last9=Khoury|first9=Joseph D.|date=2021-01|title=Translocation t(1;19)(q23;p13) in adult acute lymphoblastic leukemia - a distinct subtype with favorable prognosis|url=https://pubmed.ncbi.nlm.nih.gov/32955970|journal=Leukemia & Lymphoma|volume=62|issue=1|pages=224–228|doi=10.1080/10428194.2020.1824071|issn=1029-2403|pmc=11648456|pmid=32955970}}</ref>. 5-year event-free survival (80-88.2%)<ref>{{Cite journal|last=Jeha|first=Sima|last2=Choi|first2=John|last3=Roberts|first3=Kathryn G.|last4=Pei|first4=Deqing|last5=Coustan-Smith|first5=Elaine|last6=Inaba|first6=Hiroto|last7=Rubnitz|first7=Jeffrey E.|last8=Ribeiro|first8=Raul C.|last9=Gruber|first9=Tanja A.|date=2021-07|title=Clinical significance of novel subtypes of acute lymphoblastic leukemia in the context of minimal residual disease-directed therapy|url=https://pubmed.ncbi.nlm.nih.gov/34250504|journal=Blood Cancer Discovery|volume=2|issue=4|pages=326–337|doi=10.1158/2643-3230.bcd-20-0229|issn=2643-3249|pmc=8265990|pmid=34250504}}</ref>.
@@ Line 65: / Line 53: @@
 |No (NCCN)
 |There may be an increased relative risk of CNS relapse in these patients<ref>{{Cite journal|last=Jeha|first=S.|last2=Pei|first2=D.|last3=Raimondi|first3=S. C.|last4=Onciu|first4=M.|last5=Campana|first5=D.|last6=Cheng|first6=C.|last7=Sandlund|first7=J. T.|last8=Ribeiro|first8=R. C.|last9=Rubnitz|first9=J. E.|date=2009-08|title=Increased risk for CNS relapse in pre-B cell leukemia with the t(1;19)/TCF3-PBX1|url=https://pubmed.ncbi.nlm.nih.gov/19282835|journal=Leukemia|volume=23|issue=8|pages=1406–1409|doi=10.1038/leu.2009.42|issn=1476-5551|pmc=2731684|pmid=19282835}}</ref>. Relapsed patients appear to have a dismal prognosis.
-Although the t(1;19) translocation can be readily detected by conventional chromosome studies, FISH confirmation is often needed since a karyotypically similar t(1;19) without involvement of TCF3 or PBX1 has been reported<ref name=":0" />.
+Although the t(1;19) translocation can be readily detected by conventional chromosome studies, FISH confirmation is often needed since a karyotypically similar t(1;19) without involvement of TCF3 or PBX1 has been reported<ref name=":0">{{Cite journal|last=Akkari|first=Yassmine M. N.|last2=Bruyere|first2=Helene|last3=Hagelstrom|first3=R. Tanner|last4=Kanagal-Shamanna|first4=Rashmi|last5=Liu|first5=Jie|last6=Luo|first6=Minjie|last7=Mikhail|first7=Fady M.|last8=Pitel|first8=Beth A.|last9=Raca|first9=Gordana|date=05 2020|title=Evidence-based review of genomic aberrations in B-lymphoblastic leukemia/lymphoma: Report from the cancer genomics consortium working group for lymphoblastic leukemia|url=https://pubmed.ncbi.nlm.nih.gov/32302940|journal=Cancer Genetics|volume=243|pages=52–72|doi=10.1016/j.cancergen.2020.03.001|issn=2210-7762|pmid=32302940}}</ref>.
-|}
+|}The breakpoints of the t(1;19) translocation typically fall within intron 16 of ''TCF3'' and intron 3 of ''PBX1''. <ref name=":0" />
-<blockquote class="blockedit">{{Box-round|title=v4:Chromosomal Rearrangements (Gene Fusions)|The content below was from the old template. Please incorporate above.}}</blockquote>
-The breakpoints of the t(1;19) translocation  typically fall within intron 16 of ''TCF3'' and intron 3 of ''PBX1''. <ref name=":0">{{Cite journal|last=Akkari|first=Yassmine M. N.|last2=Bruyere|first2=Helene|last3=Hagelstrom|first3=R. Tanner|last4=Kanagal-Shamanna|first4=Rashmi|last5=Liu|first5=Jie|last6=Luo|first6=Minjie|last7=Mikhail|first7=Fady M.|last8=Pitel|first8=Beth A.|last9=Raca|first9=Gordana|date=05 2020|title=Evidence-based review of genomic aberrations in B-lymphoblastic leukemia/lymphoma: Report from the cancer genomics consortium working group for lymphoblastic leukemia|url=https://pubmed.ncbi.nlm.nih.gov/32302940|journal=Cancer Genetics|volume=243|pages=52–72|doi=10.1016/j.cancergen.2020.03.001|issn=2210-7762|pmid=32302940}}</ref>
-{| class="wikitable sortable"
-|-
-!Chromosomal Rearrangement!!Genes in Fusion (5’ or 3’ Segments)!!Pathogenic Derivative!!Prevalence
-|-
-|t(1;19)(q23;p13.3)||TCF3-PBX1||der(19)||More common (75%)
-|-
-|t(1;19)(q23;p13.3)
-|TCF3-PBX1||Balanced translocation||Less common
-|}
-<blockquote class="blockedit">
-<center>
-</blockquote>
-<blockquote class="blockedit"></blockquote>
-<blockquote class="blockedit">
-<center>
-----
-</blockquote>
 ==Individual Region Genomic Gain/Loss/LOH==
-Secondary somatic copy number aberrations are not frequently seen in ''TCF3-PBX1'' B-ALL.
-Put your text here and fill in the table <span style="color:#0070C0">(''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.'') </span>
 {| class="wikitable sortable"
 |-
@@ Line 102: / Line 64: @@
 !Clinical Relevance Details/Other Notes
 |-
-|<span class="blue-text">EXAMPLE:</span>
+|dup(1q)
+|
-|<span class="blue-text">EXAMPLE:</span> Loss
+|
-|<span class="blue-text">EXAMPLE:</span>
+|
-chr7
+|
-|<span class="blue-text">EXAMPLE:</span>
+|
-Unknown
+|
-|<span class="blue-text">EXAMPLE:</span> D, P
+|-
-|<span class="blue-text">EXAMPLE:</span> No
+|del(6q)
-|<span class="blue-text">EXAMPLE:</span>
+|
-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).
+|
+|
+|
+|
+|
 |-
-|<span class="blue-text">EXAMPLE:</span>
+| +8
+|
-|<span class="blue-text">EXAMPLE:</span> Gain
+|
-|<span class="blue-text">EXAMPLE:</span>
+|
-chr8
+|
-|<span class="blue-text">EXAMPLE:</span>
+|
-Unknown
-|<span class="blue-text">EXAMPLE:</span> D, P
 |
-|<span class="blue-text">EXAMPLE:</span>
-Common recurrent secondary finding for t(8;21) (add references).
 |-
-|<span class="blue-text">EXAMPLE:</span>
+|i(9q)
+|
-|<span class="blue-text">EXAMPLE:</span> Amp
+|
-|<span class="blue-text">EXAMPLE:</span>
+|
-q12; chr17:39,700,064-39,728,658 [hg38; 28.6 kb]
+|
-|<span class="blue-text">EXAMPLE:</span>
+|
-''ERBB2''
-|<span class="blue-text">EXAMPLE:</span> D, P, T
 |
-|<span class="blue-text">EXAMPLE:</span>
-Amplification of ''ERBB2'' is associated with HER2 overexpression in HER2 positive breast cancer (add references). Add criteria for how amplification is defined.
 |-
+|i(17q)
 |
+|
+|
+|
+|
+|
+|-
+| +21
 |
 |
@@ Line 146: / Line 112: @@
 |
 |}
-<blockquote class="blockedit">{{Box-round|title=v4:Genomic Gain/Loss/LOH|The content below was from the old template. Please incorporate above.}}</blockquote>
-Secondary somatic copy number aberrations are not frequently seen in ''TCF3-PBX1'' B-ALL
-<blockquote class="blockedit">
-<center><span style="color:Maroon">'''End of V4 Section'''</span>
-----
-</blockquote>
 ==Characteristic Chromosomal or Other Global Mutational Patterns==
@@ Line 201: / Line 159: @@
 </blockquote>
 ==Gene Mutations (SNV/INDEL)==
+Secondary somatic copy number aberrations are not frequently seen in ''TCF3-PBX1'' B-ALL<ref>WHO Classification of Tumours: Haematolymphoid Tumours [Internet; Beta Version Ahead of Print](5th ed.), International Agency for Research on Cancer (2022)</ref>.
@@ Line 232: / Line 192: @@
 |
 |<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.
+|-
+|
+|
+|
+|
+|
+|
+|
 |}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.
-<blockquote class="blockedit">{{Box-round|title=v4:Gene Mutations (SNV/INDEL)|The content below was from the old template. Please incorporate above.}}</blockquote>
-Secondary somatic DNA mutations are not frequently seen in ''TCF3-PBX1'' B-ALL. <ref name=":0" />
-===Other Mutations===
-Secondary somatic copy number aberrations and DNA mutations are not frequently seen in ''TCF3-PBX1'' B-ALL, commonly found additional abnormalities are listed below. <ref name=":0" /><ref name=":2" />
-{| class="wikitable sortable"
-|-
-!Type!!Gene/Region/Other
-|-
-|Additional abnormalities||dup(1q), del(6q), +8, i(9q), i(17q), +21
-|}
-<blockquote class="blockedit">
-<center><span style="color:Maroon">'''End of V4 Section'''</span>
-----
-</blockquote>
 ==Epigenomic Alterations==
@@ Line 256: / Line 207: @@
 ==Genes and Main Pathways Involved==
+''TCF3'' gene at 19p13.3 is important during early lymphocyte development, whereas ''PBX1'' at 1q23 is a component of a transcriptional complex that regulates embryogenesis and hematopoiesis. Fusion protein resulting from the TCF3-PBX1 translocation is a transcriptional activator which likely interferes with the normal function of these genes. Expression of this fusion protein is thought to interfere with key regulatory pathways such as WNT and apoptosis/cell cycle control pathways which may drive a leukemic process. The DNA-binding and protein dimerization domains of PBX1 replaces the TCF3 helix-loop-helix DNA-binding motif in ''TCF3-PBX1'' fusion. The remaining transcriptional activating domains of TCF3 leads to constitutive nuclear localization and transformation of PBX1 into an oncogenic transcriptional factor <ref>{{Cite journal|last=Diakos|first=Christofer|last2=Xiao|first2=Yuanyuan|last3=Zheng|first3=Shichun|last4=Kager|first4=Leo|last5=Dworzak|first5=Michael|last6=Wiemels|first6=Joseph L.|date=2014|title=Direct and indirect targets of the E2A-PBX1 leukemia-specific fusion protein|url=https://pubmed.ncbi.nlm.nih.gov/24503810|journal=PloS One|volume=9|issue=2|pages=e87602|doi=10.1371/journal.pone.0087602|issn=1932-6203|pmc=3913655|pmid=24503810}}</ref><ref name=":1">Swerdlow SH, Campo E, Harris NL, Jaffe ES, Pileri SA, Stein H, Thiele J (Eds): WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues (Revised 4th edition). IARC: Lyon 2017</ref><ref name=":0" />
-Put your text here and fill in the table <span style="color:#0070C0">(''Instructions: Please include references throughout the table. Do not delete the table.)''</span>
 {| class="wikitable sortable"
 |-
@@ Line 266: / Line 216: @@
 |Increased cell-proliferation, survival and chemotaxis
 |}
-<blockquote class="blockedit">{{Box-round|title=v4:Genes and Main Pathways Involved|The content below was from the old template. Please incorporate above.}}</blockquote>
-''TCF3'' gene at 19p13.3 is important during early lymphocyte development, whereas ''PBX1'' at 1q23 is a component of a transcriptional complex that regulates embryogenesis and hematopoiesis. Fusion protein resulting from the TCF3-PBX1 translocation is a transcriptional activator which likely interferes with the normal function of these genes. Expression of this fusion protein is thought to interfere with key regulatory pathways such as WNT and apoptosis/cell cycle control pathways which may drive a leukemic process. The DNA-binding and protein dimerization domains of PBX1 replaces the TCF3 helix-loop-helix DNA-binding motif in ''TCF3-PBX1'' fusion. The remaining transcriptional activating domains of TCF3 leads to constitutive nuclear localization and transformation of PBX1 into an oncogenic transcriptional factor <ref>{{Cite journal|last=Diakos|first=Christofer|last2=Xiao|first2=Yuanyuan|last3=Zheng|first3=Shichun|last4=Kager|first4=Leo|last5=Dworzak|first5=Michael|last6=Wiemels|first6=Joseph L.|date=2014|title=Direct and indirect targets of the E2A-PBX1 leukemia-specific fusion protein|url=https://pubmed.ncbi.nlm.nih.gov/24503810|journal=PloS One|volume=9|issue=2|pages=e87602|doi=10.1371/journal.pone.0087602|issn=1932-6203|pmc=3913655|pmid=24503810}}</ref><ref name=":1">Swerdlow SH, Campo E, Harris NL, Jaffe ES, Pileri SA, Stein H, Thiele J (Eds): WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues (Revised 4th edition). IARC: Lyon 2017</ref><ref name=":0" />
-<blockquote class="blockedit">
-<center><span style="color:Maroon">'''End of V4 Section'''</span>
-----
-</blockquote>
 ==Genetic Diagnostic Testing Methods==
@@ Line 287: / Line 228: @@
 Put your text here <span style="color:#0070C0">(''Instructions: Include associated hereditary conditions/syndromes that cause this entity or are caused by this entity.'') </span>
 ==Additional Information==
+A karyotypically identical t(1;19) has been observed in a subset of B-ALL cases, especially in hyperdiploid B-ALL. This translocation does not involve ''TCF3'' or ''PBX1''. Therefore, a FISH confirmation is often necessary to determine the nature of t(1;19). <ref name=":1" /><ref name=":0" />
-*Another translocation involving the ''TCF3'' gene is t(17;19) which results in the fusion of ''HLF'' at 17q22 with ''TCF3''. This variant translocation has been reported in approximately 1% of pediatric B-ALL patients and is associated with a poor prognosis. <ref name=":1" /><ref name=":2" />
-*A karyotypically identical t(1;19) has been observed in a subset of B-ALL cases, especially in hyperdiploid B-ALL. This translocation does not involve ''TCF3'' or ''PBX1''. Therefore, a FISH confirmation is often necessary to determine the nature of t(1;19). <ref name=":1" /><ref name=":0" />
 ==Links==
@@ Line 296: / Line 235: @@
 [[PBX1]]
-Put your links here (use "Link" icon at top of page)
 ==References==
-(use the "Cite" icon at the top of the page) <span style="color:#0070C0">(''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''</span><span style="color:#0070C0">''.''</span><span style="color:#0070C0">)</span> <references />
+<references />
-<br />
 ==Notes==
-<nowiki>*</nowiki>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.
+<nowiki>*</nowiki>''Citation of this Page'': Mancera MG. “B lymphoblastic leukaemia/lymphoma with TCF3::PBX1 fusion”. Compendium of Cancer Genome Aberrations (CCGA), Cancer Genomics Consortium (CGC), updated {{REVISIONMONTH}}/{{REVISIONDAY}}/{{REVISIONYEAR}}, <nowiki>https://ccga.io/index.php/HAEM5:B_lymphoblastic_leukaemia/lymphoma_with_TCF3::PBX1_fusion</nowiki>.
+<nowiki>*</nowiki>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.
+Prior Author(s): Binu Porath, PhD; Linda D. Cooley, MD, MBA
-<references />
-<nowiki>*</nowiki>''Citation of this Page'': “B lymphoblastic leukaemia/lymphoma with TCF3::PBX1 fusion”. Compendium of Cancer Genome Aberrations (CCGA), Cancer Genomics Consortium (CGC), updated {{REVISIONMONTH}}/{{REVISIONDAY}}/{{REVISIONYEAR}}, <nowiki>https://ccga.io/index.php/HAEM5:B_lymphoblastic_leukaemia/lymphoma_with_TCF3::PBX1_fusion</nowiki>.
 [[Category:HAEM5]]
 [[Category:DISEASE]]
 [[Category:Diseases B]]

HAEM5:B lymphoblastic leukaemia/lymphoma with TCF3::PBX1 fusion: Difference between revisions