Compendium of Cancer Genome Aberrations

HAEM5:B-lymphoblastic leukaemia/lymphoma with BCR::ABL1-like features: Difference between revisions

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{{DISPLAYTITLE:B-lymphoblastic leukaemia/lymphoma with BCR::ABL1-like features}}
{{DISPLAYTITLE:B-lymphoblastic leukaemia/lymphoma with BCR::ABL1-like features}}
[[HAEM5:Table_of_Contents|Haematolymphoid Tumours (WHO Classification, 5th ed.)]]
[[HAEM5:Table_of_Contents|Haematolymphoid Tumours (5th ed.)]]


{{Under Construction}}
{{Under Construction}}
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}}</blockquote>
}}</blockquote>


<span style="color:#0070C0">(General Instructions – The main focus of these pages is the clinically significant genetic alterations in each disease type. Use [https://www.genenames.org/ <u>HUGO-approved gene names and symbols</u>] (italicized when appropriate), [https://varnomen.hgvs.org/ 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 to a table, click nearby within the table and select the > symbol that appears to be given options. 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>
<span style="color:#0070C0">(General Instructions – The main focus of these pages is the clinically significant genetic alterations in each disease type. Use [https://www.genenames.org/ <u>HUGO-approved gene names and symbols</u>] (italicized when appropriate), [https://varnomen.hgvs.org/ 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). 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)*==
==Primary Author(s)*==
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==Clinical Features==
==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>
Put your text here and fill in the table <span style="color:#0070C0">(''Instruction: Can include references in the table'') </span>
{| class="wikitable"
{| class="wikitable"
|'''Signs and Symptoms'''
|'''Signs and Symptoms'''
|<span class="blue-text">EXAMPLE:</span> Asymptomatic (incidental finding on complete blood counts)
|EXAMPLE Asymptomatic (incidental finding on complete blood counts)


<span class="blue-text">EXAMPLE:</span> B-symptoms (weight loss, fever, night sweats)
EXAMPLE B-symptoms (weight loss, fever, night sweats)


<span class="blue-text">EXAMPLE:</span> Fatigue
EXAMPLE Fatigue


<span class="blue-text">EXAMPLE:</span> Lymphadenopathy (uncommon)
EXAMPLE Lymphadenopathy (uncommon)
|-
|-
|'''Laboratory Findings'''
|'''Laboratory Findings'''
|<span class="blue-text">EXAMPLE:</span> Cytopenias
|EXAMPLE Cytopenias


<span class="blue-text">EXAMPLE:</span> Lymphocytosis (low level)
EXAMPLE Lymphocytosis (low level)
|}
|}




<blockquote class='blockedit'>{{Box-round|title=HAEM5 Conversion Notes|Content Update To WHO 5th Edition Classification Is In Process; Content Below is Based on WHO 4th Edition Classification}}
<blockquote class='blockedit'>{{Box-round|title=v4:Clinical Features|The content below was from the old template. Please incorporate above.}}
The presenting symptoms are similar to those of other ALL patients, with the exception of potentially higher white blood cell counts<ref name=":2">Borowitz MJ, et al., (2017). B-lymphoblastic leukaemia/lymphoma with recurrent genetic abnormalities, in World Health Organization Classification of Tumours of Haematopoietic and Lymphoid Tissues, Revised 4th edition. Swerdlow SH, Campo E, Harris NL, Jaffe ES, Pileri SA, Stein H, Thiele J, Arber DA, Hasserjian RP, Le Beau MM, Orazi A, and Siebert R, Editors. IARC Press: Lyon, France, p208.</ref>.
The presenting symptoms are similar to those of other ALL patients, with the exception of potentially higher white blood cell counts<ref name=":2">Borowitz MJ, et al., (2017). B-lymphoblastic leukaemia/lymphoma with recurrent genetic abnormalities, in World Health Organization Classification of Tumours of Haematopoietic and Lymphoid Tissues, Revised 4th edition. Swerdlow SH, Campo E, Harris NL, Jaffe ES, Pileri SA, Stein H, Thiele J, Arber DA, Hasserjian RP, Le Beau MM, Orazi A, and Siebert R, Editors. IARC Press: Lyon, France, p208.</ref>.


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==Immunophenotype==
==Immunophenotype==


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>
Put your text here and fill in the table <span style="color:#0070C0">(''Instruction: Can include references in the table'') </span>


{| class="wikitable sortable"
{| class="wikitable sortable"
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!Finding!!Marker
!Finding!!Marker
|-
|-
|Positive (universal)||<span class="blue-text">EXAMPLE:</span> CD1
|Positive (universal)||EXAMPLE CD1
|-
|-
|Positive (subset)||<span class="blue-text">EXAMPLE:</span> CD2
|Positive (subset)||EXAMPLE CD2
|-
|-
|Negative (universal)||<span class="blue-text">EXAMPLE:</span> CD3
|Negative (universal)||EXAMPLE CD3
|-
|-
|Negative (subset)||<span class="blue-text">EXAMPLE:</span> CD4
|Negative (subset)||EXAMPLE CD4
|}
|}




<blockquote class='blockedit'>{{Box-round|title=HAEM5 Conversion Notes|Content Update To WHO 5th Edition Classification Is In Process; Content Below is Based on WHO 4th Edition Classification}}
<blockquote class='blockedit'>{{Box-round|title=v4:Immunophenotype|The content below was from the old template. Please incorporate above.}}
Blasts are typically CD19, TdT, and CD10-positive. By flow cytometry, a subset of cases with CRLF2 translocations show very high levels of surface protein expression<ref name=":2" />.
Blasts are typically CD19, TdT, and CD10-positive. By flow cytometry, a subset of cases with CRLF2 translocations show very high levels of surface protein expression<ref name=":2" />.


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!Notes
!Notes
|-
|-
|<span class="blue-text">EXAMPLE:</span> t(9;22)(q34;q11.2)||<span class="blue-text">EXAMPLE:</span> 3'ABL1 / 5'BCR||<span class="blue-text">EXAMPLE:</span> der(22)||<span class="blue-text">EXAMPLE:</span> 20% (COSMIC)
|EXAMPLE t(9;22)(q34;q11.2)||EXAMPLE 3'ABL1 / 5'BCR||EXAMPLE der(22)||EXAMPLE 20% (COSMIC)
<span class="blue-text">EXAMPLE:</span> 30% (add reference)
EXAMPLE 30% (add reference)
|Yes
|Yes
|No
|No
|Yes
|Yes
|<span class="blue-text">EXAMPLE:</span>
|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).
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).
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<blockquote class='blockedit'>{{Box-round|title=HAEM5 Conversion Notes|Content Update To WHO 5th Edition Classification Is In Process; Content Below is Based on WHO 4th Edition Classification}}
<blockquote class='blockedit'>{{Box-round|title=v4:Chromosomal Rearrangements (Gene Fusions)|The content below was from the old template. Please incorporate above.}}
Tyrosine kinase-type translocations are common and involve ''ABL1'' and other kinases (such as ''ABL2'', ''EPOR'', ''JAK2'', ''PDGFRB'', and ''CSF1R''); more than 30 gene partners have been described. Frequently reported examples include ''IGH''–''EPOR'' of the t(14;19)(q32;p13)/ins(14;19)(q32;p13), ''EBF1''–''PDGFRB'' of the del(5)(q32q33.3), ''NUP214''–''ABL1'' of the t(9;9)(q34;q34)/del(9)(q34q34), and ''ETV6''–''ABL1'' of the t(9;12)(q34;p13). Other notable fusions are ''BCR''–''JAK2'', ''PAX5''–''JAK2'', ''STRN3''–''JAK2'', ''RANBP2''–''ABL1'', ''RCSD1''–''ABL1'', and ''MEF2D''–''CSF1R''<ref>Heim S & Mitelman F. Cancer Cytogenetics: Chromosomal and Molecular Genetic Aberrations of Tumor Cells. John Wiley & Sons, Incorporated: Chichester, United Kingdom. 2015.</ref>.
Tyrosine kinase-type translocations are common and involve ''ABL1'' and other kinases (such as ''ABL2'', ''EPOR'', ''JAK2'', ''PDGFRB'', and ''CSF1R''); more than 30 gene partners have been described. Frequently reported examples include ''IGH''–''EPOR'' of the t(14;19)(q32;p13)/ins(14;19)(q32;p13), ''EBF1''–''PDGFRB'' of the del(5)(q32q33.3), ''NUP214''–''ABL1'' of the t(9;9)(q34;q34)/del(9)(q34q34), and ''ETV6''–''ABL1'' of the t(9;12)(q34;p13). Other notable fusions are ''BCR''–''JAK2'', ''PAX5''–''JAK2'', ''STRN3''–''JAK2'', ''RANBP2''–''ABL1'', ''RCSD1''–''ABL1'', and ''MEF2D''–''CSF1R''<ref>Heim S & Mitelman F. Cancer Cytogenetics: Chromosomal and Molecular Genetic Aberrations of Tumor Cells. John Wiley & Sons, Incorporated: Chichester, United Kingdom. 2015.</ref>.


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<blockquote class='blockedit'>{{Box-round|title=HAEM5 Conversion Notes|Please incorporate this section into the relevant tables found in:
<blockquote class='blockedit'>{{Box-round|title=v4:Clinical Significance (Diagnosis, Prognosis and Therapeutic Implications).|Please incorporate this section into the relevant tables found in:
* Chromosomal Rearrangements (Gene Fusions)
* Chromosomal Rearrangements (Gene Fusions)
* Individual Region Genomic Gain/Loss/LOH
* Individual Region Genomic Gain/Loss/LOH
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==Individual Region Genomic Gain / Loss / LOH==
==Individual Region Genomic Gain / Loss / LOH==


Put your text here and fill in the table <span style="color:#0070C0">(''Instructions: Includes aberrations not involving gene fusions. Can include references in the table. Can refer to CGC workgroup tables as linked on the homepage if applicable. Do not delete table.'') </span>
Put your text here and fill in the table <span style="color:#0070C0">(''Instructions: Includes aberrations not involving gene fusions. Can include references in the table. Can refer to CGC workgroup tables as linked on the homepage if applicable.'') </span>


{| class="wikitable sortable"
{| class="wikitable sortable"
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!Notes
!Notes
|-
|-
|<span class="blue-text">EXAMPLE:</span>
|EXAMPLE


7
7
|<span class="blue-text">EXAMPLE:</span> Loss
|EXAMPLE Loss
|<span class="blue-text">EXAMPLE:</span>
|EXAMPLE


chr7:1- 159,335,973 [hg38]
chr7:1- 159,335,973 [hg38]
|<span class="blue-text">EXAMPLE:</span>
|EXAMPLE


chr7
chr7
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|Yes
|Yes
|No
|No
|<span class="blue-text">EXAMPLE:</span>
|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 reference).
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 reference).
|-
|-
|<span class="blue-text">EXAMPLE:</span>
|EXAMPLE


8
8
|<span class="blue-text">EXAMPLE:</span> Gain
|EXAMPLE Gain
|<span class="blue-text">EXAMPLE:</span>
|EXAMPLE


chr8:1-145,138,636 [hg38]
chr8:1-145,138,636 [hg38]
|<span class="blue-text">EXAMPLE:</span>
|EXAMPLE


chr8
chr8
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|No
|No
|No
|No
|<span class="blue-text">EXAMPLE:</span>
|EXAMPLE


Common recurrent secondary finding for t(8;21) (add reference).
Common recurrent secondary finding for t(8;21) (add reference).
|}
|}


<blockquote class='blockedit'>{{Box-round|title=HAEM5 Conversion Notes|Content Update To WHO 5th Edition Classification Is In Process; Content Below is Based on WHO 4th Edition Classification}}
<blockquote class='blockedit'>{{Box-round|title=v4:Genomic Gain/Loss/LOH|The content below was from the old template. Please incorporate above.}}
Monoallelic (often partial) deletion of the IKAROS transcription factor, encoded by ''IKZF1'', is one of the most frequently observed genetic abnormalities in BCR-ABL1-like B-ALL, although this finding is not specific and not included in the definition<ref name=":3" />.  
Monoallelic (often partial) deletion of the IKAROS transcription factor, encoded by ''IKZF1'', is one of the most frequently observed genetic abnormalities in BCR-ABL1-like B-ALL, although this finding is not specific and not included in the definition<ref name=":3" />.  
</blockquote>
</blockquote>
==Characteristic Chromosomal Patterns==
==Characteristic Chromosomal Patterns==


Put your text here <span style="color:#0070C0">(''EXAMPLE PATTERNS: 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. Do not delete table.'')</span>
Put your text here <span style="color:#0070C0">(''EXAMPLE PATTERNS: 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'')</span>


{| class="wikitable sortable"
{| class="wikitable sortable"
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!Notes
!Notes
|-
|-
|<span class="blue-text">EXAMPLE:</span>
|EXAMPLE


Co-deletion of 1p and 18q
Co-deletion of 1p and 18q
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|No
|No
|No
|No
|<span class="blue-text">EXAMPLE:</span>
|EXAMPLE:


See chromosomal rearrangements table as this pattern is due to an unbalanced derivative translocation associated with oligodendroglioma (add reference).
See chromosomal rearrangements table as this pattern is due to an unbalanced derivative translocation associated with oligodendroglioma (add reference).
|}
|}


<blockquote class='blockedit'>{{Box-round|title=HAEM5 Conversion Notes|Content Update To WHO 5th Edition Classification Is In Process; Content Below is Based on WHO 4th Edition Classification}}
<blockquote class='blockedit'>{{Box-round|title=v4:Characteristic Chromosomal Aberrations / Patterns|The content below was from the old template. Please incorporate above.}}
Approximately half of cases demonstrate rearrangements resulting in overexpression of CRLF2<ref name=":7" />. These rearrangements are the result of either translocation of immunoglobin heavy chain enhance locus into ''CRLF2'' (''IGH''-''CRLF2''—more commonly seen in adults) or through a cryptic deletion on chromosome X/Y involving the PAR1 psuedoautosomal region, resulting in fusion of ''CRLF2'' to ''P2RY8'' (more commonly seen in children). Very rare alternative translocations involving ''CRLF2'' have also been observed.
Approximately half of cases demonstrate rearrangements resulting in overexpression of CRLF2<ref name=":7" />. These rearrangements are the result of either translocation of immunoglobin heavy chain enhance locus into ''CRLF2'' (''IGH''-''CRLF2''—more commonly seen in adults) or through a cryptic deletion on chromosome X/Y involving the PAR1 psuedoautosomal region, resulting in fusion of ''CRLF2'' to ''P2RY8'' (more commonly seen in children). Very rare alternative translocations involving ''CRLF2'' have also been observed.
[[File:FISH 1.jpg|thumb|none]]
[[File:FISH 1.jpg|thumb|none]]
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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 and common as well as either disease defining and/or clinically significant. Can include references 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. Do not delete table.'') </span>
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 and common as well either disease defining and/or clinically significant. Can include references 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.'') </span>


{| class="wikitable sortable"
{| class="wikitable sortable"
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!Notes
!Notes
|-
|-
|<span class="blue-text">EXAMPLE:</span> TP53; Variable LOF mutations
|EXAMPLE: TP53; Variable LOF mutations


<span class="blue-text">EXAMPLE:</span>
EXAMPLE:


EGFR; Exon 20 mutations
EGFR; Exon 20 mutations


<span class="blue-text">EXAMPLE:</span> BRAF; Activating mutations
EXAMPLE: BRAF; Activating mutations
|<span class="blue-text">EXAMPLE:</span> TSG
|EXAMPLE: TSG
|<span class="blue-text">EXAMPLE:</span> 20% (COSMIC)
|EXAMPLE: 20% (COSMIC)


<span class="blue-text">EXAMPLE:</span> 30% (add Reference)
EXAMPLE: 30% (add Reference)
|<span class="blue-text">EXAMPLE:</span> IDH1 R123H
|EXAMPLE: IDH1 R123H
|<span class="blue-text">EXAMPLE:</span> EGFR amplification
|EXAMPLE: EGFR amplification
|
|
|
|
|
|
|<span class="blue-text">EXAMPLE:</span>  Excludes hairy cell leukemia (HCL) (add reference).
|EXAMPLE:  Excludes hairy cell leukemia (HCL) (add reference).
<br />
<br />
|}
|}
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<blockquote class='blockedit'>{{Box-round|title=HAEM5 Conversion Notes|Content Update To WHO 5th Edition Classification Is In Process; Content Below is Based on WHO 4th Edition Classification}}
<blockquote class='blockedit'>{{Box-round|title=v4:Gene Mutations (SNV/INDEL)|The content below was from the old template. Please incorporate above.}}
In addition to gene translocations, gain-of-function mutations in ''CRLF2'' itself or in its partner gene, ''IL7RA'', have been seen<ref name=":8">Quesada A, Reynolds M, Jorgensen JL, et al. Cytokine receptor-like factor 2 (CRLF2) expression in precursor B-lymphoblastic leukemia. International Clinical Cytometry Society e-Newsletter. 2014;5(1).</ref>.  Alternative alterations activating kinase signaling occur, including activating mutations of ''FLT3'', as well as focal deletions of ''SH2B3'' (also known as ''LNK'')<ref>Tosi S & Reid AG. The Genetic Basis of Haematological Cancers. John Wiley & Sons, Incorporated: Chichester, United Kingdom: 2016.</ref>.
In addition to gene translocations, gain-of-function mutations in ''CRLF2'' itself or in its partner gene, ''IL7RA'', have been seen<ref name=":8">Quesada A, Reynolds M, Jorgensen JL, et al. Cytokine receptor-like factor 2 (CRLF2) expression in precursor B-lymphoblastic leukemia. International Clinical Cytometry Society e-Newsletter. 2014;5(1).</ref>.  Alternative alterations activating kinase signaling occur, including activating mutations of ''FLT3'', as well as focal deletions of ''SH2B3'' (also known as ''LNK'')<ref>Tosi S & Reid AG. The Genetic Basis of Haematological Cancers. John Wiley & Sons, Incorporated: Chichester, United Kingdom: 2016.</ref>.


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==Genes and Main Pathways Involved==
==Genes and Main Pathways Involved==


Put your text here and fill in the table <span style="color:#0070C0">(''Instructions: Can include references in the table. Do not delete table.'')</span>
Put your text here and fill in the table <span style="color:#0070C0">(''Instructions: Can include references in the table.'')</span>
{| class="wikitable sortable"
{| class="wikitable sortable"
|-
|-
!Gene; Genetic Alteration!!Pathway!!Pathophysiologic Outcome
!Gene; Genetic Alteration!!Pathway!!Pathophysiologic Outcome
|-
|-
|<span class="blue-text">EXAMPLE:</span> BRAF and MAP2K1; Activating mutations
|EXAMPLE: BRAF and MAP2K1; Activating mutations
|<span class="blue-text">EXAMPLE:</span> MAPK signaling
|EXAMPLE: MAPK signaling
|<span class="blue-text">EXAMPLE:</span> Increased cell growth and proliferation
|EXAMPLE: Increased cell growth and proliferation
|-
|-
|<span class="blue-text">EXAMPLE:</span> CDKN2A; Inactivating mutations
|EXAMPLE: CDKN2A; Inactivating mutations
|<span class="blue-text">EXAMPLE:</span> Cell cycle regulation
|EXAMPLE: Cell cycle regulation
|<span class="blue-text">EXAMPLE:</span> Unregulated cell division
|EXAMPLE: Unregulated cell division
|-
|-
|<span class="blue-text">EXAMPLE:</span>  KMT2C and ARID1A; Inactivating mutations
|EXAMPLE:  KMT2C and ARID1A; Inactivating mutations
|<span class="blue-text">EXAMPLE:</span>  Histone modification, chromatin remodeling
|EXAMPLE:  Histone modification, chromatin remodeling
|<span class="blue-text">EXAMPLE:</span>  Abnormal gene expression program
|EXAMPLE:  Abnormal gene expression program
|}
|}


<blockquote class='blockedit'>{{Box-round|title=HAEM5 Conversion Notes|Content Update To WHO 5th Edition Classification Is In Process; Content Below is Based on WHO 4th Edition Classification}}
<blockquote class='blockedit'>{{Box-round|title=v4:Genes and Main Pathways Involved|The content below was from the old template. Please incorporate above.}}


*IKAROS transcription factor:  Deletion of ''IKZF1'' results in activation of ''EBF1'', ''MSH2'', and ''MCL1'', leading to B-cell leukemogenesis<ref>{{Cite journal|last=van der Veer|first=Arian|last2=Waanders|first2=Esmé|last3=Pieters|first3=Rob|last4=Willemse|first4=Marieke E.|last5=Van Reijmersdal|first5=Simon V.|last6=Russell|first6=Lisa J.|last7=Harrison|first7=Christine J.|last8=Evans|first8=William E.|last9=van der Velden|first9=Vincent H. J.|date=2013|title=Independent prognostic value of BCR-ABL1-like signature and IKZF1 deletion, but not high CRLF2 expression, in children with B-cell precursor ALL|url=https://www.ncbi.nlm.nih.gov/pubmed/23974192|journal=Blood|volume=122|issue=15|pages=2622–2629|doi=10.1182/blood-2012-10-462358|issn=1528-0020|pmc=3795461|pmid=23974192}}</ref>.
*IKAROS transcription factor:  Deletion of ''IKZF1'' results in activation of ''EBF1'', ''MSH2'', and ''MCL1'', leading to B-cell leukemogenesis<ref>{{Cite journal|last=van der Veer|first=Arian|last2=Waanders|first2=Esmé|last3=Pieters|first3=Rob|last4=Willemse|first4=Marieke E.|last5=Van Reijmersdal|first5=Simon V.|last6=Russell|first6=Lisa J.|last7=Harrison|first7=Christine J.|last8=Evans|first8=William E.|last9=van der Velden|first9=Vincent H. J.|date=2013|title=Independent prognostic value of BCR-ABL1-like signature and IKZF1 deletion, but not high CRLF2 expression, in children with B-cell precursor ALL|url=https://www.ncbi.nlm.nih.gov/pubmed/23974192|journal=Blood|volume=122|issue=15|pages=2622–2629|doi=10.1182/blood-2012-10-462358|issn=1528-0020|pmc=3795461|pmid=23974192}}</ref>.
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