HAEM5:B-lymphoblastic leukaemia/lymphoma with high hyperdiploidy: Difference between revisions
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==Gene Rearrangements== | ==Gene Rearrangements== | ||
No recurrent gene rearrangements | No recurrent gene rearrangements have been described<ref name=":3" />. | ||
{| class="wikitable sortable" | {| class="wikitable sortable" | ||
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|<span class="blue-text">EXAMPLE:</span> ''CIC::DUX4'' | |<span class="blue-text">EXAMPLE:</span> ''CIC::DUX4'' | ||
|<span class="blue-text">EXAMPLE:</span> 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''. | |<span class="blue-text">EXAMPLE:</span> 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''. | ||
| | | | ||
|} | |} | ||
* | |||
* | |||
<blockquote class="blockedit"> | <blockquote class="blockedit"> | ||
<center> | <center> | ||
</blockquote> | </blockquote> | ||
==Individual Region Genomic Gain/Loss/LOH== | ==Individual Region Genomic Gain/Loss/LOH== | ||
* This entity is defined by a hyperdiploid pattern with a karyotype comprising 51–65 chromosomes with recurrent, non-random gains of one or more copies of entire chromosomes<ref name=":3" />. | |||
* Highly homogeneous genomes are seen for most of the leukemias, with predominantly whole chromosome gains being present in all cells<ref name=":6">{{Cite journal|last=Woodward|first=Eleanor L.|last2=Yang|first2=Minjun|last3=Moura-Castro|first3=Larissa H.|last4=van den Bos|first4=Hilda|last5=Gunnarsson|first5=Rebeqa|last6=Olsson-Arvidsson|first6=Linda|last7=Spierings|first7=Diana C. J.|last8=Castor|first8=Anders|last9=Duployez|first9=Nicolas|date=2023-03-25|title=Clonal origin and development of high hyperdiploidy in childhood acute lymphoblastic leukaemia|url=https://pubmed.ncbi.nlm.nih.gov/36966135|journal=Nature Communications|volume=14|issue=1|pages=1658|doi=10.1038/s41467-023-37356-5|issn=2041-1723|pmc=10039905|pmid=36966135}}</ref>. Below are the typical chromosomal gains described. | |||
{| class="wikitable sortable" | {| class="wikitable sortable" | ||
|- | |- | ||
| Line 107: | Line 88: | ||
|Chr21 | |Chr21 | ||
|''RUNX1'' | |''RUNX1'' | ||
|No established significance | |No established significance | ||
|No | |No (NCCN) | ||
|Chromosome 21 is universally gained in high-hyperdiploid B-ALL/LBL <ref>{{Cite journal|last=Harrison|first=Christine J.|last2=Haas|first2=Oskar|last3=Harbott|first3=Jochen|last4=Biondi|first4=Andrea|last5=Stanulla|first5=Martin|last6=Trka|first6=Jan|last7=Izraeli|first7=Shai|last8=Biology and Diagnosis Committee of International Berlin-Frankfürt-Münster study group|date=2010-10|title=Detection of prognostically relevant genetic abnormalities in childhood B-cell precursor acute lymphoblastic leukaemia: recommendations from the Biology and Diagnosis Committee of the International Berlin-Frankfürt-Münster study group|url=https://pubmed.ncbi.nlm.nih.gov/20701601|journal=British Journal of Haematology|volume=151|issue=2|pages=132–142|doi=10.1111/j.1365-2141.2010.08314.x|issn=1365-2141|pmid=20701601}}</ref> | |Chromosome 21 is universally gained in high-hyperdiploid B-ALL/LBL <ref>{{Cite journal|last=Harrison|first=Christine J.|last2=Haas|first2=Oskar|last3=Harbott|first3=Jochen|last4=Biondi|first4=Andrea|last5=Stanulla|first5=Martin|last6=Trka|first6=Jan|last7=Izraeli|first7=Shai|last8=Biology and Diagnosis Committee of International Berlin-Frankfürt-Münster study group|date=2010-10|title=Detection of prognostically relevant genetic abnormalities in childhood B-cell precursor acute lymphoblastic leukaemia: recommendations from the Biology and Diagnosis Committee of the International Berlin-Frankfürt-Münster study group|url=https://pubmed.ncbi.nlm.nih.gov/20701601|journal=British Journal of Haematology|volume=151|issue=2|pages=132–142|doi=10.1111/j.1365-2141.2010.08314.x|issn=1365-2141|pmid=20701601}}</ref>; therefore, the presence of multiple (three to five) discrete ''RUNX1'' signals seen when using ''ETV6''::''RUNX1'' FISH probes suggests the presence of high hyperdiploidy. | ||
|- | |- | ||
|X | |X | ||
| Line 115: | Line 96: | ||
|ChrX | |ChrX | ||
|None | |None | ||
|No established significance | |No established significance | ||
|No | |No (NCCN) | ||
|N/A | |N/A | ||
|- | |- | ||
| Line 123: | Line 104: | ||
|Chr6 | |Chr6 | ||
|None | |None | ||
|No established significance | |No established significance | ||
|No | |No (NCCN) | ||
|N/A | |N/A | ||
|- | |- | ||
| Line 131: | Line 112: | ||
|Chr14 | |Chr14 | ||
|None | |None | ||
|No established significance | |No established significance | ||
|No | |No (NCCN) | ||
|N/A | |N/A | ||
|- | |- | ||
| Line 140: | Line 121: | ||
|None | |None | ||
|Prognostic significance: has been correlated with a lower risk of relapse<ref name=":1">{{Cite journal|last=Moorman|first=Anthony V.|last2=Ensor|first2=Hannah M.|last3=Richards|first3=Sue M.|last4=Chilton|first4=Lucy|last5=Schwab|first5=Claire|last6=Kinsey|first6=Sally E.|last7=Vora|first7=Ajay|last8=Mitchell|first8=Chris D.|last9=Harrison|first9=Christine J.|date=2010-05|title=Prognostic effect of chromosomal abnormalities in childhood B-cell precursor acute lymphoblastic leukaemia: results from the UK Medical Research Council ALL97/99 randomised trial|url=https://pubmed.ncbi.nlm.nih.gov/20409752|journal=The Lancet. Oncology|volume=11|issue=5|pages=429–438|doi=10.1016/S1470-2045(10)70066-8|issn=1474-5488|pmid=20409752}}</ref>. | |Prognostic significance: has been correlated with a lower risk of relapse<ref name=":1">{{Cite journal|last=Moorman|first=Anthony V.|last2=Ensor|first2=Hannah M.|last3=Richards|first3=Sue M.|last4=Chilton|first4=Lucy|last5=Schwab|first5=Claire|last6=Kinsey|first6=Sally E.|last7=Vora|first7=Ajay|last8=Mitchell|first8=Chris D.|last9=Harrison|first9=Christine J.|date=2010-05|title=Prognostic effect of chromosomal abnormalities in childhood B-cell precursor acute lymphoblastic leukaemia: results from the UK Medical Research Council ALL97/99 randomised trial|url=https://pubmed.ncbi.nlm.nih.gov/20409752|journal=The Lancet. Oncology|volume=11|issue=5|pages=429–438|doi=10.1016/S1470-2045(10)70066-8|issn=1474-5488|pmid=20409752}}</ref>. | ||
|No | |No (NCCN) | ||
|N/A | |N/A | ||
|- | |- | ||
| Line 147: | Line 128: | ||
|Chr4 | |Chr4 | ||
|None | |None | ||
|The prognostic impact of the “triple trisomies”, i.e., concurrent rent +4, +10, and +17, is debated; they have been reported to be associated with low risk by the Children’s Oncology Group (COG) | |The prognostic impact of the “triple trisomies”, i.e., concurrent rent +4, +10, and +17, is debated; they have been reported to be associated with low risk by the Children’s Oncology Group (COG)<ref>{{Cite journal|last=Schultz|first=Kirk R.|last2=Pullen|first2=D. Jeanette|last3=Sather|first3=Harland N.|last4=Shuster|first4=Jonathan J.|last5=Devidas|first5=Meenakshi|last6=Borowitz|first6=Michael J.|last7=Carroll|first7=Andrew J.|last8=Heerema|first8=Nyla A.|last9=Rubnitz|first9=Jeffrey E.|date=2007-02-01|title=Risk- and response-based classification of childhood B-precursor acute lymphoblastic leukemia: a combined analysis of prognostic markers from the Pediatric Oncology Group (POG) and Children's Cancer Group (CCG)|url=https://pubmed.ncbi.nlm.nih.gov/17003380|journal=Blood|volume=109|issue=3|pages=926–935|doi=10.1182/blood-2006-01-024729|issn=0006-4971|pmc=1785141|pmid=17003380}}</ref>, but not in UK trials<ref name=":1" />. | ||
|No | |No (NCCN) | ||
|N/A | |N/A | ||
|- | |- | ||
| Line 155: | Line 136: | ||
|Chr17 | |Chr17 | ||
|None | |None | ||
|''See | |''See "prognostic significance" section for +4 above'' | ||
|No | |No (NCCN) | ||
|N/A | |N/A | ||
|- | |- | ||
| Line 163: | Line 144: | ||
|Chr10 | |Chr10 | ||
|None | |None | ||
|''See | |''See prognostic significance" section for +4 above'' | ||
|No | |No (NCCN) | ||
|N/A | |N/A | ||
|- | |- | ||
| Line 171: | Line 152: | ||
|Chr8 | |Chr8 | ||
|None | |None | ||
|No established significance | |No established significance | ||
|No | |No (NCCN) | ||
|N/A | |N/A | ||
|} | |} | ||
<blockquote class="blockedit"> | <blockquote class="blockedit"></blockquote><blockquote class="blockedit"> | ||
<center> | |||
<blockquote class="blockedit"> | |||
<center | |||
---- | ---- | ||
</blockquote> | </blockquote> | ||
==Characteristic Chromosomal or Other Global Mutational Patterns== | ==Characteristic Chromosomal or Other Global Mutational Patterns== | ||
{| class="wikitable sortable" | {| class="wikitable sortable" | ||
|- | |- | ||
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|- | |- | ||
|Hyperdiploid | |Hyperdiploid | ||
|Although pathogenetic mechanisms are poorly understood, chromosomal gains are early events in the pathogenesis | |Although pathogenetic mechanisms are poorly understood, chromosomal gains are early events in the pathogenesis, possibly already before birth, and are the main driver<ref name=":3">WHO Classification of Tumours: Haematolymphoid Tumours [Internet; Beta Version Ahead of Print](5th ed.), International Agency for Research on Cancer (2022)</ref><ref>{{Cite journal|last=Szczepański|first=T.|last2=Willemse|first2=M. J.|last3=van Wering|first3=E. R.|last4=van Weerden|first4=J. F.|last5=Kamps|first5=W. A.|last6=van Dongen|first6=J. J.|date=2001-09|title=Precursor-B-ALL with D(H)-J(H) gene rearrangements have an immature immunogenotype with a high frequency of oligoclonality and hyperdiploidy of chromosome 14|url=https://pubmed.ncbi.nlm.nih.gov/11516102|journal=Leukemia|volume=15|issue=9|pages=1415–1423|doi=10.1038/sj.leu.2402206|issn=0887-6924|pmid=11516102}}</ref><ref>{{Cite journal|last=Maia|first=A. T.|last2=van der Velden|first2=V. H. J.|last3=Harrison|first3=C. J.|last4=Szczepanski|first4=T.|last5=Williams|first5=M. D.|last6=Griffiths|first6=M. J.|last7=van Dongen|first7=J. J. M.|last8=Greaves|first8=M. F.|date=2003-11|title=Prenatal origin of hyperdiploid acute lymphoblastic leukemia in identical twins|url=https://pubmed.ncbi.nlm.nih.gov/12931229|journal=Leukemia|volume=17|issue=11|pages=2202–2206|doi=10.1038/sj.leu.2403101|issn=0887-6924|pmid=12931229}}</ref><ref>{{Cite journal|last=Maia|first=Ana Teresa|last2=Tussiwand|first2=Roxane|last3=Cazzaniga|first3=Giovanni|last4=Rebulla|first4=Paolo|last5=Colman|first5=Susan|last6=Biondi|first6=Andrea|last7=Greaves|first7=Mel|date=2004-05|title=Identification of preleukemic precursors of hyperdiploid acute lymphoblastic leukemia in cord blood|url=https://pubmed.ncbi.nlm.nih.gov/15034866|journal=Genes, Chromosomes & Cancer|volume=40|issue=1|pages=38–43|doi=10.1002/gcc.20010|issn=1045-2257|pmid=15034866}}</ref><ref name=":2" />. It was suggested that the aneuploidy in these cases likely arises by an initial tripolar mitosis in a diploid cell followed by clonal evolution. During the clonal evolution, chromosomes that changed in copy number comprised X, 8, 9, 14, 16, 17, and 21<ref name=":6" />. | ||
|Ubiquitous | |||
|D: Needs demonstration of high-hyperdiploidy status (comprising 51–65 chromosomes) by karyotyping and/or FISH | |||
P: B-ALL/LBL with high-hyperdiploidy has a very favorable prognosis, with long-term overall survival in > 90% of children<ref name=":0">{{Cite journal|last=Paulsson|first=Kajsa|last2=Forestier|first2=Erik|last3=Andersen|first3=Mette K.|last4=Autio|first4=Kirsi|last5=Barbany|first5=Gisela|last6=Borgström|first6=Georg|last7=Cavelier|first7=Lucia|last8=Golovleva|first8=Irina|last9=Heim|first9=Sverre|date=2013-09|title=High modal number and triple trisomies are highly correlated favorable factors in childhood B-cell precursor high hyperdiploid acute lymphoblastic leukemia treated according to the NOPHO ALL 1992/2000 protocols|url=https://pubmed.ncbi.nlm.nih.gov/23645689|journal=Haematologica|volume=98|issue=9|pages=1424–1432|doi=10.3324/haematol.2013.085852|issn=1592-8721|pmc=3762100|pmid=23645689}}</ref>. | |||
( | T: N/A | ||
|No (NCCN) | |||
|High event-free survival (EFS) was associated with trisomy 4, 6, 17, 18, and 22, presence of triple trisomies (4, 10, 17), and high modal numbers ( > 50 chromosomes)<ref name=":0" />. | |||
Patients with low hyperdiploidy have been reported to have a 49% EFS at 5 years compared to those with high hyperdiploidy with a five-year EFS of 71%. | |||
Negative prognostic features include > 10 years of age, male gender, and bone marrow fibrosis<ref name=":0" />. | |||
< | More recent studies have validated a risk profile determining that outcome appears to be linked to specific chromosomal gains<ref>{{Cite journal|last=Enshaei|first=Amir|last2=Vora|first2=Ajay|last3=Harrison|first3=Christine J.|last4=Moppett|first4=John|last5=Moorman|first5=Anthony V.|date=2021-11|title=Defining low-risk high hyperdiploidy in patients with paediatric acute lymphoblastic leukaemia: a retrospective analysis of data from the UKALL97/99 and UKALL2003 clinical trials|url=https://pubmed.ncbi.nlm.nih.gov/34715050|journal=The Lancet. Haematology|volume=8|issue=11|pages=e828–e839|doi=10.1016/S2352-3026(21)00304-5|issn=2352-3026|pmc=8567211|pmid=34715050}}</ref>. | ||
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|} | |} | ||
<blockquote class="blockedit"> | <blockquote class="blockedit"></blockquote> | ||
* | * | ||
<blockquote class="blockedit"> | <blockquote class="blockedit"> | ||
<center | <center> | ||
---- | ---- | ||
</blockquote> | </blockquote> | ||
==Gene Mutations (SNV/INDEL)== | ==Gene Mutations (SNV/INDEL)== | ||
Nine genes have been found to be recurrently mutated and were also either mutated more frequently than expected by chance or targeted by structural events<ref name=":2" />. | |||
{| class="wikitable sortable" | {| class="wikitable sortable" | ||
|- | |- | ||
| Line 254: | Line 210: | ||
<br /> | <br /> | ||
|Nonsynonymous single nucleotide variant (SNV) | |Nonsynonymous single nucleotide variant (SNV) in known codon 12 and 13 hotspot region, and additional mutations in codons 116 and 146<ref name=":2" /> | ||
|Oncogene | |Oncogene | ||
|Common | |Common | ||
|No | |No | ||
|No | |No | ||
|< | |''KRAS'' codons 117 and 146 may be new recurrent mutational hotspots in high hyperdiploid ALL<ref name=":2" />. | ||
|- | |- | ||
|''NRAS'' | |''NRAS'' | ||
| Line 268: | Line 224: | ||
|No | |No | ||
|No | |No | ||
| | |N/A | ||
|- | |- | ||
|''FLT3'' | |''FLT3'' | ||
| Line 276: | Line 232: | ||
|No | |No | ||
|No | |No | ||
| | |N/A | ||
|- | |- | ||
|''PTPN11'' | |''PTPN11'' | ||
| Line 284: | Line 240: | ||
|No | |No | ||
|No | |No | ||
| | |N/A | ||
|- | |- | ||
|''CREBBP'' | |''CREBBP'' | ||
| Line 292: | Line 248: | ||
|No | |No | ||
|No | |No | ||
| | |''CREBBP'' has been reported to be mutated in a high proportion of relapsing high hyperdiploid childhood ALLs<ref>{{Cite journal|last=Inthal|first=A.|last2=Zeitlhofer|first2=P.|last3=Zeginigg|first3=M.|last4=Morak|first4=M.|last5=Grausenburger|first5=R.|last6=Fronkova|first6=E.|last7=Fahrner|first7=B.|last8=Mann|first8=G.|last9=Haas|first9=O. A.|date=2012-08|title=CREBBP HAT domain mutations prevail in relapse cases of high hyperdiploid childhood acute lymphoblastic leukemia|url=https://pubmed.ncbi.nlm.nih.gov/22388726|journal=Leukemia|volume=26|issue=8|pages=1797–1803|doi=10.1038/leu.2012.60|issn=1476-5551|pmc=4194312|pmid=22388726}}</ref>. | ||
|- | |- | ||
|''WHSC1'' | |''WHSC1'' | ||
| Line 300: | Line 256: | ||
|No | |No | ||
|No | |No | ||
| | |N/A | ||
|- | |- | ||
|''SUV420H1'' | |''SUV420H1'' | ||
| Line 308: | Line 264: | ||
|No | |No | ||
|No | |No | ||
| | |N/A | ||
|- | |- | ||
|''SETD2'' | |''SETD2'' | ||
| Line 316: | Line 272: | ||
|No | |No | ||
|No | |No | ||
| | |N/A | ||
|- | |- | ||
|''EZH2'' | |''EZH2'' | ||
| Line 324: | Line 280: | ||
|No | |No | ||
|No | |No | ||
| | |N/A | ||
|}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. | |}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. | ||
==Epigenomic Alterations== | ==Epigenomic Alterations== | ||
No relevant epigenomic alterations | No relevant epigenomic alterations have been described<ref name=":3" />. | ||
==Genes and Main Pathways Involved== | ==Genes and Main Pathways Involved== | ||
{| class="wikitable sortable" | {| class="wikitable sortable" | ||
|- | |- | ||
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==Genetic Diagnostic Testing Methods== | ==Genetic Diagnostic Testing Methods== | ||
Hyperdiploidy is readily identifiable by conventional chromosome studies, FISH and CMA. CMA studies have shown that approximately 80% of hyperdiploid cases have additional genomic abnormalities with chromosomes commonly involved being 1, 9, 11, 12, and X | * Hyperdiploidy is readily identifiable by conventional chromosome studies, FISH and CMA. | ||
* CMA studies have shown that approximately 80% of hyperdiploid cases have additional genomic abnormalities with chromosomes commonly involved being 1, 9, 11, 12, and X<ref name=":4">{{Cite journal|last=Paulsson|first=Kajsa|last2=Forestier|first2=Erik|last3=Lilljebjörn|first3=Henrik|last4=Heldrup|first4=Jesper|last5=Behrendtz|first5=Mikael|last6=Young|first6=Bryan D.|last7=Johansson|first7=Bertil|date=2010-12-14|title=Genetic landscape of high hyperdiploid childhood acute lymphoblastic leukemia|url=https://pubmed.ncbi.nlm.nih.gov/21098271|journal=Proceedings of the National Academy of Sciences of the United States of America|volume=107|issue=50|pages=21719–21724|doi=10.1073/pnas.1006981107|issn=1091-6490|pmc=3003126|pmid=21098271}}</ref><ref>{{Cite journal|last=Schraders|first=Margit|last2=van Reijmersdal|first2=Simon V.|last3=Kamping|first3=Eveline J.|last4=van Krieken|first4=Johan H. J. M.|last5=van Kessel|first5=Ad Geurts|last6=Groenen|first6=Patricia J. T. A.|last7=Hoogerbrugge|first7=Peter M.|last8=Kuiper|first8=Roland P.|date=2009-05|title=High-resolution genomic profiling of pediatric lymphoblastic lymphomas reveals subtle differences with pediatric acute lymphoblastic leukemias in the B-lineage|url=https://pubmed.ncbi.nlm.nih.gov/19389505|journal=Cancer Genetics and Cytogenetics|volume=191|issue=1|pages=27–33|doi=10.1016/j.cancergencyto.2009.01.002|issn=1873-4456|pmid=19389505}}</ref><ref>{{Cite journal|last=Steeghs|first=Elisabeth M. P.|last2=Boer|first2=Judith M.|last3=Hoogkamer|first3=Alex Q.|last4=Boeree|first4=Aurélie|last5=de Haas|first5=Valerie|last6=de Groot-Kruseman|first6=Hester A.|last7=Horstmann|first7=Martin A.|last8=Escherich|first8=Gabriele|last9=Pieters|first9=Rob|date=03 15, 2019|title=Copy number alterations in B-cell development genes, drug resistance, and clinical outcome in pediatric B-cell precursor acute lymphoblastic leukemia|url=https://pubmed.ncbi.nlm.nih.gov/30874617|journal=Scientific Reports|volume=9|issue=1|pages=4634|doi=10.1038/s41598-019-41078-4|issn=2045-2322|pmc=6420659|pmid=30874617}}</ref><ref>{{Cite journal|last=Lejman|first=Monika|last2=Zawitkowska|first2=Joanna|last3=Styka|first3=Borys|last4=Babicz|first4=Mariusz|last5=Winnicka|first5=Dorota|last6=Zaucha-Prażmo|first6=Agnieszka|last7=Pastorczak|first7=Agata|last8=Taha|first8=Joanna|last9=Młynarski|first9=Wojciech|date=08 2019|title=Microarray testing as an efficient tool to redefine hyperdiploid paediatric B-cell precursor acute lymphoblastic leukaemia patients|url=https://pubmed.ncbi.nlm.nih.gov/31202078|journal=Leukemia Research|volume=83|pages=106163|doi=10.1016/j.leukres.2019.05.013|issn=1873-5835|pmid=31202078}}</ref>. | |||
<ref>{{Cite journal|last=Paulsson|first=Kajsa|last2=Forestier|first2=Erik|last3=Lilljebjörn|first3=Henrik|last4=Heldrup|first4=Jesper|last5=Behrendtz|first5=Mikael|last6=Young|first6=Bryan D.|last7=Johansson|first7=Bertil|date=2010-12-14|title=Genetic landscape of high hyperdiploid childhood acute lymphoblastic leukemia|url=https://pubmed.ncbi.nlm.nih.gov/21098271|journal=Proceedings of the National Academy of Sciences of the United States of America|volume=107|issue=50|pages=21719–21724|doi=10.1073/pnas.1006981107|issn=1091-6490|pmc=3003126|pmid=21098271}}</ref> <ref>{{Cite journal|last=Schraders|first=Margit|last2=van Reijmersdal|first2=Simon V.|last3=Kamping|first3=Eveline J.|last4=van Krieken|first4=Johan H. J. M.|last5=van Kessel|first5=Ad Geurts|last6=Groenen|first6=Patricia J. T. A.|last7=Hoogerbrugge|first7=Peter M.|last8=Kuiper|first8=Roland P.|date=2009-05|title=High-resolution genomic profiling of pediatric lymphoblastic lymphomas reveals subtle differences with pediatric acute lymphoblastic leukemias in the B-lineage|url=https://pubmed.ncbi.nlm.nih.gov/19389505|journal=Cancer Genetics and Cytogenetics|volume=191|issue=1|pages=27–33|doi=10.1016/j.cancergencyto.2009.01.002|issn=1873-4456|pmid=19389505}}</ref><ref>{{Cite journal|last=Steeghs|first=Elisabeth M. P.|last2=Boer|first2=Judith M.|last3=Hoogkamer|first3=Alex Q.|last4=Boeree|first4=Aurélie|last5=de Haas|first5=Valerie|last6=de Groot-Kruseman|first6=Hester A.|last7=Horstmann|first7=Martin A.|last8=Escherich|first8=Gabriele|last9=Pieters|first9=Rob|date=03 15, 2019|title=Copy number alterations in B-cell development genes, drug resistance, and clinical outcome in pediatric B-cell precursor acute lymphoblastic leukemia|url=https://pubmed.ncbi.nlm.nih.gov/30874617|journal=Scientific Reports|volume=9|issue=1|pages=4634|doi=10.1038/s41598-019-41078-4|issn=2045-2322|pmc=6420659|pmid=30874617}}</ref><ref>{{Cite journal|last=Lejman|first=Monika|last2=Zawitkowska|first2=Joanna|last3=Styka|first3=Borys|last4=Babicz|first4=Mariusz|last5=Winnicka|first5=Dorota|last6=Zaucha-Prażmo|first6=Agnieszka|last7=Pastorczak|first7=Agata|last8=Taha|first8=Joanna|last9=Młynarski|first9=Wojciech|date=08 2019|title=Microarray testing as an efficient tool to redefine hyperdiploid paediatric B-cell precursor acute lymphoblastic leukaemia patients|url=https://pubmed.ncbi.nlm.nih.gov/31202078|journal=Leukemia Research|volume=83|pages=106163|doi=10.1016/j.leukres.2019.05.013|issn=1873-5835|pmid=31202078}}</ref> | |||
==Familial Forms== | ==Familial Forms== | ||
No familial forms have been described | No familial forms have been described<ref name=":3" />. | ||
==Additional Information== | ==Additional Information== | ||
| Line 361: | Line 311: | ||
==References== | ==References== | ||
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