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2023-11-03T18:48:59Z

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			{{DISPLAYTITLE:B-Lymphoblastic Leukemia/Lymphoma with Hypodiploidy}}


			<blockquote class='blockedit'>{{Box-round\|title=PREVIOUS EDITION\|This page from the 4th edition of Haematolymphoid Tumours is being updated. See 5th edition [[HAEM5:Table_of_Contents\|Table of Contents]].
			}}</blockquote>
	==Primary Author(s)*==		==Primary Author(s)*==

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	~~[[Category:Karyotypic Patterns]]~~
	[[Copy Number and cn-LOH Abnormalities in ALL]		[[Copy Number and cn-LOH Abnormalities in ALL]
	[[Category:~~Recently Added Pages~~]]		[[Category:HAEM4]] [[Category:DISEASE]]

Bailey.Glen: Created page with "==Primary Author(s)*== Ashwini Yenamandra PhD FACMG Lisa Smith PhD FACMG Yassmine Akkari PhD FACMG TOC ==Cancer Category/Type== B lymphoblastic leukaemia/lymphoma, A..."

2023-11-03T18:09:24Z

Created page with "==Primary Author(s)*== Ashwini Yenamandra PhD FACMG Lisa Smith PhD FACMG Yassmine Akkari PhD FACMG __TOC__ ==Cancer Category/Type== B lymphoblastic leukaemia/lymphoma, A..."

New page

==Primary Author(s)*==

Ashwini Yenamandra PhD FACMG

Lisa Smith PhD FACMG

Yassmine Akkari PhD FACMG

__TOC__

==Cancer Category/Type==

B lymphoblastic leukaemia/lymphoma, Acute Lymphoblastic Leukemia (B-ALL)

==Cancer Sub-Classification / Subtype==

Hypodiploidy

==Definition / Description of Disease==

Hypodiploidy is a rare entity comprising approximately 5% of all B-cell acute lymphoblastic leukemias. The majority of cases (>80%) fall within the 44-45 chromosome range. However, beyond this, there are three main groups, that although rare, are associated with a very poor clinical prognosis.

[[File:Near-Haploid ALL Karyotype.jpg|Near-haploid karyotype with 26 Chromosomes in a 4-year-old. Note: Chromosomes 8, 10 and 21 have TWO copies. Courtesy of Ashwini Yenamandra, Vanderbilt University Medical Center, Nashville, TN.|frame|center]]

[[File:Doubled Haploid ALL Karyotype.jpg|Doubling of the near-haploid cell line with 52 Chromosomes. Note: Chromosomes 8, 10 and 21 have FOUR copies. Courtesy of Ashwini Yenamandra, Vanderbilt University Medical Center, Nashville, TN.|frame|center]]

==Synonyms / Terminology==

Hypodiploidy- High Hypodiploidy, Low Hypodiploidy, Near-haploidy

==Epidemiology / Prevalence==

Hypodiploid ALL accounts for about 5% of ALL cases. Approximately 1% of ALL cases with hypodiploidy have <45 chromosomes<ref name=":0">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, p206.</ref>. It is more common in children than adults and accounts for 75% of pediatric cancers<ref name=":4">Karen Seiter, MD; Chief Editor: Emmanuel C Besa, MD (2018). Acute lymphoblastic leukemia (ALL). Medscape. emedicine, Medscape Article, Drugs & Diseases, Hematology.</ref>. Hypodiploid ALL with chromosome numbers less than 44 is associated with poor prognosis.

==Clinical Features==

The clinical features are generally similar to those seen in other types of B-ALL like anemia, thrombocytopenia and neutropenia. May have very high WBC count at presentation. Malignant and poorly differentiated lymphoid cells in the bone marrow, peripheral blood and extramedullary sites<ref name=":1">{{Cite journal|last=Terwilliger|first=T.|last2=Abdul-Hay|first2=M.|date=2017|title=Acute lymphoblastic leukemia: a comprehensive review and 2017 update|url=https://www.ncbi.nlm.nih.gov/pubmed/28665419|journal=Blood Cancer Journal|volume=7|issue=6|pages=e577|doi=10.1038/bcj.2017.53|issn=2044-5385|pmc=5520400|pmid=28665419}}</ref>. Symptoms may include anemia, thrombocytopenia, leukopenia, fever, weight loss, night sweats, bleeding, bruising, fatigue<ref name=":1" />. Splenomegaly and hepatomegaly (20%), central nervous system (CNS) in 5-8% of patients<ref name=":1" />. Diagnosis: 20% of blasts or more lymphoblasts in the bone marrow, or peripheral blood<ref name=":1" />.

==Sites of Involvement==

Bone Marrow, Peripheral Blood, extra medullary sites.

==Morphologic Features==

Malignant and poorly differentiated lymphoid cells in the bone marrow, peripheral blood and extramedullary sites<ref name=":1" />. Symptoms may include anemia, thrombocytopenia, leukopenia, fever, weight loss, night sweats, bleeding, bruising, fatigue<ref name=":1" />. Splenomegaly and hepatomegaly (20%), central nervous system (CNS) in 5-8% of patients<ref name=":1" />. Diagnosis: 20% of blasts or more lymphoblasts in the bone marrow, or peripheral blood<ref name=":1" />

==Immunophenotype==

Put your text here and/or fill in the table

{| class="wikitable sortable"
|-
!Finding!!Marker
|-
|Positive||CD19
|-
|Positive||CD10
|-
|Negative (universal)||EXAMPLE CD3
|-
|Negative (subset)||EXAMPLE CD4
|}

==Chromosomal Rearrangements (Gene Fusions)==

N/A

==Characteristic Chromosomal Aberrations / Patterns==

'''Based on WHO classification'''<ref name=":0" />''', hypodiploidy is divided into:'''

1. '''Near-haploidy (NH=23-29 chromosomes)'''
This is a very rare category, has been observed in the pediatric population with virtually no adult cases reported. Nonrandom retention of the X chromosome plus chromosomes 8, 14, 18, and 21 are frequently observed.

2. '''Low Hypodiploidy (LH=33-39 chromosomes)'''
This category was reported in both children and adults. Nonrandom retention of two copies of chromosomes from the following: the sex chromosomes plus chromosomes 1,6, 8, 10, 14, 18, and19. Chromosome 21 is almost always retained in two copies.

3. '''High Hypodiploidy (HH=40-43 chromosomes)'''
This category was observed in both children and adults. Chromosome abnormalities include whole chromosome loss, specifically one sex chromosome and often chromosomes 7, 9, and/or 13. Also detected are structural anomalies especially dicentric chromosomes involving chromosomes 7, 9 or 12.

4. '''Near-diploid (ND=44-45 chromosomes)'''
This category is not often included in hypodiploid.

'''Note: A slight variation in the range of chromosome number has been reported in the literature in the classification of NH, LH, HH and NH'''<ref name=":0" /><ref name=":1" /><ref name=":2" /><ref name=":5" /><ref name=":3" /><ref>{{Cite journal|last=Safavi|first=Setareh|last2=Paulsson|first2=Kajsa|date=2017|title=Near-haploid and low-hypodiploid acute lymphoblastic leukemia: two distinct subtypes with consistently poor prognosis|url=https://www.ncbi.nlm.nih.gov/pubmed/27903530|journal=Blood|volume=129|issue=4|pages=420–423|doi=10.1182/blood-2016-10-743765|issn=1528-0020|pmid=27903530}}</ref><ref>{{Cite journal|last=Mehta|first=Parinda A.|last2=Zhang|first2=Mei-Jie|last3=Eapen|first3=Mary|last4=He|first4=Wensheng|last5=Seber|first5=Adriana|last6=Gibson|first6=Brenda|last7=Camitta|first7=Bruce M.|last8=Kitko|first8=Carrie L.|last9=Dvorak|first9=Christopher C.|date=2015|title=Transplantation Outcomes for Children with Hypodiploid Acute Lymphoblastic Leukemia|url=https://www.ncbi.nlm.nih.gov/pubmed/25865650|journal=Biology of Blood and Marrow Transplantation: Journal of the American Society for Blood and Marrow Transplantation|volume=21|issue=7|pages=1273–1277|doi=10.1016/j.bbmt.2015.04.008|issn=1523-6536|pmc=4465998|pmid=25865650}}</ref><ref>{{Cite journal|last=Mullighan|first=Charles G.|date=2012|title=Molecular genetics of B-precursor acute lymphoblastic leukemia|url=https://www.ncbi.nlm.nih.gov/pubmed/23023711|journal=The Journal of Clinical Investigation|volume=122|issue=10|pages=3407–3415|doi=10.1172/JCI61203|issn=1558-8238|pmc=3461902|pmid=23023711}}</ref><ref>{{Cite journal|last=Harrison|first=Christine J.|last2=Moorman|first2=Anthony V.|last3=Broadfield|first3=Zoë J.|last4=Cheung|first4=Kan L.|last5=Harris|first5=Rachel L.|last6=Reza Jalali|first6=G.|last7=Robinson|first7=Hazel M.|last8=Barber|first8=Kerry E.|last9=Richards|first9=Sue M.|date=2004|title=Three distinct subgroups of hypodiploidy in acute lymphoblastic leukaemia|url=https://www.ncbi.nlm.nih.gov/pubmed/15147369|journal=British Journal of Haematology|volume=125|issue=5|pages=552–559|doi=10.1111/j.1365-2141.2004.04948.x|issn=0007-1048|pmid=15147369}}</ref><ref>{{Cite journal|last=Wang|first=Yunhong|last2=Miller|first2=Sue|last3=Roulston|first3=Diane|last4=Bixby|first4=Dale|last5=Shao|first5=Lina|date=2016|title=Genome-Wide Single-Nucleotide Polymorphism Array Analysis Improves Prognostication of Acute Lymphoblastic Leukemia/Lymphoma|url=https://www.ncbi.nlm.nih.gov/pubmed/27161658|journal=The Journal of molecular diagnostics: JMD|volume=18|issue=4|pages=595–603|doi=10.1016/j.jmoldx.2016.03.004|issn=1943-7811|pmid=27161658}}</ref><ref>{{Cite journal|last=Safavi|first=Setareh|last2=Olsson|first2=Linda|last3=Biloglav|first3=Andrea|last4=Veerla|first4=Srinivas|last5=Blendberg|first5=Molly|last6=Tayebwa|first6=Johnbosco|last7=Behrendtz|first7=Mikael|last8=Castor|first8=Anders|last9=Hansson|first9=Markus|date=2015|title=Genetic and epigenetic characterization of hypodiploid acute lymphoblastic leukemia|url=https://www.ncbi.nlm.nih.gov/pubmed/26544893|journal=Oncotarget|volume=6|issue=40|pages=42793–42802|doi=10.18632/oncotarget.6000|issn=1949-2553|pmc=4767471|pmid=26544893}}</ref> <ref>{{Cite journal|last=Moorman|first=Anthony V.|date=2016|title=New and emerging prognostic and predictive genetic biomarkers in B-cell precursor acute lymphoblastic leukemia|url=https://www.ncbi.nlm.nih.gov/pubmed/27033238|journal=Haematologica|volume=101|issue=4|pages=407–416|doi=10.3324/haematol.2015.141101|issn=1592-8721|pmc=5004393|pmid=27033238}}</ref><ref>{{Cite journal|last=Fang|first=Min|last2=Becker|first2=Pamela S.|last3=Linenberger|first3=Michael|last4=Eaton|first4=Keith D.|last5=Appelbaum|first5=Frederick R.|last6=Dreyer|first6=ZoAnn|last7=Airewele|first7=Gladstone|last8=Redell|first8=Michele|last9=Lopez-Terrada|first9=Dolores|date=2015|title=Adult Low-Hypodiploid Acute B-Lymphoblastic Leukemia With IKZF3 Deletion and TP53 Mutation: Comparison With Pediatric Patients|url=https://www.ncbi.nlm.nih.gov/pubmed/26185311|journal=American Journal of Clinical Pathology|volume=144|issue=2|pages=263–270|doi=10.1309/AJCPW83OXPYKPEEN|issn=1943-7722|pmid=26185311}}</ref><ref>{{Cite journal|last=Mühlbacher|first=Verena|last2=Zenger|first2=Melanie|last3=Schnittger|first3=Susanne|last4=Weissmann|first4=Sandra|last5=Kunze|first5=Franziska|last6=Kohlmann|first6=Alexander|last7=Bellos|first7=Frauke|last8=Kern|first8=Wolfgang|last9=Haferlach|first9=Torsten|date=2014|title=Acute lymphoblastic leukemia with low hypodiploid/near triploid karyotype is a specific clinical entity and exhibits a very high TP53 mutation frequency of 93%|url=https://www.ncbi.nlm.nih.gov/pubmed/24619868|journal=Genes, Chromosomes & Cancer|volume=53|issue=6|pages=524–536|doi=10.1002/gcc.22163|issn=1098-2264|pmid=24619868}}</ref><ref>{{Cite journal|last=Woo|first=Jennifer S.|last2=Alberti|first2=Michael O.|last3=Tirado|first3=Carlos A.|date=2014|title=Childhood B-acute lymphoblastic leukemia: a genetic update|url=https://www.ncbi.nlm.nih.gov/pubmed/24949228|journal=Experimental Hematology & Oncology|volume=3|pages=16|doi=10.1186/2162-3619-3-16|issn=2162-3619|pmc=4063430|pmid=24949228}}</ref><ref>{{Cite journal|last=Collins-Underwood|first=J. R.|last2=Mullighan|first2=C. G.|date=2010|title=Genomic profiling of high-risk acute lymphoblastic leukemia|url=https://www.ncbi.nlm.nih.gov/pubmed/20739952|journal=Leukemia|volume=24|issue=10|pages=1676–1685|doi=10.1038/leu.2010.177|issn=1476-5551|pmid=20739952}}</ref><ref name=":4" /> '''[1-17].'''

Sorting patients into these three rare groups is easy. However, detecting the presence of a masked low-hypodiploid/masked near-hypodiploid group, which is endoreduplication of the low- and near-haploid groups and associated with a very poor prognosis, is difficult. Often karyotypes in these two groups, usually ranging from 56-78 chromosomes, are mistaken for hyperdiploidy/near-triploidy, which in itself is associated with a good prognosis. The key is to look for trisomies vs tetrasomies of the chromosomes. Typically, hyperdiploidy/near-triploidy should have three copies of several chromosomes (usually the X, 4, 10, 17, and 18), and four copies of 14 and 21. However, the masked low-hypodiploid/masked near-hypodiploid groups should show tetrasomies for the sex chromosomes and chromosomes 1, 14, 18, 21, and 22 while having only two copies of chromosomes 7 and 17.

When only a 56-78 chromosome count is detected, the above mentioned criteria is helpful, but SNP-array testing can also be informative. Masked near-haploidy appears to show LOH involving the chromosomes that are not gained and true hyperdiploidy will show heterozygosity. Dicentric chromosomes reportedly originated from chromosomes 9p, 12p or 20q in near diploid karyotypes<ref name=":2">{{Cite journal|last=Holmfeldt|first=Linda|last2=Wei|first2=Lei|last3=Diaz-Flores|first3=Ernesto|last4=Walsh|first4=Michael|last5=Zhang|first5=Jinghui|last6=Ding|first6=Li|last7=Payne-Turner|first7=Debbie|last8=Churchman|first8=Michelle|last9=Andersson|first9=Anna|date=2013|title=The genomic landscape of hypodiploid acute lymphoblastic leukemia|url=https://www.ncbi.nlm.nih.gov/pubmed/23334668|journal=Nature Genetics|volume=45|issue=3|pages=242–252|doi=10.1038/ng.2532|issn=1546-1718|pmc=3919793|pmid=23334668}}</ref>. In near haploid aneuploidy of chromosomes 1 through 7, 9, 11, 13, 15-17, 19,20, 22 while in low hypodiploid aneuploidy of chromosomes 2 through 4, 7, 9, 12, 13, 15 and 17 were reported<ref name=":2" />.

Near haploidy may be the primary event with loss of chromosomes, followed by a secondary event of doubling of chromosomes indicating uniparental isodisomy (UPID), microdeletions if any may occur after the secondary event<ref name=":5">{{Cite journal|last=Safavi|first=S.|last2=Forestier|first2=E.|last3=Golovleva|first3=I.|last4=Barbany|first4=G.|last5=Nord|first5=K. H.|last6=Moorman|first6=A. V.|last7=Harrison|first7=C. J.|last8=Johansson|first8=B.|last9=Paulsson|first9=K.|date=2013|title=Loss of chromosomes is the primary event in near-haploid and low-hypodiploid acute lymphoblastic leukemia|url=https://www.ncbi.nlm.nih.gov/pubmed/22889820|journal=Leukemia|volume=27|issue=1|pages=248–250|doi=10.1038/leu.2012.227|issn=1476-5551|pmid=22889820}}</ref>.

In hypodiploid ALL, molecular mutations are equally as important as chromosome number, or as a result of chromosome number, molecular mutations have a driving effect. Both LH and NH have common mutations involved in the disease process. In near haploid ALL (NH) ''RTK'' and ''RAS'' (71%) signaling were a hallmark<ref name=":2" />. In addition, lymphoid transcription factor gene ''IKZF3'' (13%, encoding AIOLOS) and deletions of histone cluster at 6p22 (19%) were also reported<ref name=":2" />. In low hypodiploid (LH) ALL mutations involved ''TP53'' (91.2%) and ''IKZF2'' (53%, encoding HELIOS, 2q34), and ''RB1'' genes (41%) loci<ref name=":2" />. Both NH and LH had activation of RAS signaling and P13K signaling pathways and sensitive to P13K inhibitors indicating these drugs may offer a new therapeutic option<ref name=":2" />. Inn this group, several studies have not only identified a high percentage of pediatric patients with ''TP53'' mutations, but close to half displayed germline mutations, suggesting that LH ALL is a manifestation of Li-Fraumeni syndrome in children. Adults also showed a high incidence of ''TP53'' (91%) in low hypodiploid ALL mutations, but these mutations appear to be somatic in origin. In NH, mutations appear in genes involving receptor tyrosine kinase (RTK) pathway, Ras signaling, ''IKZF3'' (17q21.1), and histone clusters, but rarely ''IZFK2'', ''RB1'', or ''TP53''<ref name=":2" />.

Copy number alterations and sequence mutations have been reported in ''FLT3'', ''NF1'', ''KRAS'', ''NRAS'', ''PTPN11'', ''RTK'', ''RAS'', ''IKZF1'', ''IKZF2'', ''IKZF3'', ''TP53'', ''RB1'', Histone, 6q22, ''CDKN2A'', ''CDKN2B'', ''PAX5'', and ''PAG1'' gene loci<ref name=":2" />.

The most significant observation by Holmfeldt et al.,<ref name=":2" /> is that a global difference in the gene expression profiles distinguishes subgroups of hypodiploid ALL. More than 600 genes had subtype specific enrichment on gene set enrichment analysis<ref name=":2" />. In addition, RAS pathway, ''RB1'' and ''TP53'' mutations mimic solid tumor pathways<ref name=":2" />.

==Genomic Gain/Loss/LOH==

{| class="wikitable sortable"
|-
!Chromosome Number!!Gain/Loss/Amp/LOH!!Region
|-
|17||Gain||SOX9
|-
|9||Loss||CDKN2A/CDKN2B (22-50%)
|}

==Gene Mutations (SNV/INDEL)==

{| class="wikitable sortable"
|-
!Gene!!Mutation!!Oncogene/Tumor Suppressor/Other!!Presumed Mechanism (LOF/GOF/Other; Driver/Passenger)!!Prevalence (COSMIC/TCGA/Other)
|-
|TP53||R280S, Y220C and several other mutations, please see reference<ref name=":2" />.||Tumor Suppressor||Missense/Nonsense/Insertion/Splice||in Low Hypodiploid about 90%
|}

===Other Mutations===

'''RTK-RAS signaling pathways''': About two-thirds of near haploid ALL (71%) had activation of RTK-RAS signaling pathways including deletion, amplification and sequence mutation of ''NF1'', ''NRAS'', ''KRAS'', ''MAPK1'', ''FLT3'' and ''PTPN11''<ref name=":2" />. ''NF1'' mutation was reported in 44% of near haploid cases with a biallelic mutation of ''NF1'' in 77% of the near haploid cases. In 68% of the cases, the ''NF1'' deletions were intragenic involving exons 15 through 35<ref name=":2" />. The focal deletion results in deletion of ''GAP''<ref name=":2" />.

'''''PAG1'' mutations''': Recurrent alterations of ''PAG1'' was reported in 10.3% of near haploid ALL, ''PAG1'' mutations are rare in other hypodiploid cases<ref name=":2" />. ''PAG1'' was identified as a putative RAS signaling inhibitor and have a negative regulatory function in proximal B-cell receptor signaling<ref name=":2" />.

'''''TP53'' mutations''': High mutation rate was observed (91%) in low hypodiploid than in non-low hypodiploid (5%) B-ALL; In low hypodiploid ALL, 43% were observed in non-tumor hematopoietic cells, suggesting either an inherited or a germline ''de novo'' origin of the mutation<ref name=":2" />.

==Epigenomics (Methylation)==

In near haploid 19% of the cases had focal deletions of histone gene cluster at 6p22, however, non-hypodiploid ALL had 8%, lower frequency of these deletions<ref name=":2" />.

Of the 25 next generation sequenced haploid cases 16 (64%) cases had twenty six histone modifier gene mutations and of the 15 low hypodiploid ALL cases 9 (60%) cases had 9 mutations; the most common mutation (32%) of the near haploid cases was transcriptional co-activator and histone acetyltransferase ''CREBBP''<ref name=":2" />.

==Genes and Main Pathways Involved==

RTK and RAS pathway alterations as ''de novo'' germline mutations or in primitive hematopoietic progenitor cells<ref name=":2" />.

==Diagnostic Testing Methods==

FLOW, Hematopathology, Cytogenetics, Fluorescence insitu Hybridization (FISH), Next Generation sequencing (NGS), Exome sequencing, Microarray.

==Clinical Significance (Diagnosis, Prognosis and Therapeutic Implications)==

B-lymphoblastic leukemia/lymphoma (B-ALL/LBL) is the most common cause of cancer in pediatric patients. It is characterized by recurrent genetic abnormalities of chromosome number, deletions, duplications and translocations. Hypodiploidy, a neoplasm of lymphoblasts containing less than 46 chromosomes<ref name=":0" />. Hypodiploid ALL has poor prognosis and near haploid with worst prognosis<ref name=":0" /><ref name=":2" /><ref name=":3">{{Cite journal|last=Nachman|first=James B.|last2=Heerema|first2=Nyla A.|last3=Sather|first3=Harland|last4=Camitta|first4=Bruce|last5=Forestier|first5=Erik|last6=Harrison|first6=Christine J.|last7=Dastugue|first7=Nicole|last8=Schrappe|first8=Martin|last9=Pui|first9=Ching-Hon|date=2007|title=Outcome of treatment in children with hypodiploid acute lymphoblastic leukemia|url=https://www.ncbi.nlm.nih.gov/pubmed/17473063|journal=Blood|volume=110|issue=4|pages=1112–1115|doi=10.1182/blood-2006-07-038299|issn=0006-4971|pmc=1939895|pmid=17473063}}</ref>.

Patients with 44 chromosomes had a better event free survival (EFS) than patients with fewer than 44 chromosomes<ref name=":3" />. However, patients with 44 chromosomes and monosomy 7 or a dicentric chromosome had worse EFS<ref name=":3" />. Children and adults with less than 44 chromosomes had poor outcome despite contemporary therapy<ref name=":3" />.

In near haploid cases, two-thirds had activation of RAS signaling and P13K signaling pathways; these are sensitive to P13K inhibitors indicating these drugs may offer a new therapeutic option<ref name=":2" />.

==Familial Forms==

In Low hypodiploid (LH), several studies have not only identified a high percentage of pediatric patients with ''TP53'' mutations, but close to half displayed germline mutations, suggesting that LH ALL is a manifestation of Li-Fraumeni syndrome in children.

Adults also showed a high incidence of ''TP53'' mutations, but these mutations appear to be somatic in origin. In NH, mutations of genes of receptor tyrosine kinase (RTK) pathway, Ras signaling, ''IKZF3'' (17q21.1) and histone clusters, but mutations of ''IZFK2'', ''RB1'', or ''TP53'' were rare.

==Other Information==

Genetic abnormalities involving ''TP53'', ''RB1'' and ''IKZF2'' are hallmarks of low hypodiploid ALL, where as near haploid ALL has ''RTK'', ''RAS'' and ''IKZF3'' alterations<ref name=":2" />.

==Links==

N/A

==References==
<references />
==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.

[[Category:Karyotypic Patterns]]
[[Copy Number and cn-LOH Abnormalities in ALL]
[[Category:Recently Added Pages]]

HAEM4:B-Lymphoblastic Leukemia/Lymphoma with Hypodiploidy - Revision history

Bailey.Glen at 18:48, 3 November 2023

Bailey.Glen: Created page with "==Primary Author(s)*== Ashwini Yenamandra PhD FACMG Lisa Smith PhD FACMG Yassmine Akkari PhD FACMG __TOC__ ==Cancer Category/Type== B lymphoblastic leukaemia/lymphoma, A..."

Bailey.Glen: Created page with "==Primary Author(s)*== Ashwini Yenamandra PhD FACMG Lisa Smith PhD FACMG Yassmine Akkari PhD FACMG TOC ==Cancer Category/Type== B lymphoblastic leukaemia/lymphoma, A..."