Compendium of Cancer Genome Aberrations

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HAEM5:ALK-positive anaplastic large cell lymphoma (view source)

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{{DISPLAYTITLE:ALK-positive anaplastic large cell lymphoma}}
 
{{DISPLAYTITLE:ALK-positive anaplastic large cell lymphoma}}
 +
 
[[HAEM5:Table_of_Contents|Haematolymphoid Tumours (5th ed.)]]
 
[[HAEM5:Table_of_Contents|Haematolymphoid Tumours (5th ed.)]]
    
{{Under Construction}}
 
{{Under Construction}}
   −
<blockquote class='blockedit'>{{Box-round|title=HAEM5 Conversion Notes|This page was converted to the new template on 2023-12-07. The original page can be found at [[HAEM4:Anaplastic Large Cell Lymphoma, ALK-Positive]].
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<blockquote class="blockedit">{{Box-round|title=HAEM5 Conversion Notes|This page was converted to the new template on 2023-12-07. The original page can be found at [[HAEM4:Anaplastic Large Cell Lymphoma, ALK-Positive]].
 
}}</blockquote>
 
}}</blockquote>
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==Primary Author(s)*==
 
==Primary Author(s)*==
   −
Put your text here<span style="color:#0070C0"> (''Name and affiliation; example:'' Jane Smith, PhD, Institute of Genomics) </span>
+
Miguel Gonzalez Mancera, MD, Cedars-Sinai, Los Angeles, CA
 +
 
 +
Sumire Kitahara, MD, Cedars-Sinai, Los Angeles, CA
    
__TOC__
 
__TOC__
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{| class="wikitable"
 
{| class="wikitable"
 
|'''Signs and Symptoms'''
 
|'''Signs and Symptoms'''
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|EXAMPLE Asymptomatic (incidental finding on complete blood counts)
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|Most patients (70%) present with advanced (stage III-IV) disease and B-symptoms.<ref name=":19" />
−
 
  −
EXAMPLE B-symptoms (weight loss, fever, night sweats)
  −
 
  −
EXAMPLE Fatigue
  −
 
  −
EXAMPLE Lymphadenopathy (uncommon)
   
|-
 
|-
 
|'''Laboratory Findings'''
 
|'''Laboratory Findings'''
−
|EXAMPLE Cytopenias
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|Noncontributory
−
 
  −
EXAMPLE Lymphocytosis (low level)
   
|}
 
|}
      −
<blockquote class='blockedit'>{{Box-round|title=v4:Clinical Features|The content below was from the old template. Please incorporate above.}}
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<blockquote class="blockedit">{{Box-round|title=v4:Clinical Features|The content below was from the old template. Please incorporate above.}}
   −
*Most patients (70%) present with advanced (stage III-IV) disease and B-symptoms.<ref>{{Cite journal|last=Savage|first=Kerry J.|last2=Harris|first2=Nancy Lee|last3=Vose|first3=Julie M.|last4=Ullrich|first4=Fred|last5=Jaffe|first5=Elaine S.|last6=Connors|first6=Joseph M.|last7=Rimsza|first7=Lisa|last8=Pileri|first8=Stefano A.|last9=Chhanabhai|first9=Mukesh|date=2008-06-15|title=ALK- anaplastic large-cell lymphoma is clinically and immunophenotypically different from both ALK+ ALCL and peripheral T-cell lymphoma, not otherwise specified: report from the International Peripheral T-Cell Lymphoma Project|url=https://pubmed.ncbi.nlm.nih.gov/18385450/|journal=Blood|volume=111|issue=12|pages=5496–5504|doi=10.1182/blood-2008-01-134270|issn=1528-0020|pmid=18385450}}</ref>
+
*Most patients (70%) present with advanced (stage III-IV) disease and B-symptoms.<ref name=":19">{{Cite journal|last=Savage|first=Kerry J.|last2=Harris|first2=Nancy Lee|last3=Vose|first3=Julie M.|last4=Ullrich|first4=Fred|last5=Jaffe|first5=Elaine S.|last6=Connors|first6=Joseph M.|last7=Rimsza|first7=Lisa|last8=Pileri|first8=Stefano A.|last9=Chhanabhai|first9=Mukesh|date=2008-06-15|title=ALK- anaplastic large-cell lymphoma is clinically and immunophenotypically different from both ALK+ ALCL and peripheral T-cell lymphoma, not otherwise specified: report from the International Peripheral T-Cell Lymphoma Project|url=https://pubmed.ncbi.nlm.nih.gov/18385450/|journal=Blood|volume=111|issue=12|pages=5496–5504|doi=10.1182/blood-2008-01-134270|issn=1528-0020|pmid=18385450}}</ref>
    
</blockquote>
 
</blockquote>
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*Lymph nodes and extranodal sites (most commonly skin, bone, soft tissue, lungs and liver)
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*Lymph nodes and extranodal sites (most commonly skin, bone, soft tissue, lungs and liver)<ref name=":0" />
 
*Bone marrow involvement detected in 30% when using immunohistochemistry (CD30 and EMA). Can miss marrow involvement by H&E evaluation alone, which detects involvement with ~10% incidence.<ref>{{Cite journal|last=M|first=Fraga|last2=P|first2=Brousset|last3=D|first3=Schlaifer|last4=C|first4=Payen|last5=A|first5=Robert|last6=H|first6=Rubie|last7=F|first7=Huguet-Rigal|last8=G|first8=Delsol|date=1995|title=Bone marrow involvement in anaplastic large cell lymphoma. Immunohistochemical detection of minimal disease and its prognostic significance|url=https://pubmed.ncbi.nlm.nih.gov/7817951/|language=en|pmid=7817951}}</ref>
 
*Bone marrow involvement detected in 30% when using immunohistochemistry (CD30 and EMA). Can miss marrow involvement by H&E evaluation alone, which detects involvement with ~10% incidence.<ref>{{Cite journal|last=M|first=Fraga|last2=P|first2=Brousset|last3=D|first3=Schlaifer|last4=C|first4=Payen|last5=A|first5=Robert|last6=H|first6=Rubie|last7=F|first7=Huguet-Rigal|last8=G|first8=Delsol|date=1995|title=Bone marrow involvement in anaplastic large cell lymphoma. Immunohistochemical detection of minimal disease and its prognostic significance|url=https://pubmed.ncbi.nlm.nih.gov/7817951/|language=en|pmid=7817951}}</ref>
      −
<blockquote class='blockedit'>{{Box-round|title=Unassigned References|The following referenees were placed in the header. Please place them into the appropriate locations in the text.}}<ref name=":0" /></blockquote>
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<blockquote class="blockedit">{{Box-round|title=Unassigned References|The following referenees were placed in the header. Please place them into the appropriate locations in the text.}}<ref name=":0" /></blockquote>
 
==Morphologic Features==
 
==Morphologic Features==
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!Finding!!Marker
 
!Finding!!Marker
 
|-
 
|-
−
|Positive (universal)||EXAMPLE CD1
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|Positive (universal) - Cell membrane and Golgi; large lymphoma cells show strongest staining; smaller cells may show weak, partial to negative staining||CD30
 
|-
 
|-
−
|Positive (subset)||EXAMPLE CD2
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|Positive (universal) - Cellular location of ALK staining varies depending on ALK translocation partner. In the most common t(2;5), most cases show both cytoplasmic and nuclear||ALK
 
|-
 
|-
−
|Negative (universal)||EXAMPLE CD3
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|Positive (subset) ||EMA
 
|-
 
|-
−
|Negative (subset)||EXAMPLE CD4
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|Negative - >75% of cases are CD3-negative||CD3
 +
|-
 +
|Positive (70%)
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|CD4
 +
|-
 +
|Negative in majority of cases
 +
|CD8
 +
|-
 +
|Positive in majority of cases
 +
|CD2
 +
|-
 +
|Positive in majority of cases
 +
|CD5
 +
|-
 +
|Positive
 +
|TIA1
 +
|-
 +
|Positive
 +
|Granzyme B
 +
|-
 +
|Positive
 +
|Perforin
 +
|-
 +
|Variably positive
 +
|CD45
 +
|-
 +
|Positive (universal)
 +
|CD25
 +
|-
 +
|Negative (universal)
 +
|BCL2
 
|}
 
|}
      −
<blockquote class='blockedit'>{{Box-round|title=v4:Immunophenotype|The content below was from the old template. Please incorporate above.}}
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<blockquote class="blockedit">{{Box-round|title=v4:Immunophenotype|The content below was from the old template. Please incorporate above.}}
 
[[ALK]]+ ALCL show the following staining pattern<ref>{{Cite journal|last=Montes-Mojarro|first=Ivonne A.|last2=Steinhilber|first2=Julia|last3=Bonzheim|first3=Irina|last4=Quintanilla-Martinez|first4=Leticia|last5=Fend|first5=Falko|date=2018-04-04|title=The Pathological Spectrum of Systemic Anaplastic Large Cell Lymphoma (ALCL)|url=https://pubmed.ncbi.nlm.nih.gov/29617304/|journal=Cancers|volume=10|issue=4|pages=E107|doi=10.3390/cancers10040107|issn=2072-6694|pmc=5923362|pmid=29617304}}</ref><ref>{{Cite journal|last=Stein|first=H.|last2=Foss|first2=H. D.|last3=Dürkop|first3=H.|last4=Marafioti|first4=T.|last5=Delsol|first5=G.|last6=Pulford|first6=K.|last7=Pileri|first7=S.|last8=Falini|first8=B.|date=2000-12-01|title=CD30(+) anaplastic large cell lymphoma: a review of its histopathologic, genetic, and clinical features|url=https://pubmed.ncbi.nlm.nih.gov/11090048/|journal=Blood|volume=96|issue=12|pages=3681–3695|issn=0006-4971|pmid=11090048}}</ref>:
 
[[ALK]]+ ALCL show the following staining pattern<ref>{{Cite journal|last=Montes-Mojarro|first=Ivonne A.|last2=Steinhilber|first2=Julia|last3=Bonzheim|first3=Irina|last4=Quintanilla-Martinez|first4=Leticia|last5=Fend|first5=Falko|date=2018-04-04|title=The Pathological Spectrum of Systemic Anaplastic Large Cell Lymphoma (ALCL)|url=https://pubmed.ncbi.nlm.nih.gov/29617304/|journal=Cancers|volume=10|issue=4|pages=E107|doi=10.3390/cancers10040107|issn=2072-6694|pmc=5923362|pmid=29617304}}</ref><ref>{{Cite journal|last=Stein|first=H.|last2=Foss|first2=H. D.|last3=Dürkop|first3=H.|last4=Marafioti|first4=T.|last5=Delsol|first5=G.|last6=Pulford|first6=K.|last7=Pileri|first7=S.|last8=Falini|first8=B.|date=2000-12-01|title=CD30(+) anaplastic large cell lymphoma: a review of its histopathologic, genetic, and clinical features|url=https://pubmed.ncbi.nlm.nih.gov/11090048/|journal=Blood|volume=96|issue=12|pages=3681–3695|issn=0006-4971|pmid=11090048}}</ref>:
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!Notes
 
!Notes
 
|-
 
|-
−
|EXAMPLE t(9;22)(q34;q11.2)||EXAMPLE 3'ABL1 / 5'BCR||EXAMPLE der(22)||EXAMPLE 20% (COSMIC)
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|t(2;5)(p23;q35)||3' ''ALK'' / 5' ''NPM1''<ref name=":20" />||''NPM1::ALK'' fusion protein||84%<ref name=":0" />
−
EXAMPLE 30% (add reference)
+
|No
−
|Yes
   
|No
 
|No
 
|Yes
 
|Yes
−
|EXAMPLE
+
|ALK inhibition ([https://www.fda.gov/drugs/drug-approvals-and-databases/fda-approves-crizotinib-children-and-young-adults-relapsed-or-refractory-systemic-anaplastic-large#:~:text=Approvals%20and%20Databases-,FDA%20approves%20crizotinib%20for%20children%20and%20young%20adults%20with%20relapsed,systemic%20anaplastic%20large%20cell%20lymphoma&text=On%20January%2014%2C%202021%2C%20the,(Xalkori%2C%20Pfizer%20Inc.) crizotinib]) can be an effective 2nd-line therapeutic strategy as ALK is essential for the proliferation and survival of ALK+ ALCL cells<ref name=":21" /><ref name=":2" /><ref name=":22" />
   −
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).
+
*Drug resistance may develop due to:
 +
*#Mutations of the ALK gene impairing binding of the inhibitor<ref name=":3" />; other ALK inhibitors are not currently FDA-approved for use in ALK+ ALCL
 +
*#See also gene mutations section above
 +
*#Engagement of other cell signaling pathways
 +
|-
 +
|t(1;2)(q25;p23)<ref name=":10" />
 +
|3' ''ALK'' / 5' ''TPM3''
 +
|''TPM3::ALK'' Fusion protein
 +
|13%<ref name=":10" />
 +
|No
 +
|No
 +
|No
 +
|
 +
|-
 +
|inv(2)(p23q35)<ref name=":11" />
 +
|3' ''ALK'' / 5' ''ATIC''
 +
|''ATIC::ALK'' fusion protein
 +
|1% <ref name=":11" />
 +
|No
 +
|No
 +
|No
 +
|
 +
|-
 +
|t(2;3)(p23;q12.2)<ref name=":12" />
 +
|3' ''ALK'' / 5' ''TFG''
 +
|''TFG::ALK'' fusion protein
 +
|<1%
 +
|No
 +
|No
 +
|No
 +
|
 +
|-
 +
|t(2;17)(p23;q23)<ref name=":13" />
 +
|3' ''ALK'' / 5' ''CLTC''
 +
|''CLTC::ALK'' fusion protein
 +
|<1%
 +
|No
 +
|No
 +
|No
 +
|
 +
|-
 +
|t(X;2)(q11-22;p23)<ref name=":14" />
 +
|3' ''ALK'' / 5' ''MSN''
 +
|''MSN::ALK'' fusion protein
 +
|<1%
 +
|No
 +
|No
 +
|No
 +
|
 +
|-
 +
|t(2;19)(p23;p13.1)<ref name=":6" />
 +
|3' ''ALK'' / 5' ''TPM4''
 +
|''TPM4::ALK'' fusion protein
 +
|<1%
 +
|No
 +
|No
 +
|No
 +
|
 +
|-
 +
|t(2;22)(p23;q11.2)<ref name=":15" />
 +
|3' ''ALK'' / 5' ''MYH9''
 +
|''MYH9::ALK'' fusion protein
 +
|<1%
 +
|No
 +
|No
 +
|No
 +
|
 +
|-
 +
|t(2;17)(p23;q25)<ref name=":6" />
 +
|3' ''ALK'' / 5' ''RNF213''
 +
|''RNF213::ALK'' fusion protein
 +
|<1%
 +
|No
 +
|No
 +
|No
 +
|
 +
|-
 +
|t(2;9)(p23;q33)<ref name=":16" />
 +
|3' ''ALK'' / 5' ''TRAF-1''
 +
|''TRAF-1::ALK'' fusion protein
 +
|<1%
 +
|No
 +
|No
 +
|No
 +
|
 
|}
 
|}
 
 
   −
<blockquote class='blockedit'>{{Box-round|title=v4:Chromosomal Rearrangements (Gene Fusions)|The content below was from the old template. Please incorporate above.}}
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<blockquote class="blockedit">{{Box-round|title=v4:Chromosomal Rearrangements (Gene Fusions)|The content below was from the old template. Please incorporate above.}}
    
*ALK(+) ALCL is characterized by chromosomal translocations involving ''ALK'' gene, a receptor tyrosine kinase domain at 2p23.
 
*ALK(+) ALCL is characterized by chromosomal translocations involving ''ALK'' gene, a receptor tyrosine kinase domain at 2p23.
−
*Approximately 80% of cases show a cytogenetic translocation t(2;5) (NPM1-ALK, t(2;5)(p23;q35)) which fuses the ''ALK'' gene to the nucleophosmine (NPM) gene at 5q35, resulting in the overexpression and constitutive activation of a chimeric ALK fusion protein, which plays an important role in ALK-mediated oncogenesis.<ref>{{Cite journal|last=Morris|first=S. W.|last2=Kirstein|first2=M. N.|last3=Valentine|first3=M. B.|last4=Dittmer|first4=K. G.|last5=Shapiro|first5=D. N.|last6=Saltman|first6=D. L.|last7=Look|first7=A. T.|date=1994-03-04|title=Fusion of a kinase gene, ALK, to a nucleolar protein gene, NPM, in non-Hodgkin's lymphoma|url=https://pubmed.ncbi.nlm.nih.gov/8122112/|journal=Science (New York, N.Y.)|volume=263|issue=5151|pages=1281–1284|doi=10.1126/science.8122112|issn=0036-8075|pmid=8122112}}</ref>
+
*Approximately 80% of cases show a cytogenetic translocation t(2;5) (NPM1-ALK, t(2;5)(p23;q35)) which fuses the ''ALK'' gene to the nucleophosmine (NPM) gene at 5q35, resulting in the overexpression and constitutive activation of a chimeric ALK fusion protein, which plays an important role in ALK-mediated oncogenesis.<ref name=":20">{{Cite journal|last=Morris|first=S. W.|last2=Kirstein|first2=M. N.|last3=Valentine|first3=M. B.|last4=Dittmer|first4=K. G.|last5=Shapiro|first5=D. N.|last6=Saltman|first6=D. L.|last7=Look|first7=A. T.|date=1994-03-04|title=Fusion of a kinase gene, ALK, to a nucleolar protein gene, NPM, in non-Hodgkin's lymphoma|url=https://pubmed.ncbi.nlm.nih.gov/8122112/|journal=Science (New York, N.Y.)|volume=263|issue=5151|pages=1281–1284|doi=10.1126/science.8122112|issn=0036-8075|pmid=8122112}}</ref>
 
**
 
**
 
*''ALK'' translocations may be seen in multiple malignancies including epithelial malignancies<ref>{{Cite journal|last=Holla|first=Vijaykumar R.|last2=Elamin|first2=Yasir Y.|last3=Bailey|first3=Ann Marie|last4=Johnson|first4=Amber M.|last5=Litzenburger|first5=Beate C.|last6=Khotskaya|first6=Yekaterina B.|last7=Sanchez|first7=Nora S.|last8=Zeng|first8=Jia|last9=Shufean|first9=Md Abu|date=2017-1|title=ALK: a tyrosine kinase target for cancer therapy|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5171696/|journal=Cold Spring Harbor Molecular Case Studies|volume=3|issue=1|pages=a001115|doi=10.1101/mcs.a001115|issn=2373-2873|pmc=5171696|pmid=28050598}}</ref><ref>{{Cite journal|last=Amatu|first=Alessio|last2=Somaschini|first2=Alessio|last3=Cerea|first3=Giulio|last4=Bosotti|first4=Roberta|last5=Valtorta|first5=Emanuele|last6=Buonandi|first6=Pasquale|last7=Marrapese|first7=Giovanna|last8=Veronese|first8=Silvio|last9=Luo|first9=David|date=2015-12-22|title=Novel CAD-ALK gene rearrangement is drugable by entrectinib in colorectal cancer|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4701996/|journal=British Journal of Cancer|volume=113|issue=12|pages=1730–1734|doi=10.1038/bjc.2015.401|issn=0007-0920|pmc=4701996|pmid=26633560}}</ref><ref>{{Cite journal|last=Camidge|first=D. Ross|last2=Kono|first2=Scott A.|last3=Lu|first3=Xian|last4=Okuyama|first4=Sonia|last5=Barón|first5=Anna E.|last6=Oton|first6=Ana B.|last7=Davies|first7=Angela M.|last8=Varella-Garcia|first8=Marileila|last9=Franklin|first9=Wilbur|date=2011-04|title=Anaplastic lymphoma kinase gene rearrangements in non-small cell lung cancer are associated with prolonged progression-free survival on pemetrexed|url=https://pubmed.ncbi.nlm.nih.gov/21336183/|journal=Journal of Thoracic Oncology: Official Publication of the International Association for the Study of Lung Cancer|volume=6|issue=4|pages=774–780|doi=10.1097/JTO.0b013e31820cf053|issn=1556-1380|pmc=3626562|pmid=21336183}}</ref><ref>{{Cite journal|last=Choi|first=Young Lim|last2=Takeuchi|first2=Kengo|last3=Soda|first3=Manabu|last4=Inamura|first4=Kentaro|last5=Togashi|first5=Yuki|last6=Hatano|first6=Satoko|last7=Enomoto|first7=Munehiro|last8=Hamada|first8=Toru|last9=Haruta|first9=Hidenori|date=2008-07-01|title=Identification of novel isoforms of the EML4-ALK transforming gene in non-small cell lung cancer|url=https://pubmed.ncbi.nlm.nih.gov/18593892/|journal=Cancer Research|volume=68|issue=13|pages=4971–4976|doi=10.1158/0008-5472.CAN-07-6158|issn=1538-7445|pmid=18593892}}</ref><ref>{{Cite journal|last=Kelly|first=Lindsey M.|last2=Barila|first2=Guillermo|last3=Liu|first3=Pengyuan|last4=Evdokimova|first4=Viktoria N.|last5=Trivedi|first5=Sumita|last6=Panebianco|first6=Federica|last7=Gandhi|first7=Manoj|last8=Carty|first8=Sally E.|last9=Hodak|first9=Steven P.|date=2014-03-18|title=Identification of the transforming STRN-ALK fusion as a potential therapeutic target in the aggressive forms of thyroid cancer|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3964116/|journal=Proceedings of the National Academy of Sciences of the United States of America|volume=111|issue=11|pages=4233–4238|doi=10.1073/pnas.1321937111|issn=0027-8424|pmc=3964116|pmid=24613930}}</ref><ref>{{Cite journal|last=Ambrosini|first=Margherita|last2=Del Re|first2=Marzia|last3=Manca|first3=Paolo|last4=Hendifar|first4=Andrew|last5=Drilon|first5=Alexander|last6=Harada|first6=Guilherme|last7=Ree|first7=Anne Hansen|last8=Klempner|first8=Samuel|last9=Mælandsmo|first9=Gunhild Mari|date=2022-04|title=ALK Inhibitors in Patients With ALK Fusion-Positive GI Cancers: An International Data Set and a Molecular Case Series|url=https://pubmed.ncbi.nlm.nih.gov/35476549/|journal=JCO precision oncology|volume=6|pages=e2200015|doi=10.1200/PO.22.00015|issn=2473-4284|pmid=35476549}}</ref>, inflammatory myofibroblastic tumor<ref>{{Cite journal|last=Bridge|first=Julia A.|last2=Kanamori|first2=Masahiko|last3=Ma|first3=Zhigui|last4=Pickering|first4=Diane|last5=Hill|first5=D. Ashley|last6=Lydiatt|first6=William|last7=Lui|first7=Man Yee|last8=Colleoni|first8=Gisele W. B.|last9=Antonescu|first9=Cristina R.|date=2001-8|title=Fusion of the ALK Gene to the Clathrin Heavy Chain Gene, CLTC, in Inflammatory Myofibroblastic Tumor|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1850566/|journal=The American Journal of Pathology|volume=159|issue=2|pages=411–415|issn=0002-9440|pmc=1850566|pmid=11485898}}</ref><ref>{{Cite journal|last=Lawrence|first=B.|last2=Perez-Atayde|first2=A.|last3=Hibbard|first3=M. K.|last4=Rubin|first4=B. P.|last5=Dal Cin|first5=P.|last6=Pinkus|first6=J. L.|last7=Pinkus|first7=G. S.|last8=Xiao|first8=S.|last9=Yi|first9=E. S.|date=2000-08|title=TPM3-ALK and TPM4-ALK oncogenes in inflammatory myofibroblastic tumors|url=https://pubmed.ncbi.nlm.nih.gov/10934142/|journal=The American Journal of Pathology|volume=157|issue=2|pages=377–384|doi=10.1016/S0002-9440(10)64550-6|issn=0002-9440|pmc=1850130|pmid=10934142}}</ref><ref>{{Cite journal|last=Ma|first=Zhigui|last2=Hill|first2=D. Ashley|last3=Collins|first3=Margaret H.|last4=Morris|first4=Stephan W.|last5=Sumegi|first5=Janos|last6=Zhou|first6=Ming|last7=Zuppan|first7=Craig|last8=Bridge|first8=Julia A.|date=2003-05|title=Fusion of ALK to the Ran-binding protein 2 (RANBP2) gene in inflammatory myofibroblastic tumor|url=https://pubmed.ncbi.nlm.nih.gov/12661011/|journal=Genes, Chromosomes & Cancer|volume=37|issue=1|pages=98–105|doi=10.1002/gcc.10177|issn=1045-2257|pmid=12661011}}</ref>, non-Hodgkin's lymphoma<ref>{{Cite journal|last=Pan|first=Zenggang|last2=Hu|first2=Shimin|last3=Li|first3=Min|last4=Zhou|first4=Yi|last5=Kim|first5=Young S.|last6=Reddy|first6=Vishnu|last7=Sanmann|first7=Jennifer N.|last8=Smith|first8=Lynette M.|last9=Chen|first9=Mingyi|date=2017-01|title=ALK-positive Large B-cell Lymphoma: A Clinicopathologic Study of 26 Cases With Review of Additional 108 Cases in the Literature|url=https://pubmed.ncbi.nlm.nih.gov/27740969/|journal=The American Journal of Surgical Pathology|volume=41|issue=1|pages=25–38|doi=10.1097/PAS.0000000000000753|issn=1532-0979|pmid=27740969}}</ref><ref>{{Cite journal|last=Laurent|first=Camille|last2=Do|first2=Catherine|last3=Gascoyne|first3=Randy D.|last4=Lamant|first4=Laurence|last5=Ysebaert|first5=Loïc|last6=Laurent|first6=Guy|last7=Delsol|first7=Georges|last8=Brousset|first8=Pierre|date=2009-09-01|title=Anaplastic lymphoma kinase-positive diffuse large B-cell lymphoma: a rare clinicopathologic entity with poor prognosis|url=https://pubmed.ncbi.nlm.nih.gov/19636007/|journal=Journal of Clinical Oncology: Official Journal of the American Society of Clinical Oncology|volume=27|issue=25|pages=4211–4216|doi=10.1200/JCO.2008.21.5020|issn=1527-7755|pmid=19636007}}</ref><ref>{{Cite journal|last=Sakamoto|first=Kana|last2=Nakasone|first2=Hideki|last3=Togashi|first3=Yuki|last4=Sakata|first4=Seiji|last5=Tsuyama|first5=Naoko|last6=Baba|first6=Satoko|last7=Dobashi|first7=Akito|last8=Asaka|first8=Reimi|last9=Tsai|first9=Chien-Chen|date=2016-04|title=ALK-positive large B-cell lymphoma: identification of EML4-ALK and a review of the literature focusing on the ALK immunohistochemical staining pattern|url=https://pubmed.ncbi.nlm.nih.gov/26781614/|journal=International Journal of Hematology|volume=103|issue=4|pages=399–408|doi=10.1007/s12185-016-1934-1|issn=1865-3774|pmid=26781614}}</ref>, and ALK+ histiocytosis <ref>{{Cite journal|last=Takeyasu|first=Yuki|last2=Okuma|first2=Hitomi S.|last3=Kojima|first3=Yuki|last4=Nishikawa|first4=Tadaaki|last5=Tanioka|first5=Maki|last6=Sudo|first6=Kazuki|last7=Shimoi|first7=Tatsunori|last8=Noguchi|first8=Emi|last9=Arakawa|first9=Ayumu|date=2021|title=Impact of ALK Inhibitors in Patients With ALK-Rearranged Nonlung Solid Tumors|url=https://pubmed.ncbi.nlm.nih.gov/34036223/|journal=JCO precision oncology|volume=5|pages=PO.20.00383|doi=10.1200/PO.20.00383|issn=2473-4284|pmc=8140781|pmid=34036223}}</ref><ref>{{Cite journal|last=Chang|first=Kenneth Tou En|last2=Tay|first2=Amos Zhi En|last3=Kuick|first3=Chik Hong|last4=Chen|first4=Huiyi|last5=Algar|first5=Elizabeth|last6=Taubenheim|first6=Nadine|last7=Campbell|first7=Janine|last8=Mechinaud|first8=Francoise|last9=Campbell|first9=Martin|date=2019-05|title=ALK-positive histiocytosis: an expanded clinicopathologic spectrum and frequent presence of KIF5B-ALK fusion|url=https://pubmed.ncbi.nlm.nih.gov/30573850/|journal=Modern Pathology: An Official Journal of the United States and Canadian Academy of Pathology, Inc|volume=32|issue=5|pages=598–608|doi=10.1038/s41379-018-0168-6|issn=1530-0285|pmid=30573850}}</ref><ref>{{Cite journal|last=Chan|first=John K. C.|last2=Lamant|first2=Laurence|last3=Algar|first3=Elizabeth|last4=Delsol|first4=Georges|last5=Tsang|first5=William Y. W.|last6=Lee|first6=King C.|last7=Tiedemann|first7=Karin|last8=Chow|first8=Chung W.|date=2008-10-01|title=ALK+ histiocytosis: a novel type of systemic histiocytic proliferative disorder of early infancy|url=https://pubmed.ncbi.nlm.nih.gov/18660380/|journal=Blood|volume=112|issue=7|pages=2965–2968|doi=10.1182/blood-2008-03-147017|issn=1528-0020|pmid=18660380}}</ref>.
 
*''ALK'' translocations may be seen in multiple malignancies including epithelial malignancies<ref>{{Cite journal|last=Holla|first=Vijaykumar R.|last2=Elamin|first2=Yasir Y.|last3=Bailey|first3=Ann Marie|last4=Johnson|first4=Amber M.|last5=Litzenburger|first5=Beate C.|last6=Khotskaya|first6=Yekaterina B.|last7=Sanchez|first7=Nora S.|last8=Zeng|first8=Jia|last9=Shufean|first9=Md Abu|date=2017-1|title=ALK: a tyrosine kinase target for cancer therapy|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5171696/|journal=Cold Spring Harbor Molecular Case Studies|volume=3|issue=1|pages=a001115|doi=10.1101/mcs.a001115|issn=2373-2873|pmc=5171696|pmid=28050598}}</ref><ref>{{Cite journal|last=Amatu|first=Alessio|last2=Somaschini|first2=Alessio|last3=Cerea|first3=Giulio|last4=Bosotti|first4=Roberta|last5=Valtorta|first5=Emanuele|last6=Buonandi|first6=Pasquale|last7=Marrapese|first7=Giovanna|last8=Veronese|first8=Silvio|last9=Luo|first9=David|date=2015-12-22|title=Novel CAD-ALK gene rearrangement is drugable by entrectinib in colorectal cancer|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4701996/|journal=British Journal of Cancer|volume=113|issue=12|pages=1730–1734|doi=10.1038/bjc.2015.401|issn=0007-0920|pmc=4701996|pmid=26633560}}</ref><ref>{{Cite journal|last=Camidge|first=D. Ross|last2=Kono|first2=Scott A.|last3=Lu|first3=Xian|last4=Okuyama|first4=Sonia|last5=Barón|first5=Anna E.|last6=Oton|first6=Ana B.|last7=Davies|first7=Angela M.|last8=Varella-Garcia|first8=Marileila|last9=Franklin|first9=Wilbur|date=2011-04|title=Anaplastic lymphoma kinase gene rearrangements in non-small cell lung cancer are associated with prolonged progression-free survival on pemetrexed|url=https://pubmed.ncbi.nlm.nih.gov/21336183/|journal=Journal of Thoracic Oncology: Official Publication of the International Association for the Study of Lung Cancer|volume=6|issue=4|pages=774–780|doi=10.1097/JTO.0b013e31820cf053|issn=1556-1380|pmc=3626562|pmid=21336183}}</ref><ref>{{Cite journal|last=Choi|first=Young Lim|last2=Takeuchi|first2=Kengo|last3=Soda|first3=Manabu|last4=Inamura|first4=Kentaro|last5=Togashi|first5=Yuki|last6=Hatano|first6=Satoko|last7=Enomoto|first7=Munehiro|last8=Hamada|first8=Toru|last9=Haruta|first9=Hidenori|date=2008-07-01|title=Identification of novel isoforms of the EML4-ALK transforming gene in non-small cell lung cancer|url=https://pubmed.ncbi.nlm.nih.gov/18593892/|journal=Cancer Research|volume=68|issue=13|pages=4971–4976|doi=10.1158/0008-5472.CAN-07-6158|issn=1538-7445|pmid=18593892}}</ref><ref>{{Cite journal|last=Kelly|first=Lindsey M.|last2=Barila|first2=Guillermo|last3=Liu|first3=Pengyuan|last4=Evdokimova|first4=Viktoria N.|last5=Trivedi|first5=Sumita|last6=Panebianco|first6=Federica|last7=Gandhi|first7=Manoj|last8=Carty|first8=Sally E.|last9=Hodak|first9=Steven P.|date=2014-03-18|title=Identification of the transforming STRN-ALK fusion as a potential therapeutic target in the aggressive forms of thyroid cancer|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3964116/|journal=Proceedings of the National Academy of Sciences of the United States of America|volume=111|issue=11|pages=4233–4238|doi=10.1073/pnas.1321937111|issn=0027-8424|pmc=3964116|pmid=24613930}}</ref><ref>{{Cite journal|last=Ambrosini|first=Margherita|last2=Del Re|first2=Marzia|last3=Manca|first3=Paolo|last4=Hendifar|first4=Andrew|last5=Drilon|first5=Alexander|last6=Harada|first6=Guilherme|last7=Ree|first7=Anne Hansen|last8=Klempner|first8=Samuel|last9=Mælandsmo|first9=Gunhild Mari|date=2022-04|title=ALK Inhibitors in Patients With ALK Fusion-Positive GI Cancers: An International Data Set and a Molecular Case Series|url=https://pubmed.ncbi.nlm.nih.gov/35476549/|journal=JCO precision oncology|volume=6|pages=e2200015|doi=10.1200/PO.22.00015|issn=2473-4284|pmid=35476549}}</ref>, inflammatory myofibroblastic tumor<ref>{{Cite journal|last=Bridge|first=Julia A.|last2=Kanamori|first2=Masahiko|last3=Ma|first3=Zhigui|last4=Pickering|first4=Diane|last5=Hill|first5=D. Ashley|last6=Lydiatt|first6=William|last7=Lui|first7=Man Yee|last8=Colleoni|first8=Gisele W. B.|last9=Antonescu|first9=Cristina R.|date=2001-8|title=Fusion of the ALK Gene to the Clathrin Heavy Chain Gene, CLTC, in Inflammatory Myofibroblastic Tumor|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1850566/|journal=The American Journal of Pathology|volume=159|issue=2|pages=411–415|issn=0002-9440|pmc=1850566|pmid=11485898}}</ref><ref>{{Cite journal|last=Lawrence|first=B.|last2=Perez-Atayde|first2=A.|last3=Hibbard|first3=M. K.|last4=Rubin|first4=B. P.|last5=Dal Cin|first5=P.|last6=Pinkus|first6=J. L.|last7=Pinkus|first7=G. S.|last8=Xiao|first8=S.|last9=Yi|first9=E. S.|date=2000-08|title=TPM3-ALK and TPM4-ALK oncogenes in inflammatory myofibroblastic tumors|url=https://pubmed.ncbi.nlm.nih.gov/10934142/|journal=The American Journal of Pathology|volume=157|issue=2|pages=377–384|doi=10.1016/S0002-9440(10)64550-6|issn=0002-9440|pmc=1850130|pmid=10934142}}</ref><ref>{{Cite journal|last=Ma|first=Zhigui|last2=Hill|first2=D. Ashley|last3=Collins|first3=Margaret H.|last4=Morris|first4=Stephan W.|last5=Sumegi|first5=Janos|last6=Zhou|first6=Ming|last7=Zuppan|first7=Craig|last8=Bridge|first8=Julia A.|date=2003-05|title=Fusion of ALK to the Ran-binding protein 2 (RANBP2) gene in inflammatory myofibroblastic tumor|url=https://pubmed.ncbi.nlm.nih.gov/12661011/|journal=Genes, Chromosomes & Cancer|volume=37|issue=1|pages=98–105|doi=10.1002/gcc.10177|issn=1045-2257|pmid=12661011}}</ref>, non-Hodgkin's lymphoma<ref>{{Cite journal|last=Pan|first=Zenggang|last2=Hu|first2=Shimin|last3=Li|first3=Min|last4=Zhou|first4=Yi|last5=Kim|first5=Young S.|last6=Reddy|first6=Vishnu|last7=Sanmann|first7=Jennifer N.|last8=Smith|first8=Lynette M.|last9=Chen|first9=Mingyi|date=2017-01|title=ALK-positive Large B-cell Lymphoma: A Clinicopathologic Study of 26 Cases With Review of Additional 108 Cases in the Literature|url=https://pubmed.ncbi.nlm.nih.gov/27740969/|journal=The American Journal of Surgical Pathology|volume=41|issue=1|pages=25–38|doi=10.1097/PAS.0000000000000753|issn=1532-0979|pmid=27740969}}</ref><ref>{{Cite journal|last=Laurent|first=Camille|last2=Do|first2=Catherine|last3=Gascoyne|first3=Randy D.|last4=Lamant|first4=Laurence|last5=Ysebaert|first5=Loïc|last6=Laurent|first6=Guy|last7=Delsol|first7=Georges|last8=Brousset|first8=Pierre|date=2009-09-01|title=Anaplastic lymphoma kinase-positive diffuse large B-cell lymphoma: a rare clinicopathologic entity with poor prognosis|url=https://pubmed.ncbi.nlm.nih.gov/19636007/|journal=Journal of Clinical Oncology: Official Journal of the American Society of Clinical Oncology|volume=27|issue=25|pages=4211–4216|doi=10.1200/JCO.2008.21.5020|issn=1527-7755|pmid=19636007}}</ref><ref>{{Cite journal|last=Sakamoto|first=Kana|last2=Nakasone|first2=Hideki|last3=Togashi|first3=Yuki|last4=Sakata|first4=Seiji|last5=Tsuyama|first5=Naoko|last6=Baba|first6=Satoko|last7=Dobashi|first7=Akito|last8=Asaka|first8=Reimi|last9=Tsai|first9=Chien-Chen|date=2016-04|title=ALK-positive large B-cell lymphoma: identification of EML4-ALK and a review of the literature focusing on the ALK immunohistochemical staining pattern|url=https://pubmed.ncbi.nlm.nih.gov/26781614/|journal=International Journal of Hematology|volume=103|issue=4|pages=399–408|doi=10.1007/s12185-016-1934-1|issn=1865-3774|pmid=26781614}}</ref>, and ALK+ histiocytosis <ref>{{Cite journal|last=Takeyasu|first=Yuki|last2=Okuma|first2=Hitomi S.|last3=Kojima|first3=Yuki|last4=Nishikawa|first4=Tadaaki|last5=Tanioka|first5=Maki|last6=Sudo|first6=Kazuki|last7=Shimoi|first7=Tatsunori|last8=Noguchi|first8=Emi|last9=Arakawa|first9=Ayumu|date=2021|title=Impact of ALK Inhibitors in Patients With ALK-Rearranged Nonlung Solid Tumors|url=https://pubmed.ncbi.nlm.nih.gov/34036223/|journal=JCO precision oncology|volume=5|pages=PO.20.00383|doi=10.1200/PO.20.00383|issn=2473-4284|pmc=8140781|pmid=34036223}}</ref><ref>{{Cite journal|last=Chang|first=Kenneth Tou En|last2=Tay|first2=Amos Zhi En|last3=Kuick|first3=Chik Hong|last4=Chen|first4=Huiyi|last5=Algar|first5=Elizabeth|last6=Taubenheim|first6=Nadine|last7=Campbell|first7=Janine|last8=Mechinaud|first8=Francoise|last9=Campbell|first9=Martin|date=2019-05|title=ALK-positive histiocytosis: an expanded clinicopathologic spectrum and frequent presence of KIF5B-ALK fusion|url=https://pubmed.ncbi.nlm.nih.gov/30573850/|journal=Modern Pathology: An Official Journal of the United States and Canadian Academy of Pathology, Inc|volume=32|issue=5|pages=598–608|doi=10.1038/s41379-018-0168-6|issn=1530-0285|pmid=30573850}}</ref><ref>{{Cite journal|last=Chan|first=John K. C.|last2=Lamant|first2=Laurence|last3=Algar|first3=Elizabeth|last4=Delsol|first4=Georges|last5=Tsang|first5=William Y. W.|last6=Lee|first6=King C.|last7=Tiedemann|first7=Karin|last8=Chow|first8=Chung W.|date=2008-10-01|title=ALK+ histiocytosis: a novel type of systemic histiocytic proliferative disorder of early infancy|url=https://pubmed.ncbi.nlm.nih.gov/18660380/|journal=Blood|volume=112|issue=7|pages=2965–2968|doi=10.1182/blood-2008-03-147017|issn=1528-0020|pmid=18660380}}</ref>.
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<blockquote class='blockedit'>{{Box-round|title=v4:Clinical Significance (Diagnosis, Prognosis and Therapeutic Implications).|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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*CD30 expression on ALCL (ALK+ or ALK-) allows for targeted therapy<ref name=":2">{{Cite journal|displayauthors=1|last=National Comprehensive Cancer Network|first=|date=January 2021|title=NCCN Clinical Practice Guidelines in Oncology: T-cell lymphomas|url=https://www.nccn.org/professionals/physician_gls/pdf/t-cell.pdf|journal=|volume=|pages=|via=}}</ref>
 
*CD30 expression on ALCL (ALK+ or ALK-) allows for targeted therapy<ref name=":2">{{Cite journal|displayauthors=1|last=National Comprehensive Cancer Network|first=|date=January 2021|title=NCCN Clinical Practice Guidelines in Oncology: T-cell lymphomas|url=https://www.nccn.org/professionals/physician_gls/pdf/t-cell.pdf|journal=|volume=|pages=|via=}}</ref>
 
**First-line therapy: [https://www.fda.gov/drugs/fda-approves-brentuximab-vedotin-previously-untreated-salcl-and-cd30-expressing-ptcl Brentuximab] (anti-CD30) vedotin + CHP (cyclophosphamide, doxorubicin, and prednisone)
 
**First-line therapy: [https://www.fda.gov/drugs/fda-approves-brentuximab-vedotin-previously-untreated-salcl-and-cd30-expressing-ptcl Brentuximab] (anti-CD30) vedotin + CHP (cyclophosphamide, doxorubicin, and prednisone)
−
*ALK inhibition ([https://www.fda.gov/drugs/drug-approvals-and-databases/fda-approves-crizotinib-children-and-young-adults-relapsed-or-refractory-systemic-anaplastic-large#:~:text=Approvals%20and%20Databases-,FDA%20approves%20crizotinib%20for%20children%20and%20young%20adults%20with%20relapsed,systemic%20anaplastic%20large%20cell%20lymphoma&text=On%20January%2014%2C%202021%2C%20the,(Xalkori%2C%20Pfizer%20Inc.) crizotinib]) can be an effective 2nd-line therapeutic strategy as ALK is essential for the proliferation and survival of ALK+ ALCL cells<ref>{{Cite journal|last=Werner|first=Michael T.|last2=Zhao|first2=Chen|last3=Zhang|first3=Qian|last4=Wasik|first4=Mariusz A.|date=02 16, 2017|title=Nucleophosmin-anaplastic lymphoma kinase: the ultimate oncogene and therapeutic target|url=https://pubmed.ncbi.nlm.nih.gov/27879258|journal=Blood|volume=129|issue=7|pages=823–831|doi=10.1182/blood-2016-05-717793|issn=1528-0020|pmid=27879258}}</ref><ref name=":2" /><ref>{{Cite journal|displayauthors=1|last=Food and Drug Administration|first=|date=January 2021|title=FDA approves crizotinib for children and young adults with relapsed or refractory, systemic anaplastic large cell lymphoma|url=https://www.fda.gov/drugs/drug-approvals-and-databases/fda-approves-crizotinib-children-and-young-adults-relapsed-or-refractory-systemic-anaplastic-large?utm_medium=email&utm_source=govdelivery|journal=|volume=|pages=|via=}}</ref>
+
*ALK inhibition ([https://www.fda.gov/drugs/drug-approvals-and-databases/fda-approves-crizotinib-children-and-young-adults-relapsed-or-refractory-systemic-anaplastic-large#:~:text=Approvals%20and%20Databases-,FDA%20approves%20crizotinib%20for%20children%20and%20young%20adults%20with%20relapsed,systemic%20anaplastic%20large%20cell%20lymphoma&text=On%20January%2014%2C%202021%2C%20the,(Xalkori%2C%20Pfizer%20Inc.) crizotinib]) can be an effective 2nd-line therapeutic strategy as ALK is essential for the proliferation and survival of ALK+ ALCL cells<ref name=":21">{{Cite journal|last=Werner|first=Michael T.|last2=Zhao|first2=Chen|last3=Zhang|first3=Qian|last4=Wasik|first4=Mariusz A.|date=02 16, 2017|title=Nucleophosmin-anaplastic lymphoma kinase: the ultimate oncogene and therapeutic target|url=https://pubmed.ncbi.nlm.nih.gov/27879258|journal=Blood|volume=129|issue=7|pages=823–831|doi=10.1182/blood-2016-05-717793|issn=1528-0020|pmid=27879258}}</ref><ref name=":2" /><ref name=":22">{{Cite journal|displayauthors=1|last=Food and Drug Administration|first=|date=January 2021|title=FDA approves crizotinib for children and young adults with relapsed or refractory, systemic anaplastic large cell lymphoma|url=https://www.fda.gov/drugs/drug-approvals-and-databases/fda-approves-crizotinib-children-and-young-adults-relapsed-or-refractory-systemic-anaplastic-large?utm_medium=email&utm_source=govdelivery|journal=|volume=|pages=|via=}}</ref>
 
**Drug resistance may develop due to:  
 
**Drug resistance may develop due to:  
 
**#Mutations of the ALK gene impairing binding of the inhibitor<ref name=":3">{{Cite journal|last=Zdzalik|first=Daria|last2=Dymek|first2=Barbara|last3=Grygielewicz|first3=Paulina|last4=Gunerka|first4=Pawel|last5=Bujak|first5=Anna|last6=Lamparska-Przybysz|first6=Monika|last7=Wieczorek|first7=Maciej|last8=Dzwonek|first8=Karolina|date=2014-04|title=Activating mutations in ALK kinase domain confer resistance to structurally unrelated ALK inhibitors in NPM-ALK-positive anaplastic large-cell lymphoma|url=https://pubmed.ncbi.nlm.nih.gov/24509625|journal=Journal of Cancer Research and Clinical Oncology|volume=140|issue=4|pages=589–598|doi=10.1007/s00432-014-1589-3|issn=1432-1335|pmc=3949014|pmid=24509625}}</ref>; other ALK inhibitors are not currently FDA-approved for use in ALK+ ALCL
 
**#Mutations of the ALK gene impairing binding of the inhibitor<ref name=":3">{{Cite journal|last=Zdzalik|first=Daria|last2=Dymek|first2=Barbara|last3=Grygielewicz|first3=Paulina|last4=Gunerka|first4=Pawel|last5=Bujak|first5=Anna|last6=Lamparska-Przybysz|first6=Monika|last7=Wieczorek|first7=Maciej|last8=Dzwonek|first8=Karolina|date=2014-04|title=Activating mutations in ALK kinase domain confer resistance to structurally unrelated ALK inhibitors in NPM-ALK-positive anaplastic large-cell lymphoma|url=https://pubmed.ncbi.nlm.nih.gov/24509625|journal=Journal of Cancer Research and Clinical Oncology|volume=140|issue=4|pages=589–598|doi=10.1007/s00432-014-1589-3|issn=1432-1335|pmc=3949014|pmid=24509625}}</ref>; other ALK inhibitors are not currently FDA-approved for use in ALK+ ALCL
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!Notes
 
!Notes
 
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<blockquote class='blockedit'>{{Box-round|title=v4:Genomic Gain/Loss/LOH|The content below was from the old template. Please incorporate above.}}
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<blockquote class="blockedit">{{Box-round|title=v4:Genomic Gain/Loss/LOH|The content below was from the old template. Please incorporate above.}}
    
Frequent secondary chromosomal imbalances are seen in ALK+ ALCL (58% of cases), as based on comparative genomic hybridization analysis<ref>{{Cite journal|last=I|first=Salaverria|last2=S|first2=Beà|last3=A|first3=Lopez-Guillermo|last4=V|first4=Lespinet|last5=M|first5=Pinyol|last6=B|first6=Burkhardt|last7=L|first7=Lamant|last8=A|first8=Zettl|last9=D|first9=Horsman|date=2008|title=Genomic profiling reveals different genetic aberrations in systemic ALK-positive and ALK-negative anaplastic large cell lymphomas|url=https://pubmed.ncbi.nlm.nih.gov/18275429/|language=en|pmid=18275429}}</ref>.
 
Frequent secondary chromosomal imbalances are seen in ALK+ ALCL (58% of cases), as based on comparative genomic hybridization analysis<ref>{{Cite journal|last=I|first=Salaverria|last2=S|first2=Beà|last3=A|first3=Lopez-Guillermo|last4=V|first4=Lespinet|last5=M|first5=Pinyol|last6=B|first6=Burkhardt|last7=L|first7=Lamant|last8=A|first8=Zettl|last9=D|first9=Horsman|date=2008|title=Genomic profiling reveals different genetic aberrations in systemic ALK-positive and ALK-negative anaplastic large cell lymphomas|url=https://pubmed.ncbi.nlm.nih.gov/18275429/|language=en|pmid=18275429}}</ref>.
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See other sections.
 
See other sections.
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<blockquote class="blockedit">{{Box-round|title=v4:Gene Mutations (SNV/INDEL)|The content below was from the old template. Please incorporate above.}}
    
*Limited literature on somatic mutations in ALK+ ALCL
 
*Limited literature on somatic mutations in ALK+ ALCL
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*
 
*
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(use the "Cite" icon at the top of the page) <span style="color:#0070C0">(''Instructions: Add each reference into the text above by clicking on where you want to insert the reference, selecting the “Cite” icon at the top of the page, and using the “Automatic” tab option to search such as by PMID to select the reference to insert. The reference list in this section will be automatically generated and sorted.''</span> <span style="color:#0070C0">''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''</span><span style="color:#0070C0">''.''</span><span style="color:#0070C0">) </span> <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 on where you want to insert the reference, selecting the “Cite” icon at the top of the page, and using the “Automatic” tab option to search such as by PMID to select the reference to insert. The reference list in this section will be automatically generated and sorted.''</span> <span style="color:#0070C0">''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''</span><span style="color:#0070C0">''.''</span><span style="color:#0070C0">) </span> <references />
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==Notes==
 
==Notes==
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__TOC__
 
__TOC__
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[[Category:HAEM5]][[Category:DISEASE]][[Category:Diseases A]]
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[[Category:HAEM5]]
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[[Category:DISEASE]]
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[[Category:Diseases A]]
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