Compendium of Cancer Genome Aberrations

HAEM5:Classic Hodgkin lymphoma: Difference between revisions

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|gain
|gain
|2p13
|2p13
|REL
|''REL''
|P
|P
|No
|No
|REL amplification promotes NF-κB signaling activation <ref>{{Cite journal|last=Joos|first=Stefan|last2=Menz|first2=Christiane K.|last3=Wrobel|first3=Gunnar|last4=Siebert|first4=Reiner|last5=Gesk|first5=Stefan|last6=Ohl|first6=Sibylle|last7=Mechtersheimer|first7=Gunhild|last8=Trümper|first8=Lorenz|last9=Möller|first9=Peter|date=2002-02-15|title=Classical Hodgkin lymphoma is characterized by recurrent copy number gains of the short arm of chromosome 2|url=https://pubmed.ncbi.nlm.nih.gov/11830490|journal=Blood|volume=99|issue=4|pages=1381–1387|doi=10.1182/blood.v99.4.1381|issn=0006-4971|pmid=11830490}}</ref><ref>{{Cite journal|last=Martín-Subero|first=José I.|last2=Gesk|first2=Stefan|last3=Harder|first3=Lana|last4=Sonoki|first4=Takashi|last5=Tucker|first5=Philip W.|last6=Schlegelberger|first6=Brigitte|last7=Grote|first7=Werner|last8=Novo|first8=Francisco J.|last9=Calasanz|first9=María J.|date=2002-02-15|title=Recurrent involvement of the REL and BCL11A loci in classical Hodgkin lymphoma|url=https://pubmed.ncbi.nlm.nih.gov/11830502|journal=Blood|volume=99|issue=4|pages=1474–1477|doi=10.1182/blood.v99.4.1474|issn=0006-4971|pmid=11830502}}</ref><ref name=":2">{{Cite journal|last=Steidl|first=Christian|last2=Telenius|first2=Adele|last3=Shah|first3=Sohrab P.|last4=Farinha|first4=Pedro|last5=Barclay|first5=Lorena|last6=Boyle|first6=Merrill|last7=Connors|first7=Joseph M.|last8=Horsman|first8=Douglas E.|last9=Gascoyne|first9=Randy D.|date=2010-07-22|title=Genome-wide copy number analysis of Hodgkin Reed-Sternberg cells identifies recurrent imbalances with correlations to treatment outcome|url=https://pubmed.ncbi.nlm.nih.gov/20339089|journal=Blood|volume=116|issue=3|pages=418–427|doi=10.1182/blood-2009-12-257345|issn=1528-0020|pmid=20339089}}</ref>
|REL amplification promotes NF-κB signaling activation that promotes HRS cell survival and proliferation.<ref>{{Cite journal|last=Joos|first=Stefan|last2=Menz|first2=Christiane K.|last3=Wrobel|first3=Gunnar|last4=Siebert|first4=Reiner|last5=Gesk|first5=Stefan|last6=Ohl|first6=Sibylle|last7=Mechtersheimer|first7=Gunhild|last8=Trümper|first8=Lorenz|last9=Möller|first9=Peter|date=2002-02-15|title=Classical Hodgkin lymphoma is characterized by recurrent copy number gains of the short arm of chromosome 2|url=https://pubmed.ncbi.nlm.nih.gov/11830490|journal=Blood|volume=99|issue=4|pages=1381–1387|doi=10.1182/blood.v99.4.1381|issn=0006-4971|pmid=11830490}}</ref><ref>{{Cite journal|last=Martín-Subero|first=José I.|last2=Gesk|first2=Stefan|last3=Harder|first3=Lana|last4=Sonoki|first4=Takashi|last5=Tucker|first5=Philip W.|last6=Schlegelberger|first6=Brigitte|last7=Grote|first7=Werner|last8=Novo|first8=Francisco J.|last9=Calasanz|first9=María J.|date=2002-02-15|title=Recurrent involvement of the REL and BCL11A loci in classical Hodgkin lymphoma|url=https://pubmed.ncbi.nlm.nih.gov/11830502|journal=Blood|volume=99|issue=4|pages=1474–1477|doi=10.1182/blood.v99.4.1474|issn=0006-4971|pmid=11830502}}</ref><ref name=":2">{{Cite journal|last=Steidl|first=Christian|last2=Telenius|first2=Adele|last3=Shah|first3=Sohrab P.|last4=Farinha|first4=Pedro|last5=Barclay|first5=Lorena|last6=Boyle|first6=Merrill|last7=Connors|first7=Joseph M.|last8=Horsman|first8=Douglas E.|last9=Gascoyne|first9=Randy D.|date=2010-07-22|title=Genome-wide copy number analysis of Hodgkin Reed-Sternberg cells identifies recurrent imbalances with correlations to treatment outcome|url=https://pubmed.ncbi.nlm.nih.gov/20339089|journal=Blood|volume=116|issue=3|pages=418–427|doi=10.1182/blood-2009-12-257345|issn=1528-0020|pmid=20339089}}</ref>
|-
|-
|9p
|9p
|Gain
|Gain
|9p24.1
|9p24.1
|CD274 (PD-L1), PDCD1LG2 (PD-L2), JAK2
|''CD274'' (PD-L1), ''PDCD1LG2'' (PD-L2), JAK2
|T, P
|T, P
|Yes <ref name=":1" />
|Yes <ref name=":1" />
|9p24.1 amplification drives PD-L1/PD-L2 overexpression, relevant for immune checkpoint inhibitor therapy <ref name=":1">{{Cite journal|last=Green|first=Michael R.|last2=Monti|first2=Stefano|last3=Rodig|first3=Scott J.|last4=Juszczynski|first4=Przemyslaw|last5=Currie|first5=Treeve|last6=O'Donnell|first6=Evan|last7=Chapuy|first7=Bjoern|last8=Takeyama|first8=Kunihiko|last9=Neuberg|first9=Donna|date=2010-10-28|title=Integrative analysis reveals selective 9p24.1 amplification, increased PD-1 ligand expression, and further induction via JAK2 in nodular sclerosing Hodgkin lymphoma and primary mediastinal large B-cell lymphoma|url=https://pubmed.ncbi.nlm.nih.gov/20628145|journal=Blood|volume=116|issue=17|pages=3268–3277|doi=10.1182/blood-2010-05-282780|issn=1528-0020|pmc=2995356|pmid=20628145}}</ref><ref>{{Cite journal|last=Roemer|first=Margaretha G. M.|last2=Advani|first2=Ranjana H.|last3=Ligon|first3=Azra H.|last4=Natkunam|first4=Yasodha|last5=Redd|first5=Robert A.|last6=Homer|first6=Heather|last7=Connelly|first7=Courtney F.|last8=Sun|first8=Heather H.|last9=Daadi|first9=Sarah E.|date=2016-08-10|title=PD-L1 and PD-L2 Genetic Alterations Define Classical Hodgkin Lymphoma and Predict Outcome|url=https://pmc.ncbi.nlm.nih.gov/articles/PMC5019753/|journal=Journal of Clinical Oncology: Official Journal of the American Society of Clinical Oncology|volume=34|issue=23|pages=2690–2697|doi=10.1200/JCO.2016.66.4482|issn=1527-7755|pmc=5019753|pmid=27069084}}</ref>
|9p24.1 amplification drives PD-L1/PD-L2 overexpression leading to immune suppression. Relevant for immune checkpoint inhibitor therapy <ref name=":1">{{Cite journal|last=Green|first=Michael R.|last2=Monti|first2=Stefano|last3=Rodig|first3=Scott J.|last4=Juszczynski|first4=Przemyslaw|last5=Currie|first5=Treeve|last6=O'Donnell|first6=Evan|last7=Chapuy|first7=Bjoern|last8=Takeyama|first8=Kunihiko|last9=Neuberg|first9=Donna|date=2010-10-28|title=Integrative analysis reveals selective 9p24.1 amplification, increased PD-1 ligand expression, and further induction via JAK2 in nodular sclerosing Hodgkin lymphoma and primary mediastinal large B-cell lymphoma|url=https://pubmed.ncbi.nlm.nih.gov/20628145|journal=Blood|volume=116|issue=17|pages=3268–3277|doi=10.1182/blood-2010-05-282780|issn=1528-0020|pmc=2995356|pmid=20628145}}</ref><ref>{{Cite journal|last=Roemer|first=Margaretha G. M.|last2=Advani|first2=Ranjana H.|last3=Ligon|first3=Azra H.|last4=Natkunam|first4=Yasodha|last5=Redd|first5=Robert A.|last6=Homer|first6=Heather|last7=Connelly|first7=Courtney F.|last8=Sun|first8=Heather H.|last9=Daadi|first9=Sarah E.|date=2016-08-10|title=PD-L1 and PD-L2 Genetic Alterations Define Classical Hodgkin Lymphoma and Predict Outcome|url=https://pmc.ncbi.nlm.nih.gov/articles/PMC5019753/|journal=Journal of Clinical Oncology: Official Journal of the American Society of Clinical Oncology|volume=34|issue=23|pages=2690–2697|doi=10.1200/JCO.2016.66.4482|issn=1527-7755|pmc=5019753|pmid=27069084}}</ref>
|-
|-
|17p
|17q
|Gain
|Gain
|17q21
|17q21
|MAP3K14
|''MAP3K14''
|P
|P
|No
|No
|MAP3K14 (NIK) gain activates alternative NF-κB signaling <ref name=":2" />
|MAP3K14 (NIK) gain activates alternative NF-κB signaling <ref name=":2" />
|-
|19q
|Gain
|19q13.3
|''RELB''
|P
|No
|Overexpression of RELB leads to enhanced NF-kB signaling and HRS cell survival. <ref>{{Cite journal|last=Slovak|first=Marilyn L.|last2=Bedell|first2=Victoria|last3=Hsu|first3=Ya-Hsuan|last4=Estrine|first4=Dolores B.|last5=Nowak|first5=Norma J.|last6=Delioukina|first6=Maria L.|last7=Weiss|first7=Lawrence M.|last8=Smith|first8=David D.|last9=Forman|first9=Stephen J.|date=2011-05-15|title=Molecular karyotypes of Hodgkin and Reed-Sternberg cells at disease onset reveal distinct copy number alterations in chemosensitive versus refractory Hodgkin lymphoma|url=https://pubmed.ncbi.nlm.nih.gov/21385932|journal=Clinical Cancer Research: An Official Journal of the American Association for Cancer Research|volume=17|issue=10|pages=3443–3454|doi=10.1158/1078-0432.CCR-10-1071|issn=1557-3265|pmc=3096736|pmid=21385932}}</ref>
|-
|20q
|Gain
|20q13
|''CD40''
|P
|No
|Over expression of CD40 activates NF-kB signaling, promotes proliferation and immune evasion.<ref>{{Cite journal|last=Alibrahim|first=Mohamed N.|last2=Gloghini|first2=Annunziata|last3=Carbone|first3=Antonino|date=2024-12-05|title=Pathobiological Features and Therapeutic Opportunities Linked to TNF Family Member Expression in Classic Hodgkin Lymphoma|url=https://pubmed.ncbi.nlm.nih.gov/39682256|journal=Cancers|volume=16|issue=23|pages=4070|doi=10.3390/cancers16234070|issn=2072-6694|pmc=11640334|pmid=39682256}}</ref><ref>{{Cite journal|last=De Re|first=Valli|last2=Caggiari|first2=Laura|last3=Repetto|first3=Ombretta|last4=Mussolin|first4=Lara|last5=Mascarin|first5=Maurizio|date=2019-10-02|title=Classical Hodgkin's Lymphoma in the Era of Immune Checkpoint Inhibition|url=https://pubmed.ncbi.nlm.nih.gov/31581738|journal=Journal of Clinical Medicine|volume=8|issue=10|pages=1596|doi=10.3390/jcm8101596|issn=2077-0383|pmc=6832444|pmid=31581738}}</ref>
|-
|-
|6q
|6q
|Loss
|Loss
|6q23-24
|6q23-24
|TNFAIP3
|''TNFAIP3''
|P
|No
|Loss of TNFAIP3 (A20), a negative regulator of NF‑κB,  enhance NF-kB signling <ref name=":0">{{Cite journal|last=Schmitz|first=Roland|last2=Hansmann|first2=Martin-Leo|last3=Bohle|first3=Verena|last4=Martin-Subero|first4=Jose Ignacio|last5=Hartmann|first5=Sylvia|last6=Mechtersheimer|first6=Gunhild|last7=Klapper|first7=Wolfram|last8=Vater|first8=Inga|last9=Giefing|first9=Maciej|date=2009-05-11|title=TNFAIP3 (A20) is a tumor suppressor gene in Hodgkin lymphoma and primary mediastinal B cell lymphoma|url=https://pubmed.ncbi.nlm.nih.gov/19380639|journal=The Journal of Experimental Medicine|volume=206|issue=5|pages=981–989|doi=10.1084/jem.20090528|issn=1540-9538|pmc=2715030|pmid=19380639}}</ref>
|-
|13q
|Loss
|13q14
|''RB1''
|P
|P
|No
|No
|Loss of TNFAIP3 (A20) disrupts NF-κB regulation <ref name=":0">{{Cite journal|last=Schmitz|first=Roland|last2=Hansmann|first2=Martin-Leo|last3=Bohle|first3=Verena|last4=Martin-Subero|first4=Jose Ignacio|last5=Hartmann|first5=Sylvia|last6=Mechtersheimer|first6=Gunhild|last7=Klapper|first7=Wolfram|last8=Vater|first8=Inga|last9=Giefing|first9=Maciej|date=2009-05-11|title=TNFAIP3 (A20) is a tumor suppressor gene in Hodgkin lymphoma and primary mediastinal B cell lymphoma|url=https://pubmed.ncbi.nlm.nih.gov/19380639|journal=The Journal of Experimental Medicine|volume=206|issue=5|pages=981–989|doi=10.1084/jem.20090528|issn=1540-9538|pmc=2715030|pmid=19380639}}</ref>
|loss of tumor suppressors and contribute to HRS cell survival
|}
|}


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