Compendium of Cancer Genome Aberrations

HAEM5:EBV-positive diffuse large B-cell lymphoma: Difference between revisions

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|Mutations in ''CCR6'' may act as oncogenic drivers—especially in MALT lymphoma—by disrupting β-arrestin–mediated receptor desensitization, leading to unchecked intracellular signaling.<ref name=":2" /><ref>{{Cite journal|last=Moody|first=Sarah|last2=Thompson|first2=Joe Sneath|last3=Chuang|first3=Shih-Sung|last4=Liu|first4=Hongxiang|last5=Raderer|first5=Markus|last6=Vassiliou|first6=George|last7=Wlodarska|first7=Iwona|last8=Wu|first8=Fangtian|last9=Cogliatti|first9=Sergio|date=2018-08|title=Novel GPR34 and CCR6 mutation and distinct genetic profiles in MALT lymphomas of different sites|url=http://www.haematologica.org/lookup/doi/10.3324/haematol.2018.191601|journal=Haematologica|language=en|volume=103|issue=8|pages=1329–1336|doi=10.3324/haematol.2018.191601|issn=0390-6078|pmc=6068028|pmid=29674500}}</ref>
|Mutations in ''CCR6'' may act as oncogenic drivers—especially in MALT lymphoma—by disrupting β-arrestin–mediated receptor desensitization, leading to unchecked intracellular signaling.<ref name=":2" /><ref>{{Cite journal|last=Moody|first=Sarah|last2=Thompson|first2=Joe Sneath|last3=Chuang|first3=Shih-Sung|last4=Liu|first4=Hongxiang|last5=Raderer|first5=Markus|last6=Vassiliou|first6=George|last7=Wlodarska|first7=Iwona|last8=Wu|first8=Fangtian|last9=Cogliatti|first9=Sergio|date=2018-08|title=Novel GPR34 and CCR6 mutation and distinct genetic profiles in MALT lymphomas of different sites|url=http://www.haematologica.org/lookup/doi/10.3324/haematol.2018.191601|journal=Haematologica|language=en|volume=103|issue=8|pages=1329–1336|doi=10.3324/haematol.2018.191601|issn=0390-6078|pmc=6068028|pmid=29674500}}</ref>
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|''CCR7'' upregulation in EBV-infected cells may promote lymphoid homing and viral persistence, and recurrent ''CCR7'' mutations in EBV+ DLBCL could similarly enhance proliferation and migration, as seen in other cancers.<ref name=":2" /><ref>{{Cite journal|last=Kocks|first=Jessica R|last2=Adler|first2=Heiko|last3=Danzer|first3=Heike|last4=Hoffmann|first4=Katharina|last5=Jonigk|first5=Danny|last6=Lehmann|first6=Ulrich|last7=Förster|first7=Reinhold|date=2009-06-01|title=Chemokine Receptor CCR7 Contributes to a Rapid and Efficient Clearance of Lytic Murine γ-Herpes Virus 68 from the Lung, Whereas Bronchus-Associated Lymphoid Tissue Harbors Virus during Latency|url=https://academic.oup.com/jimmunol/article/182/11/6861/8007100|journal=The Journal of Immunology|language=en|volume=182|issue=11|pages=6861–6869|doi=10.4049/jimmunol.0801826|issn=1550-6606}}</ref>
|''CCR7'' upregulation in EBV-infected cells may promote lymphoid homing and viral persistence, and recurrent ''CCR7'' mutations in EBV+ DLBCL could similarly enhance proliferation and migration, as seen in other cancers.<ref name=":2" /><ref>{{Cite journal|last=Kocks|first=Jessica R|last2=Adler|first2=Heiko|last3=Danzer|first3=Heike|last4=Hoffmann|first4=Katharina|last5=Jonigk|first5=Danny|last6=Lehmann|first6=Ulrich|last7=Förster|first7=Reinhold|date=2009-06-01|title=Chemokine Receptor CCR7 Contributes to a Rapid and Efficient Clearance of Lytic Murine γ-Herpes Virus 68 from the Lung, Whereas Bronchus-Associated Lymphoid Tissue Harbors Virus during Latency|url=https://academic.oup.com/jimmunol/article/182/11/6861/8007100|journal=The Journal of Immunology|language=en|volume=182|issue=11|pages=6861–6869|doi=10.4049/jimmunol.0801826|issn=1550-6606}}</ref>
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|Oncogenic ''DAPK1'' mutations appear to be '''unique to EBV+ DLBCL'''<ref name=":2" />. Prior studies have shown poor prognosis associated with hypermethylation - loss of function mutations in ''DAPK1'' and may similarly contribute to adverse prognosis.<ref name=":6" />
|Oncogenic ''DAPK1'' mutations appear to be '''unique/ exclusive to EBV+ DLBCL'''<ref name=":2" />. Prior studies have shown poor prognosis associated with hypermethylation - loss of function mutations in ''DAPK1'' and may similarly contribute to adverse prognosis.<ref name=":6" />
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|''TNFRSF21''<ref name=":2" />
|''TNFRSF21''<ref name=":2" />
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|Impaired ''TNFRSF21/DR6'' function has been associated with increased cell proliferation and reduced apoptosis in B- and T-cell malignancies, including EBV-associated AITL<ref>{{Cite journal|last=Wang|first=Ming|last2=Zhang|first2=Shaowei|last3=Chuang|first3=Shih-Sung|last4=Ashton-Key|first4=Margaret|last5=Ochoa|first5=Eguzkine|last6=Bolli|first6=Niccolo|last7=Vassiliou|first7=George|last8=Gao|first8=Zifen|last9=Du|first9=Ming-Qing|date=2017-03-14|title=Angioimmunoblastic T cell lymphoma: novel molecular insights by mutation profiling|url=https://www.oncotarget.com/lookup/doi/10.18632/oncotarget.14846|journal=Oncotarget|language=en|volume=8|issue=11|pages=17763–17770|doi=10.18632/oncotarget.14846|issn=1949-2553|pmc=5392284|pmid=28148900}}</ref>
|Impaired ''TNFRSF21/DR6'' function has been associated with increased cell proliferation and reduced apoptosis in B- and T-cell malignancies, including EBV-associated AITL<ref>{{Cite journal|last=Wang|first=Ming|last2=Zhang|first2=Shaowei|last3=Chuang|first3=Shih-Sung|last4=Ashton-Key|first4=Margaret|last5=Ochoa|first5=Eguzkine|last6=Bolli|first6=Niccolo|last7=Vassiliou|first7=George|last8=Gao|first8=Zifen|last9=Du|first9=Ming-Qing|date=2017-03-14|title=Angioimmunoblastic T cell lymphoma: novel molecular insights by mutation profiling|url=https://www.oncotarget.com/lookup/doi/10.18632/oncotarget.14846|journal=Oncotarget|language=en|volume=8|issue=11|pages=17763–17770|doi=10.18632/oncotarget.14846|issn=1949-2553|pmc=5392284|pmid=28148900}}</ref>
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|''CSNK2B'', another alteration uniquely seen in EBV⁺ DLBCL, remains poorly characterized and its oncogenic role is not yet well understood.<ref name=":2" />
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|''YY1''<ref name=":2" />
|''YY1''<ref name=":2" />
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|''YY1'' is a known oncogenic driver in DLBCL, where its overexpression promotes B-cell transformation and tumor progression, independent of EBV status.<ref name=":2" />
|''YY1'' is a known oncogenic driver in DLBCL, where its overexpression promotes B-cell transformation and tumor progression, independent of EBV status.<ref name=":2" />
|}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.
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