HAEM5:EBV-positive diffuse large B-cell lymphoma: Difference between revisions
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|Mutations in | |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''<ref name=":2" /> | |''CCR7''<ref name=":2" /> | ||
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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> | ||
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|''DAPK1''<ref name=":2" /> | |''DAPK1''<ref name=":2" /> | ||