Compendium of Cancer Genome Aberrations

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

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==Gene Rearrangements==
==Gene Rearrangements==
Put your text here and fill in the table <span style="color:#0070C0">(''Instructions: Details on clinical significance such as prognosis and other important information can be provided in the notes section. Please include references throughout the table. Do not delete the table.'')</span>
Detection of clonal IGH and IGK gene rearrangements supports a neoplastic process and helps differentiate EBV-positive DLBCL from reactive, polyclonal B-cell proliferations.<ref name=":4">{{Cite journal|title=BlueBooksOnline|url=https://tumourclassification.iarc.who.int/chaptercontent/63/149}}</ref> However, the major oncogenic driver rearrangements seen in other aggressive B-cell lymphoma such as the ‘double/triple-hit’ rearrangements involving ''MYC, BCL2, or BCL6'' are rare in EBV-positive DLBCL<ref>{{Cite journal|last=Liu|first=Hui|last2=Xu-Monette|first2=Zijun Y|last3=Tang|first3=Guilin|last4=Wang|first4=Wei|last5=Kim|first5=Young|last6=Yuan|first6=Ji|last7=Li|first7=Yu|last8=Chen|first8=Weina|last9=Li|first9=Yanping|date=2022|title=EBV+ high-grade B cell lymphoma with MYC and BCL2 and/or BCL6 rearrangements: a multi-institutional study|url=https://onlinelibrary.wiley.com/doi/abs/10.1111/his.14585|journal=Histopathology|language=en|volume=80|issue=3|pages=575–588|doi=10.1111/his.14585|issn=1365-2559}}</ref><ref name=":1">{{Cite journal|last=Frontzek|first=Fabian|last2=Staiger|first2=Annette M.|last3=Wullenkord|first3=Ramona|last4=Grau|first4=Michael|last5=Zapukhlyak|first5=Myroslav|last6=Kurz|first6=Katrin S.|last7=Horn|first7=Heike|last8=Erdmann|first8=Tabea|last9=Fend|first9=Falko|date=2023-03|title=Molecular profiling of EBV associated diffuse large B-cell lymphoma|url=https://www.nature.com/articles/s41375-022-01804-w|journal=Leukemia|language=en|volume=37|issue=3|pages=670–679|doi=10.1038/s41375-022-01804-w|issn=1476-5551|pmc=9991915|pmid=36604606}}</ref>. Its pathogenesis is driven more by EBV-related mechanisms and distinct genetic alterations than by these characteristic translocations. ''IRF4'' rearrangements involving known partners such as ''IGH'' and more recently ''RHOH'' have also been described in EBV-positive DLBCL<ref name=":0">{{Cite journal|last=Zhang|first=Yuxiu|last2=Li|first2=Anqi|last3=Li|first3=Yimin|last4=Ouyang|first4=Binshen|last5=Wang|first5=Xuan|last6=Zhang|first6=Lei|last7=Xu|first7=Haimin|last8=Gu|first8=Yijin|last9=Lu|first9=Xinyuan|date=2024-11|title=Clinicopathological and Molecular Characteristics of Rare EBV-associated Diffuse Large B-cell Lymphoma With IRF4 Rearrangement|url=https://journals.lww.com/10.1097/PAS.0000000000002301|journal=American Journal of Surgical Pathology|language=en|volume=48|issue=11|pages=1341–1348|doi=10.1097/PAS.0000000000002301|issn=0147-5185}}</ref>. ''RHOH'', is an RHO GTPase family member and negative regulator of cell growth, has been described as a fusion partner in other lymphoid neoplasms but is more commonly linked to non-coding somatic hypermutation in DLBCL<ref name=":0" /> Clinically, morphologically as well as at the molecular level, EBV+DLBCL-''IRF4''-R resemble and behave like EBV+DLBCL<ref name=":0" />
{| class="wikitable sortable"
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!Established Clinical Significance Per Guidelines - Yes or No (Source)
!Established Clinical Significance Per Guidelines - Yes or No (Source)
!Clinical Relevance Details/Other Notes
!Clinical Relevance Details/Other Notes
|-
|<span class="blue-text">EXAMPLE:</span> ''ABL1''||<span class="blue-text">EXAMPLE:</span> ''BCR::ABL1''||<span class="blue-text">EXAMPLE:</span> The pathogenic derivative is the der(22) resulting in fusion of 5’ BCR and 3’ABL1.||<span class="blue-text">EXAMPLE:</span> t(9;22)(q34;q11.2)
|<span class="blue-text">EXAMPLE:</span> Common (CML)
|<span class="blue-text">EXAMPLE:</span> D, P, T
|<span class="blue-text">EXAMPLE:</span> Yes (WHO, NCCN)
|<span class="blue-text">EXAMPLE:</span>
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). BCR::ABL1 is generally favorable in CML (add reference).
|-
|<span class="blue-text">EXAMPLE:</span> ''CIC''
|<span class="blue-text">EXAMPLE:</span> ''CIC::DUX4''
|<span class="blue-text">EXAMPLE:</span> Typically, the last exon of ''CIC'' is fused to ''DUX4''. The fusion breakpoint in ''CIC'' is usually intra-exonic and removes an inhibitory sequence, upregulating ''PEA3'' genes downstream of ''CIC'' including ''ETV1'', ''ETV4'', and ''ETV5''.
|<span class="blue-text">EXAMPLE:</span> t(4;19)(q25;q13)
|<span class="blue-text">EXAMPLE:</span> Common (CIC-rearranged sarcoma)
|<span class="blue-text">EXAMPLE:</span> D
|
|<span class="blue-text">EXAMPLE:</span>
''DUX4'' has many homologous genes; an alternate translocation in a minority of cases is t(10;19), but this is usually indistinguishable from t(4;19) by short-read sequencing (add references).
|-
|<span class="blue-text">EXAMPLE:</span> ''ALK''
|<span class="blue-text">EXAMPLE:</span> ''ELM4::ALK''
Other fusion partners include ''KIF5B, NPM1, STRN, TFG, TPM3, CLTC, KLC1''
|<span class="blue-text">EXAMPLE:</span> Fusions result in constitutive activation of the ''ALK'' tyrosine kinase. The most common ''ALK'' fusion is ''EML4::ALK'', with breakpoints in intron 19 of ''ALK''. At the transcript level, a variable (5’) partner gene is fused to 3’ ''ALK'' at exon 20. Rarely, ''ALK'' fusions contain exon 19 due to breakpoints in intron 18.
|<span class="blue-text">EXAMPLE:</span> N/A
|<span class="blue-text">EXAMPLE:</span> Rare (Lung adenocarcinoma)
|<span class="blue-text">EXAMPLE:</span> T
|
|<span class="blue-text">EXAMPLE:</span>
Both balanced and unbalanced forms are observed by FISH (add references).
|-
|<span class="blue-text">EXAMPLE:</span> ''ABL1''
|<span class="blue-text">EXAMPLE:</span> N/A
|<span class="blue-text">EXAMPLE:</span> Intragenic deletion of exons 2–7 in ''EGFR'' removes the ligand-binding domain, resulting in a constitutively active tyrosine kinase with downstream activation of multiple oncogenic pathways.
|<span class="blue-text">EXAMPLE:</span> N/A
|<span class="blue-text">EXAMPLE:</span> Recurrent (IDH-wildtype Glioblastoma)
|<span class="blue-text">EXAMPLE:</span> D, P, T
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==Individual Region Genomic Gain/Loss/LOH==
==Individual Region Genomic Gain/Loss/LOH==
Put your text here and fill in the table <span style="color:#0070C0">(''Instructions: Includes aberrations not involving gene rearrangements. Details on clinical significance such as prognosis and other important information can be provided in the notes section. Can refer to CGC workgroup tables as linked on the homepage if applicable. Please include references throughout the table. Do not delete the table.'') </span>
None reported so far.
 
{| class="wikitable sortable"
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!Established Clinical Significance Per Guidelines - Yes or No (Source)
!Established Clinical Significance Per Guidelines - Yes or No (Source)
!Clinical Relevance Details/Other Notes
!Clinical Relevance Details/Other Notes
|-
|<span class="blue-text">EXAMPLE:</span>
7
|<span class="blue-text">EXAMPLE:</span> Loss
|<span class="blue-text">EXAMPLE:</span>
chr7
|<span class="blue-text">EXAMPLE:</span>
Unknown
|<span class="blue-text">EXAMPLE:</span> D, P
|<span class="blue-text">EXAMPLE:</span> No
|<span class="blue-text">EXAMPLE:</span>
Presence of monosomy 7 (or 7q deletion) is sufficient for a diagnosis of AML with MDS-related changes when there is ≥20% blasts and no prior therapy (add reference).  Monosomy 7/7q deletion is associated with a poor prognosis in AML (add references).
|-
|<span class="blue-text">EXAMPLE:</span>
8
|<span class="blue-text">EXAMPLE:</span> Gain
|<span class="blue-text">EXAMPLE:</span>
chr8
|<span class="blue-text">EXAMPLE:</span>
Unknown
|<span class="blue-text">EXAMPLE:</span> D, P
|
|<span class="blue-text">EXAMPLE:</span>
Common recurrent secondary finding for t(8;21) (add references).
|-
|<span class="blue-text">EXAMPLE:</span>
17
|<span class="blue-text">EXAMPLE:</span> Amp
|<span class="blue-text">EXAMPLE:</span>
17q12; chr17:39,700,064-39,728,658 [hg38; 28.6 kb]
|<span class="blue-text">EXAMPLE:</span>
''ERBB2''
|<span class="blue-text">EXAMPLE:</span> D, P, T
|
|<span class="blue-text">EXAMPLE:</span>
Amplification of ''ERBB2'' is associated with HER2 overexpression in HER2 positive breast cancer (add references). Add criteria for how amplification is defined.
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==Characteristic Chromosomal or Other Global Mutational Patterns==
==Characteristic Chromosomal or Other Global Mutational Patterns==
Put your text here and fill in the table <span style="color:#0070C0">(I''nstructions: Included in this category are alterations such as hyperdiploid; gain of odd number chromosomes including typically chromosome 1, 3, 5, 7, 11, and 17; co-deletion of 1p and 19q; complex karyotypes without characteristic genetic findings; chromothripsis; microsatellite instability; homologous recombination deficiency; mutational signature pattern; etc. Details on clinical significance such as prognosis and other important information can be provided in the notes section. Please include references throughout the table. Do not delete the table.'')</span>
According to the most recent literature, EBV-positive DLBCL shows frequent structural genomic alterations, including recurrent '''6q deletions''' (44%)<ref name=":2" />, often involving important tumor-suppressor genes like '''''PRDM1 and A20''''', which play key roles in B-cell lymphoma development,''',''' although these cases show fewer'''''ANKRD11''1''' and'''''NOTCH2''2''' mutations. Multiple focal amplifications are prominent, most notably '''6p25.3''' containing ''IRF4'' (35%) and '''9p24.1''' including ''PD-L1/PD-L2'' and ''JAK2'' (20%), with PD-L1 amplification strongly correlating with protein overexpression. Additional immune-escape and oncogenic amplifications include '''1q24.3 (FASL)''' (22%), '''11q24.3 (ETS1/FLI1)''' (20%), and '''2q31.3''' containing the lncRNA ''SChLAP1''. Deletions are less common but include broad losses of '''18p/18q''' and a recurrent focal deletion at '''11p15.3''' impacting the tumor-suppressor ''DKK3''. These structural alterations did not correspond to distinct gene-expression profiles.
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==Gene Mutations (SNV/INDEL)==
==Gene Mutations (SNV/INDEL)==
The mutation landscape is primarily characterized by frequent alterations in the NF-κB, WNT, and IL-6/JAK/STAT pathways, distinguishing it from the mutation profile seen in EBV-negative DLBCL-NOS.<ref name=":4" /><ref name=":1" /><ref name=":2" />
According to the most recent literature,<ref name=":2" /> frequent mutations in '''''ARID1A''', '''KMT2A''', '''ANKRD11''', '''NOTCH2''', and '''KMT2D''''' (30-45% of cases) are observed in EBV-positive DLBCL, with higher frequencies compared to EBV-negative DLBCL. Additionally, '''''CCR6''', '''CCR7''', '''DAPK1''', '''TNFRSF21''', and '''YY1''''' were identified as recurrent and specific mutations in EBV-positive DLBCL, differentiating it from other DLBCL subtypes.<ref name=":4" /><ref name=":2" />
Put your text here and fill in the table <span style="color:#0070C0">(''Instructions: This table is not meant to be an exhaustive list; please include only genes/alterations that are recurrent or common as well either disease defining and/or clinically significant. If a gene has multiple mechanisms depending on the type or site of the alteration, add multiple entries in the table. For clinical significance, denote associations with FDA-approved therapy (not an extensive list of applicable drugs) and NCCN or other national guidelines if applicable; Can also refer to CGC workgroup tables as linked on the homepage if applicable as well as any high impact papers or reviews of gene mutations in this entity. Details on clinical significance such as prognosis and other important information such as concomitant and mutually exclusive mutations can be provided in the notes section. Please include references throughout the table. Do not delete the table.'') </span>
Put your text here and fill in the table <span style="color:#0070C0">(''Instructions: This table is not meant to be an exhaustive list; please include only genes/alterations that are recurrent or common as well either disease defining and/or clinically significant. If a gene has multiple mechanisms depending on the type or site of the alteration, add multiple entries in the table. For clinical significance, denote associations with FDA-approved therapy (not an extensive list of applicable drugs) and NCCN or other national guidelines if applicable; Can also refer to CGC workgroup tables as linked on the homepage if applicable as well as any high impact papers or reviews of gene mutations in this entity. Details on clinical significance such as prognosis and other important information such as concomitant and mutually exclusive mutations can be provided in the notes section. Please include references throughout the table. Do not delete the table.'') </span>
{| class="wikitable sortable"
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!Clinical Relevance Details/Other Notes
!Clinical Relevance Details/Other Notes
|-
|-
|<span class="blue-text">EXAMPLE:</span>''EGFR''
|''SOCS1''<ref name=":1" /><ref name=":2">{{Cite journal|last=Gebauer|first=Niklas|last2=Künstner|first2=Axel|last3=Ketzer|first3=Julius|last4=Witte|first4=Hanno M.|last5=Rausch|first5=Tobias|last6=Benes|first6=Vladimir|last7=Zimmermann|first7=Jürgen|last8=Gebauer|first8=Judith|last9=Merz|first9=Hartmut|date=2021-05-26|title=Genomic insights into the pathogenesis of Epstein–Barr virus-associated diffuse large B-cell lymphoma by whole-genome and targeted amplicon sequencing|url=https://www.nature.com/articles/s41408-021-00493-5|journal=Blood Cancer Journal|language=en|volume=11|issue=5|pages=102|doi=10.1038/s41408-021-00493-5|issn=2044-5385|pmc=8155002|pmid=34039950}}</ref><ref name=":3">{{Cite journal|last=Takahashi|first=Takumi|last2=Sawada|first2=Keisuke|last3=Yamashita|first3=Takahisa|last4=Yamamoto|first4=Wataru|last5=Iijima|first5=Yosuke|last6=Adachi|first6=Akiko|last7=Kashimura|first7=Makoto|last8=Tabayashi|first8=Takayuki|last9=Kizaki|first9=Masahiro|date=2025|title=Genetic Profiling Reveals the Distinctions Among MTX-Associated DLBCL, EBV-Positive Mucocutaneous Ulcer, and EBV + DLBCL|url=https://onlinelibrary.wiley.com/doi/abs/10.1111/cas.70111|journal=Cancer Science|language=en|volume=116|issue=8|pages=2306–2316|doi=10.1111/cas.70111|issn=1349-7006|pmc=12317404|pmid=40458922}}</ref>


<br />
<br />
|<span class="blue-text">EXAMPLE:</span> Exon 18-21 activating mutations
|Loss of function aberration in the SH2 domain<ref name=":1" />
|<span class="blue-text">EXAMPLE:</span> Oncogene
|Tumor Suppressor gene<ref>{{Cite journal|last=Liau|first=Nicholas P. D.|last2=Laktyushin|first2=Artem|last3=Lucet|first3=Isabelle S.|last4=Murphy|first4=James M.|last5=Yao|first5=Shenggen|last6=Whitlock|first6=Eden|last7=Callaghan|first7=Kimberley|last8=Nicola|first8=Nicos A.|last9=Kershaw|first9=Nadia J.|date=2018-04-19|title=The molecular basis of JAK/STAT inhibition by SOCS1|url=https://www.nature.com/articles/s41467-018-04013-1|journal=Nature Communications|language=en|volume=9|issue=1|pages=1558|doi=10.1038/s41467-018-04013-1|issn=2041-1723|pmc=5908791|pmid=29674694}}</ref>
|<span class="blue-text">EXAMPLE:</span> Common (lung cancer)
|Common<ref name=":1" /><ref name=":2" /><ref name=":3" />
|<span class="blue-text">EXAMPLE:</span> T
|P, T
|<span class="blue-text">EXAMPLE:</span> Yes (NCCN)
|<span class="blue-text">EXAMPLE:</span> Yes (NCCN)
|<span class="blue-text">EXAMPLE:</span> Exons 18, 19, and 21 mutations are targetable for therapy. Exon 20 T790M variants cause resistance to first generation TKI therapy and are targetable by second and third generation TKIs (add references).
|SOCS1 mutations, especially affecting SOCS-BOX domain, improve prognosis with better PFS and OS, likely due to their role in modulating the JAK-STAT pathway.<ref>{{Cite journal|last=Zhang|first=Xin-Yi|last2=Xing|first2=Tong-Yao|last3=Hua|first3=Wei|last4=Li|first4=Yue|last5=Kong|first5=Yi-Lin|last6=Pan|first6=Bi-Hui|last7=Zhang|first7=Xin-Yu|last8=Wu|first8=Jia-Zhu|last9=Shen|first9=Hao-Rui|date=2025-08-31|title=Prognostic Role of SOCS1 Mutations in Diffuse Large B-Cell Lymphoma|url=https://www.e-crt.org/journal/view.php?doi=10.4143/crt.2025.420|journal=Cancer Research and Treatment|language=English|doi=10.4143/crt.2025.420|issn=1598-2998}}</ref>
|-
|-
|<span class="blue-text">EXAMPLE:</span> ''TP53''; Variable LOF mutations
|''STAT3''<ref name=":1" /><ref name=":2" />
<br />
<br />
|<span class="blue-text">EXAMPLE:</span> Variable LOF mutations
|Activating missense mutations<ref name=":1" />  
|<span class="blue-text">EXAMPLE:</span> Tumor Supressor Gene
|Oncogene/ Tumor suppressor gene<ref>{{Cite journal|last=Carpenter|first=Richard|last2=Lo|first2=Hui-Wen|date=2014-04-16|title=STAT3 Target Genes Relevant to Human Cancers|url=https://www.mdpi.com/2072-6694/6/2/897|journal=Cancers|language=en|volume=6|issue=2|pages=897–925|doi=10.3390/cancers6020897|issn=2072-6694|pmc=4074809|pmid=24743777}}</ref>
|<span class="blue-text">EXAMPLE:</span> Common (breast cancer)
|Common<ref name=":1" /><ref name=":2" />
|<span class="blue-text">EXAMPLE:</span> P
|T
|
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|<span class="blue-text">EXAMPLE:</span> >90% are somatic; rare germline alterations associated with Li-Fraumeni syndrome (add reference). Denotes a poor prognosis in breast cancer.
|STAT3 is an effective molecular target for ABC-like DLBCL therapy<ref>{{Cite journal|last=Scuto|first=Anna|last2=Kujawski|first2=Maciej|last3=Kowolik|first3=Claudia|last4=Krymskaya|first4=Ludmila|last5=Wang|first5=Lin|last6=Weiss|first6=Lawrence M.|last7=DiGiusto|first7=David|last8=Yu|first8=Hua|last9=Forman|first9=Stephen|date=2011-05-01|title=STAT3 Inhibition Is a Therapeutic Strategy for ABC-like Diffuse Large B-Cell Lymphoma|url=https://aacrjournals.org/cancerres/article/71/9/3182/575555/STAT3-Inhibition-Is-a-Therapeutic-Strategy-for-ABC|journal=Cancer Research|language=en|volume=71|issue=9|pages=3182–3188|doi=10.1158/0008-5472.CAN-10-2380|issn=0008-5472}}</ref>
|-
|-
|<span class="blue-text">EXAMPLE:</span> ''BRAF''; Activating mutations
|''KMT2D''<ref name=":1" /><ref name=":2" /><ref name=":5">{{Cite journal|last=Zhou|first=Yangying|last2=Xu|first2=Zhijie|last3=Lin|first3=Wei|last4=Duan|first4=Yumei|last5=Lu|first5=Can|last6=Liu|first6=Wei|last7=Su|first7=Weiping|last8=Yan|first8=Yuanliang|last9=Liu|first9=Huan|date=2019-07-25|title=Comprehensive Genomic Profiling of EBV-Positive Diffuse Large B-cell Lymphoma and the Expression and Clinicopathological Correlations of Some Related Genes|url=https://www.frontiersin.org/article/10.3389/fonc.2019.00683/full|journal=Frontiers in Oncology|volume=9|doi=10.3389/fonc.2019.00683|issn=2234-943X|pmc=6669985|pmid=31403034}}</ref>
|<span class="blue-text">EXAMPLE:</span> Activating mutations
|<span class="blue-text">EXAMPLE:</span> Oncogene
|<span class="blue-text">EXAMPLE:</span> Common (melanoma)
|<span class="blue-text">EXAMPLE:</span> T
|
|
|Tumor Suppressor Gene<ref>{{Cite journal|title=OncoKB™ - MSK's Precision Oncology Knowledge Base|url=https://www.oncokb.org/|language=en}}</ref>
|Common<ref name=":1" /><ref name=":2" /><ref name=":5" />
|D
|No
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|}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.
==Epigenomic Alterations==
==Epigenomic Alterations==
Put your text here
None identified so far.
==Genes and Main Pathways Involved==
==Genes and Main Pathways Involved==
Put your text here and fill in the table <span style="color:#0070C0">(''Instructions: Please include references throughout the table. Do not delete the table.)''</span>
Put your text here and fill in the table <span style="color:#0070C0">(''Instructions: Please include references throughout the table. Do not delete the table.)''</span>
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==References==
==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 where you want to insert the reference, selecting the “Cite” icon at the top of the wiki page, and using the “Automatic” tab option to search by PMID to select the reference to insert. 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. To insert the same reference again later in the page, select the “Cite” icon and “Re-use” to find the reference; DO NOT insert the same reference twice using the “Automatic” tab as it will be treated as two separate references. The reference list in this section will be automatically generated and sorted''</span><span style="color:#0070C0">''.''</span><span style="color:#0070C0">)</span>
 
# https://tumourclassification.iarc.who.int/chaptercontent/63/149
# Liu H, Xu-Monette ZY, Tang G, Wang W, Kim Y, Yuan J, Li Y, Chen W, Li Y, Fedoriw GY, Zhu F, Fang X, Luedke C, Medeiros LJ, Young KH & Hu S (2022) ''Histopathology'' 80, 575–588. <nowiki>https://doi.org/10.1111/his.14585</nowiki> EBV+ high-grade B cell lymphoma with ''MYC'' and ''BCL2'' and/or ''BCL6'' rearrangements: a multi-institutional study
# Frontzek, F., Staiger, A.M., Wullenkord, R. ''et al.'' Molecular profiling of EBV associated diffuse large B-cell lymphoma. ''Leukemia'' 37, 670–679 (2023). <nowiki>https://doi.org/10.1038/s41375-022-01804-w</nowiki>
# Zhang, Yuxiu MD*; Li, Anqi MD, PhD*; Li, Yimin MD, PhD*; Ouyang, Binshen MD, PhD*; Wang, Xuan MD, PhD*; Zhang, Lei MSc*; Xu, Haimin BSMT*; Gu, Yijin MSc*; Lu, Xinyuan MD, PhD†; Dong, Lei MD, PhD*; Yi, Hongmei MD, PhD*; Wang, Chaofu MD, PhD*. Clinicopathological and Molecular Characteristics of Rare EBV-associated Diffuse Large B-cell Lymphoma With IRF4 Rearrangement. The American Journal of Surgical Pathology 48(11):p 1341-1348, November 2024. | DOI: 10.1097/PAS.0000000000002301
# Gebauer, N., Künstner, A., Ketzer, J. ''et al.'' Genomic insights into the pathogenesis of Epstein–Barr virus-associated diffuse large B-cell lymphoma by whole-genome and targeted amplicon sequencing. ''Blood Cancer J.'' 11, 102 (2021). <nowiki>https://doi.org/10.1038/s41408-021-00493-5</nowiki>
# Takahashi, T., Sawada, K., Yamashita, T., Yamamoto, W., Iijima, Y., Adachi, A., Kashimura, M., Tabayashi, T., Kizaki, M., Kaneko, T., Tamaru, J.-i., Higashi, M. and Momose, S. (2025), Genetic Profiling Reveals the Distinctions Among MTX-Associated DLBCL, EBV-Positive Mucocutaneous Ulcer, and EBV + DLBCL. Cancer Sci, 116: 2306-2316. <nowiki>https://doi.org/10.1111/cas.70111</nowiki>
# Liau, N.P.D., Laktyushin, A., Lucet, I.S. ''et al.'' The molecular basis of JAK/STAT inhibition by SOCS1. ''Nat Commun'' 9, 1558 (2018). <nowiki>https://doi.org/10.1038/s41467-018-04013-1</nowiki>  
# Zhang XY, Xing TY, Hua W, Li Y, Kong YL, Pan BH, Zhang XY, Wu JZ, Shen HR, Yin H, Wang L, Li JY, Gao R, Liang JH, Xu W. Prognostic Role of SOCS1 Mutations in Diffuse Large B-Cell Lymphoma. Cancer Res Treat. ;0.0. doi: 10.4143/crt.2025.420
# Carpenter, R. L., & Lo, H.-W. (2014). STAT3 Target Genes Relevant to Human Cancers. ''Cancers'', ''6''(2), 897-925. <nowiki>https://doi.org/10.3390/cancers6020897</nowiki>


==Notes==
==Notes==
Retrieved from "https://test.ccga.io/index.php/HAEM5:EBV-positive_diffuse_large_B-cell_lymphoma"