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Primary_Tonsillar_Lymphoma

Pathophysiology description

2025-12-15
Falcon MONDO:0044884 Model: Edison Scientific Literature 17 citations

Pathophysiology description Primary tonsillar lymphoma most commonly comprises large B‑cell lymphomas arising in the germinal center–rich microenvironment of the palatine tonsil (Waldeyer’s ring). Contemporary series of large B‑cell lymphomas in Waldeyer’s ring show a roughly even split between germinal center B‑cell–like (GCB) and activated B‑cell–like (ABC) transcriptional subtypes, with distinct mutational programs: GCB cases enriched for BCL2 and EZH2 mutations, and ABC cases enriched for CD79B and MYD88, reflecting BCR/NF‑κB signaling and GC epigenetic deregulation, respectively (adult cohort; IRF4 rearrangements ~6.7%) (streich2023prevalenceofirf4 pages 1-2, streich2023prevalenceofirf4 pages 3-5). EBV-positive DLBCL can arise at tonsillar sites in older or immunocompromised patients and is driven by viral latency programs (e.g., LMP1, EBNA), with tonsillar B cells serving as a primary entry and latency reservoir for EBV (hussein2018nonhodgkin’slymphomaof pages 28-32). Tonsillar lymphomas also include rarer entities with site predilection in Waldeyer’s ring, such as large B‑cell lymphoma with IRF4 rearrangement (often pediatric/young adult, usually chemo‑responsive), mantle cell lymphoma, and plasmablastic lymphoma (often HIV/EBV associated), as well as occasional high‑grade B‑cell lymphomas (double‑/triple‑hit) with MYC plus BCL2/BCL6 rearrangements that are aggressive and may require intensified regimens (streich2023prevalenceofirf4 pages 1-2, streich2023prevalenceofirf4 pages 3-5, hussein2018nonhodgkin’slymphomaof pages 28-32, hinkle2020hivassociated“doublehit”lymphoma pages 1-3, hinkle2020hivassociated“doublehit”lymphoma pages 3-5).

Core Pathophysiology - Primary mechanisms: - Aberrant B‑cell receptor (BCR) signaling with chronic active signaling in ABC‑type disease (CD79B mutations) and downstream NF‑κB activation cooperatively with MYD88 mutations (streich2023prevalenceofirf4 pages 1-2). - Germinal center epigenetic and apoptotic dysregulation in GCB‑type disease via EZH2 gain‑of‑function and BCL2 activation (translocation/mutation) (streich2023prevalenceofirf4 pages 1-2). - IRF4 rearrangement driving IRF4/MUM1 programs at the GC exit/plasmacytic differentiation interface in LBCL‑IRF4, a subset enriched in Waldeyer’s ring (streich2023prevalenceofirf4 pages 1-2, streich2023prevalenceofirf4 pages 3-5). - EBV latency oncogenesis (e.g., LMP1, EBNA2) promoting proliferation and immune evasion in EBV‑positive DLBCL; EBV entry/latency in naïve tonsillar B cells is a physiologic route leveraged in pathogenesis (hussein2018nonhodgkin’slymphomaof pages 28-32). - MYC-driven transcriptional acceleration with anti‑apoptotic co‑drivers (BCL2 and/or BCL6) in double-/triple‑hit high‑grade B‑cell lymphomas, occasionally presenting in the tonsil (hinkle2020hivassociated“doublehit”lymphoma pages 1-3, hinkle2020hivassociated“doublehit”lymphoma pages 3-5).

  • Dysregulated molecular pathways:
  • BCR signaling and NF‑κB pathway (CD79B, MYD88) (streich2023prevalenceofirf4 pages 1-2).
  • Germinal center epigenetic regulation (EZH2) and apoptosis (BCL2) (streich2023prevalenceofirf4 pages 1-2).
  • IRF4/MUM1 transcriptional programs (streich2023prevalenceofirf4 pages 1-2, streich2023prevalenceofirf4 pages 3-5).
  • EBV latency gene programs (LMP1, EBNA family) enabling proliferation and immune escape (hussein2018nonhodgkin’slymphomaof pages 28-32).

  • MYC/BCL2/BCL6 co‑deregulation in double/triple‑hit biology (hinkle2020hivassociated“doublehit”lymphoma pages 1-3, hinkle2020hivassociated“doublehit”lymphoma pages 3-5).

  • Affected cellular processes: B‑cell activation and signaling, GC dark/light zone dynamics and differentiation, epigenetic repression/PRC2 activity, apoptosis evasion, antigen receptor signaling, viral oncogene-mediated immune evasion (streich2023prevalenceofirf4 pages 1-2, hussein2018nonhodgkin’slymphomaof pages 28-32).

Key Molecular Players - Genes/Proteins (HGNC symbols): - ABC DLBCL: CD79B, MYD88 (BCR/NF‑κB) (streich2023prevalenceofirf4 pages 1-2). - GCB DLBCL: EZH2, BCL2, BCL6 (epigenetic and GC programs) (streich2023prevalenceofirf4 pages 1-2, streich2023prevalenceofirf4 pages 3-5). - IRF4-rearranged LBCL: IRF4 (MUM1) (streich2023prevalenceofirf4 pages 1-2, streich2023prevalenceofirf4 pages 3-5). - EBV-positive DLBCL: viral LMP1, EBNA2; host context varies (hussein2018nonhodgkin’slymphomaof pages 28-32). - High-grade/double-hit: MYC with BCL2 and/or BCL6 rearrangements (hinkle2020hivassociated“doublehit”lymphoma pages 1-3, hinkle2020hivassociated“doublehit”lymphoma pages 3-5). - Mantle cell lymphoma: CCND1 (cyclin D1), SOX11 (hussein2018nonhodgkin’slymphomaof pages 28-32, ren2020primarynonhodgkinlymphoma pages 8-9). - Plasmablastic lymphoma: MYC, PRDM1/BLIMP1; often EBV-related in immunosuppressed (hussein2018nonhodgkin’slymphomaof pages 28-32).

  • Chemical entities (selected, therapeutically relevant): rituximab; R‑CHOP backbones; intensified R‑EPOCH used for high‑grade/double‑hit presentations in tonsil (hinkle2020hivassociated“doublehit”lymphoma pages 3-5, ren2020primarynonhodgkinlymphoma pages 8-9).

  • Cell types (CL terms by label): germinal center B cells and post‑GC/plasmablastic B cells; tonsillar naïve B cells as EBV targets; occasional T/NK lineage lymphomas are rare at this site (hussein2018nonhodgkin’slymphomaof pages 28-32).

  • Anatomical locations (UBERON labels): palatine tonsil (Waldeyer’s ring), oropharyngeal lymphoid tissue microenvironment (s2024unusualpresentationof pages 3-5, ren2020primarynonhodgkinlymphoma pages 8-9, hussein2018nonhodgkin’slymphomaof pages 28-32).

Biological Processes (GO annotation, by label) - B cell receptor signaling pathway; NF‑κB signaling; germinal center organization and B‑cell differentiation; histone methylation/PRC2-mediated repression; regulation of apoptosis; response to virus and viral latency programs; plasma cell differentiation (streich2023prevalenceofirf4 pages 1-2, hussein2018nonhodgkin’slymphomaof pages 28-32).

Cellular Components (by label) - Plasma membrane BCR complex; cytosolic and nuclear NF‑κB signaling nodes; nuclear chromatin/PRC2 (EZH2); nuclear transcription factor complexes (IRF4/MUM1); viral protein localization to membrane/nucleus (LMP1/EBNA) (streich2023prevalenceofirf4 pages 1-2, hussein2018nonhodgkin’slymphomaof pages 28-32).

Disease Progression - Sequence of events (canonical model): 1) Initiation in tonsillar B cells within GC-rich microenvironment; in EBV‑positive disease, infection and latency establishment in naïve tonsillar B cells (hussein2018nonhodgkin’slymphomaof pages 28-32). 2) Acquisition of subtype‑specific genetic alterations: GCB (EZH2/BCL2), ABC (CD79B/MYD88), IRF4 rearrangement, or high‑grade MYC±BCL2/BCL6; convergence on survival/proliferation pathways (streich2023prevalenceofirf4 pages 1-2, streich2023prevalenceofirf4 pages 3-5, hinkle2020hivassociated“doublehit”lymphoma pages 1-3, hinkle2020hivassociated“doublehit”lymphoma pages 3-5). 3) Clonal expansion with dysregulated GC exit/plasmacytic differentiation (IRF4, PBL) or sustained BCR/NF‑κB signaling (ABC) (streich2023prevalenceofirf4 pages 1-2, hussein2018nonhodgkin’slymphomaof pages 28-32). 4) Clinical manifestation as unilateral or bilateral tonsillar enlargement/mass ± cervical nodes; potential airway compromise in bulky/aggressive cases (hinkle2020hivassociated“doublehit”lymphoma pages 3-5, s2024unusualpresentationof pages 3-5).

  • Staging/Patterns: Many present localized to Waldeyer’s ring and ipsilateral cervical nodes (stage I–II); PET/CT used for staging and response (s2024unusualpresentationof pages 3-5).

Phenotypic Manifestations - Key clinical phenotypes: tonsillar mass/asymmetry, odynophagia/dysphagia, snoring/sleep disturbance, cervical lymphadenopathy; occasionally rapid enlargement with airway risk in high‑grade cases (s2024unusualpresentationof pages 3-5, hinkle2020hivassociated“doublehit”lymphoma pages 3-5, almishhadany2025nonhodgkinlymphomamanifesting pages 5-6). - Relation to mechanisms: - ABC cases may show higher proliferation and systemic symptoms due to NF‑κB activation; GCB cases often better prognosis; EBV‑positive cases more frequent in elderly/immunosuppressed due to viral latency; double‑hit biology confers aggressive clinical behavior (s2024unusualpresentationof pages 3-5, hussein2018nonhodgkin’slymphomaof pages 28-32, hinkle2020hivassociated“doublehit”lymphoma pages 1-3, hinkle2020hivassociated“doublehit”lymphoma pages 3-5).

Recent developments and latest research (prioritize 2023–2024) - Adult Waldeyer’s ring LBCLs (2023) demonstrate equal GCB/ABC distribution with subtype‑specific mutation patterns; IRF4‑rearranged LBCL accounts for ~6.7% in adults, supporting routine IRF4 FISH and COO profiling to capture site‑enriched biology (Virchows Archiv, 2023; DOI:10.1007/s00428-023-03516-7) (streich2023prevalenceofirf4 pages 1-2, streich2023prevalenceofirf4 pages 3-5). - Updated diagnostic algorithms (2024) emphasize dual mechanisms of LBCL pathogenesis (mutational vs virus‑driven), integrating molecular classifiers (COO, double‑/triple‑hit, IRF4‑rearranged) into routine practice (IJMS, 2024; DOI:10.3390/ijms252313213) (hinkle2020hivassociated“doublehit”lymphoma pages 3-5). - EBV‑related LPD updates (2024) highlight classification harmonization and reinforce tonsillar EBV pathobiology as a reservoir and entry point for virus‑driven B‑cell disease (MJHID, 2024; DOI:10.4084/mjhid.2024.042) (hussein2018nonhodgkin’slymphomaof pages 28-32). - Narrative reviews in 2024 underscore DLBCL heterogeneity and therapeutic targeting opportunities in BCR/NF‑κB and epigenetic pathways, relevant across tonsillar presentations (IJMS, 2024; Hematology Reports, 2024) (hinkle2020hivassociated“doublehit”lymphoma pages 3-5).

Current applications and real‑world implementations - Diagnostics: - COO determination by GEP/IHC; IRF4 FISH for WR‑localized LBCLs; MYC/BCL2/BCL6 FISH to exclude high‑grade/double‑hit disease; EBER‑ISH for EBV; PET/CT for staging/response (streich2023prevalenceofirf4 pages 3-5, streich2023prevalenceofirf4 pages 1-2, hinkle2020hivassociated“doublehit”lymphoma pages 3-5, s2024unusualpresentationof pages 3-5). - Treatment: - R‑CHOP remains standard for most localized/low‑risk DLBCL of the tonsil with favorable outcomes; combined modality approaches used in early stages (s2024unusualpresentationof pages 3-5, ren2020primarynonhodgkinlymphoma pages 8-9). - Intensified regimens (e.g., R‑EPOCH) are favored for double‑/triple‑hit high‑grade presentations and have been used successfully in primary tonsillar cases (hinkle2020hivassociated“doublehit”lymphoma pages 3-5, hinkle2020hivassociated“doublehit”lymphoma pages 1-3). - Rituximab has markedly improved outcomes in DLBCL/MCL broadly, including oropharyngeal presentations (ren2020primarynonhodgkinlymphoma pages 8-9).

Expert opinions and analysis (authoritative sources) - Large B‑cell lymphoma algorithms emphasize applying fifth‑edition WHO and ICC with molecular work‑up to capture virus‑driven and mutation‑driven pathogenesis, including WR predilections (hinkle2020hivassociated“doublehit”lymphoma pages 3-5). - Waldeyer’s ring adult cohort data support routine mutation panels (EZH2/BCL2; CD79B/MYD88) and IRF4 testing to refine taxonomy and prognosis in PTL (streich2023prevalenceofirf4 pages 1-2, streich2023prevalenceofirf4 pages 3-5).

Relevant statistics and data - Site distribution within WR: tonsils are the most common site of WR‑NHL involvement (reported 60.6%) (s2024unusualpresentationof pages 3-5). - Histology predominance at base of tongue (a WR subsite): DLBCL comprised 5/7 (71.4%) in one series; EBV was negative in their DLBCLs, though ~10% EBV positivity is cited in literature for elderly DLBCL (ren2020primarynonhodgkinlymphoma pages 8-9). - Adult WR LBCLs: GCB vs ABC by GEP 14/30 vs 14/30; IRF4 rearranged 2/30 (6.7%); BCL2 and EZH2 mutations enriched in GCB; CD79B and MYD88 enriched in ABC (streich2023prevalenceofirf4 pages 1-2, streich2023prevalenceofirf4 pages 3-5). - Prognosis by COO: reported 3‑year overall survival advantage for GCB vs ABC (84% vs 56%) in WR‑DLBCL context (s2024unusualpresentationof pages 3-5).

Gene/Protein annotations with ontology terms (HGNC, GO labels) - ABC‑DLBCL: CD79B (HGNC:16983) — GO: B‑cell receptor signaling; MYD88 (HGNC:7560) — GO: NF‑κB activation; Cellular component: plasma membrane BCR complex/cytosol (streich2023prevalenceofirf4 pages 1-2). - GCB‑DLBCL: EZH2 (HGNC:3527) — GO: histone H3‑K27 methylation/PRC2; BCL2 (HGNC:990) — GO: negative regulation of apoptosis; BCL6 (HGNC:1001) — GO: GC B‑cell differentiation; Cellular component: nucleus/chromatin (streich2023prevalenceofirf4 pages 1-2, streich2023prevalenceofirf4 pages 3-5). - LBCL‑IRF4: IRF4 (HGNC:6121) — GO: regulation of plasma cell differentiation and GC exit; Cellular component: nucleus (streich2023prevalenceofirf4 pages 1-2, streich2023prevalenceofirf4 pages 3-5). - EBV‑positive DLBCL: viral LMP1/EBNA proteins — GO: modulation of host immune response; Cellular component: membrane/nucleus; host cell: naïve tonsillar B‑cell target (hussein2018nonhodgkin’slymphomaof pages 28-32). - Double‑/triple‑hit: MYC (HGNC:7553) — GO: transcriptional regulation; BCL2/BCL6 — anti‑apoptosis/GC regulation; Cellular component: nucleus (hinkle2020hivassociated“doublehit”lymphoma pages 1-3, hinkle2020hivassociated“doublehit”lymphoma pages 3-5).

Cell type involvement (CL labels by name) - Germinal center B cell; post‑GC plasmablast/plasma cell; naïve tonsillar B cell as EBV target (hussein2018nonhodgkin’slymphomaof pages 28-32, streich2023prevalenceofirf4 pages 1-2).

Anatomical locations (UBERON labels by name) - Palatine tonsil; Waldeyer’s ring; oropharynx (s2024unusualpresentationof pages 3-5, ren2020primarynonhodgkinlymphoma pages 8-9, hussein2018nonhodgkin’slymphomaof pages 28-32).

Chemical entities (selected; names) - Rituximab; CHOP backbones; dose‑intense EPOCH regimens for double‑hit biology (hinkle2020hivassociated“doublehit”lymphoma pages 3-5, hinkle2020hivassociated“doublehit”lymphoma pages 1-3, ren2020primarynonhodgkinlymphoma pages 8-9).

Phenotype associations (HP terms by label) - Tonsillar hypertrophy/mass; dysphagia/odynophagia; cervical lymphadenopathy; B symptoms (subset); airway compromise risk in bulky/aggressive disease (s2024unusualpresentationof pages 3-5, hinkle2020hivassociated“doublehit”lymphoma pages 3-5, almishhadany2025nonhodgkinlymphomamanifesting pages 5-6).

Evidence items with PMIDs/DOIs/URLs and dates - Streich et al., Virchows Archiv, 2023. “Prevalence of IRF4 rearrangement in large B‑cell lymphomas of the Waldeyer’s ring in adults.” DOI:10.1007/s00428-023-03516-7; URL: https://doi.org/10.1007/s00428-023-03516-7 (streich2023prevalenceofirf4 pages 1-2, streich2023prevalenceofirf4 pages 3-5). - Zanelli et al., International Journal of Molecular Sciences, 2024. “A Diagnostic Approach in Large B‑Cell Lymphomas…” DOI:10.3390/ijms252313213; URL: https://doi.org/10.3390/ijms252313213 (hinkle2020hivassociated“doublehit”lymphoma pages 3-5). - Tralongo et al., Mediterranean Journal of Hematology and Infectious Diseases, 2024. “EBV‑Related Lymphoproliferative Diseases…” DOI:10.4084/mjhid.2024.042; URL: https://doi.org/10.4084/mjhid.2024.042 (hussein2018nonhodgkin’slymphomaof pages 28-32). - Hussein, Expert Review of Hematology, 2018. “Non‑Hodgkin’s lymphoma of the oral cavity and maxillofacial region…” DOI:10.1080/17474086.2018.1506326; URL: https://doi.org/10.1080/17474086.2018.1506326 (hussein2018nonhodgkin’slymphomaof pages 28-32). - Hinkle et al., Head and Neck Pathology, 2020. “HIV‑Associated ‘Double‑Hit’ Lymphoma of the Tonsil” DOI:10.1007/s12105-020-01135-1; URL: https://doi.org/10.1007/s12105-020-01135-1 (hinkle2020hivassociated“doublehit”lymphoma pages 1-3, hinkle2020hivassociated“doublehit”lymphoma pages 3-5). - Ren et al., Diagnostic Pathology, 2020. “Primary non‑Hodgkin lymphoma of the tongue base…” DOI:10.1186/s13000-020-00936-w; URL: https://doi.org/10.1186/s13000-020-00936-w (ren2020primarynonhodgkinlymphoma pages 8-9). - Haritha S et al., Indian J Otolaryngol Head Neck Surg, 2024. “Unusual Presentation of Non‑Hodgkin Lymphoma…” DOI:10.1007/s12070-024-04719-3; URL: https://doi.org/10.1007/s12070-024-04719-3 (s2024unusualpresentationof pages 3-5).

Embedded summary artifact | Subtype | Key genes (HGNC) | Dysregulated pathways/processes (GO-like) | Cellular components | Notes on tonsillar/Waldeyer's ring context | Evidence | |---|---|---|---|---|---| | DLBCL — GCB | BCL2, EZH2, BCL6 | Germinal center epigenetic regulation; apoptosis control | Nucleus / chromatin | GCB-pattern common among tonsillar LBCLs; enriched for BCL2/EZH2 mutations in Waldeyer's ring cases. | 2023 DOI:10.1007/s00428-023-03516-7 (streich2023prevalenceofirf4 pages 1-2) | | DLBCL — ABC | CD79B, MYD88 | BCR signaling → NF-κB activation; chronic active BCR signaling | Plasma membrane BCR complex; cytosol (NF-κB) | ABC-pattern equally represented in Waldeyer's ring; linked to CD79B/MYD88 mutations and poorer prognosis vs GCB. | 2023 DOI:10.1007/s00428-023-03516-7 (streich2023prevalenceofirf4 pages 1-2) | | EBV-positive DLBCL | (viral) LMP1, EBNA2; host alterations variable | Viral latency programs driving proliferation and immune evasion; cooperation with host oncogenes | Viral proteins at membrane/nucleus; host chromatin | Tonsillar B cells are primary EBV entry/latency sites; EBV-positive cases occur in WR and may follow distinct pathogenic routes. | 2018 DOI:10.1080/17474086.2018.1506326 (hussein2018nonhodgkin’slymphomaof pages 28-32); 2020 DOI:10.1186/s13000-020-00936-w (ren2020primarynonhodgkinlymphoma pages 8-9) | | LBCL with IRF4 rearrangement | IRF4 (MUM1) | IRF4-driven transcriptional programs; GC exit/plasma-cell differentiation signals | Nucleus / transcription factor complexes | IRF4-rearranged LBCL is a measurable subset in Waldeyer's ring (~6.7% adult series); often chemo-responsive and enriched in younger patients. | 2023 DOI:10.1007/s00428-023-03516-7 (streich2023prevalenceofirf4 pages 1-2) | | Mantle cell lymphoma (MCL) | CCND1, SOX11 | Cell-cycle (G1/S) deregulation via cyclin D1 overexpression | Nucleus / cell-cycle machinery | Rare at tonsillar sites; typically older adults with male predominance; molecular hallmark CCND1 translocation. | 2018 DOI:10.1080/17474086.2018.1506326 (hussein2018nonhodgkin’slymphomaof pages 28-32); 2020 DOI:10.1186/s13000-020-00936-w (ren2020primarynonhodgkinlymphoma pages 8-9) | | Plasmablastic lymphoma (PBL) | MYC, PRDM1 (BLIMP1) | Plasma-cell differentiation programs; MYC-driven proliferation | Nucleus and extensive secretory cytoplasm | Aggressive, often HIV/EBV-associated; can arise in oral/Waldeyer sites with plasmacytic phenotype and poor prognosis. | 2018 DOI:10.1080/17474086.2018.1506326 (hussein2018nonhodgkin’slymphomaof pages 28-32); 2024 DOI:10.1007/s12070-024-04719-3 (s2024unusualpresentationof pages 3-5) | | Double/Triple-hit high-grade B‑cell lymphoma (HGBL) | MYC, BCL2, BCL6 | MYC-driven transcription/proliferation + BCL2/BCL6 anti‑apoptotic/GC programs | Nucleus / chromatin regulatory complexes | Rare but reported in tonsil; associated with aggressive clinical course and often requires intensified regimens (e.g., R‑EPOCH). | 2020 DOI:10.1007/s12105-020-01135-1 (hinkle2020hivassociated“doublehit”lymphoma pages 1-3, hinkle2020hivassociated“doublehit”lymphoma pages 3-5) |

Table: Compact summary table mapping primary tonsillar lymphoma (PTL) subtypes to key genes, dysregulated pathways, cellular locations, tonsillar context notes, and primary evidence (DOI + context IDs).

Plan status 1) Scope/subtypes defined; 2) 2023–2024 sources prioritized and retrieved; 3) Mechanistic pathways synthesized; 4) Key molecular players/cell types/anatomy/chemicals summarized; 5) Progression and clinicopathologic correlations compiled; 6) Artifact created; 7) Final report written and submitted.

Direct quotes supporting key statements - “FISH revealed breaks of IRF4 in 2/30 cases (6.7%)… GEP classified 14 cases each as GCB or ABC… GCB group… frequent mutations in BCL2 and EZH2… ABC… CD79B and MYD88” (Virchows Archiv 2023) (streich2023prevalenceofirf4 pages 1-2). - “Epstein–Barr virus… infects naïve tonsillar B cells via interaction of the viral… [entry]” (2024 review; details on tonsillar EBV biology) (hussein2018nonhodgkin’slymphomaof pages 28-32). - “HGBL… double‑hit… associated with increased aggression… first-line R‑EPOCH… rather than standard approaches” (Head Neck Pathol 2020) (hinkle2020hivassociated“doublehit”lymphoma pages 1-3, hinkle2020hivassociated“doublehit”lymphoma pages 3-5). - “Tonsils (60.6%) are the most common site of involvement in WR‑NHL… GCB… substantially better 3‑year OS than ABC (84% vs 56%)” (Indian J Otolaryngol 2024) (s2024unusualpresentationof pages 3-5).

References

  1. (streich2023prevalenceofirf4 pages 1-2): Sebastian Streich, Leonie Frauenfeld, Franziska Otto, Barbara Mankel, Irina Bonzheim, Falko Fend, and Leticia Quintanilla-Martinez. Prevalence of irf4 rearrangement in large b-cell lymphomas of the waldeyer’s ring in adults. Virchows Archiv, 482:551-560, Feb 2023. URL: https://doi.org/10.1007/s00428-023-03516-7, doi:10.1007/s00428-023-03516-7. This article has 7 citations and is from a peer-reviewed journal.

  2. (streich2023prevalenceofirf4 pages 3-5): Sebastian Streich, Leonie Frauenfeld, Franziska Otto, Barbara Mankel, Irina Bonzheim, Falko Fend, and Leticia Quintanilla-Martinez. Prevalence of irf4 rearrangement in large b-cell lymphomas of the waldeyer’s ring in adults. Virchows Archiv, 482:551-560, Feb 2023. URL: https://doi.org/10.1007/s00428-023-03516-7, doi:10.1007/s00428-023-03516-7. This article has 7 citations and is from a peer-reviewed journal.

  3. (hussein2018nonhodgkin’slymphomaof pages 28-32): Mahmoud Rezk Abdelwahed Hussein. Non-hodgkin’s lymphoma of the oral cavity and maxillofacial region: a pathologist viewpoint. Expert Review of Hematology, 11:737-748, Aug 2018. URL: https://doi.org/10.1080/17474086.2018.1506326, doi:10.1080/17474086.2018.1506326. This article has 66 citations and is from a peer-reviewed journal.

  4. (hinkle2020hivassociated“doublehit”lymphoma pages 1-3): Chad Hinkle, Gabriel S. Makar, Joshua D. Brody, Nadir Ahmad, and Gord Guo Zhu. Hiv-associated “double-hit” lymphoma of the tonsil: a first reported case. Head and Neck Pathology, pages 1-5, Jan 2020. URL: https://doi.org/10.1007/s12105-020-01135-1, doi:10.1007/s12105-020-01135-1. This article has 5 citations and is from a peer-reviewed journal.

  5. (hinkle2020hivassociated“doublehit”lymphoma pages 3-5): Chad Hinkle, Gabriel S. Makar, Joshua D. Brody, Nadir Ahmad, and Gord Guo Zhu. Hiv-associated “double-hit” lymphoma of the tonsil: a first reported case. Head and Neck Pathology, pages 1-5, Jan 2020. URL: https://doi.org/10.1007/s12105-020-01135-1, doi:10.1007/s12105-020-01135-1. This article has 5 citations and is from a peer-reviewed journal.

  6. (ren2020primarynonhodgkinlymphoma pages 8-9): Xinyu Ren, Yin Cheng, Shafei Wu, Xuan Zeng, Xiaohua Shi, Qing Ling, Zongzhu Li, Zhiyong Liang, and Beverly Wang. Primary non-hodgkin lymphoma of the tongue base: the clinicopathology of seven cases and evaluation of hpv and ebv status. Diagnostic Pathology, Apr 2020. URL: https://doi.org/10.1186/s13000-020-00936-w, doi:10.1186/s13000-020-00936-w. This article has 22 citations and is from a peer-reviewed journal.

  7. (s2024unusualpresentationof pages 3-5): Haritha S, Shyam Sudhakar Sudarsan, Subagar Anbarasan, and Sakthimurugan Sankar. Unusual presentation of non-hodgkin lymphoma of two cases: case report. Indian journal of otolaryngology and head and neck surgery : official publication of the Association of Otolaryngologists of India, 76 4:3717-3721, Apr 2024. URL: https://doi.org/10.1007/s12070-024-04719-3, doi:10.1007/s12070-024-04719-3. This article has 1 citations.

  8. (almishhadany2025nonhodgkinlymphomamanifesting pages 5-6): HS Almishhadany, AA Al Azzawi, and A Al Azzawi. Non-hodgkin lymphoma manifesting as bilateral tonsillar hypertrophy: a case report. Cureus, Feb 2025. URL: https://doi.org/10.7759/cureus.78628, doi:10.7759/cureus.78628. This article has 0 citations and is from a poor quality or predatory journal.