Lymphoma (Hodgkin & Non-Hodgkin)

Meet the patient

A 24-year-old man notices a painless lump above his left collarbone that has grown over two months. He has been waking drenched in sweat and has dropped 6 kg without trying. A chest X-ray shows a mediastinal mass.[1]

The second patient is a 62-year-old with a rapidly enlarging abdominal mass and abdominal pain; a CT reveals an ileocaecal mass with widespread nodes, and his LDH is markedly raised.[8]

The first is Hodgkin lymphoma — a contiguous, curable disease of young adults. The second is Burkitt lymphoma — the fastest-growing human tumour, treated as an emergency within hours. The single decision that runs the whole topic is the Reed-Sternberg cell, and the single non-negotiable diagnostic step is the excisional biopsy.[1][8]

One cell splits the family — the Reed-Sternberg test

Lymphoma is a clonal malignancy of lymphocytes (B cells in the great majority) arising in lymphoid tissue — nodes, spleen, marrow, Waldeyer ring, MALT — and sometimes at extranodal sites. It is the commonest haematological malignancy.[1]

The one histological criterion that splits the entire family is the Reed-Sternberg cell: a large, often binucleate cell with owl-eye nucleoli in a reactive inflammatory background. Reed-Sternberg present — Hodgkin lymphoma (HL); absent — non-Hodgkin lymphoma (NHL). The split is not cosmetic: it governs pattern of spread (contiguous in HL, disseminated in NHL), the first-line regimen (ABVD versus R-CHOP), and prognosis.[1][12]

NHL vastly outnumbers HL (roughly 90 percent versus 10 percent), is the commonest blood cancer overall, and its incidence rises with age. HL has a characteristic bimodal age distribution (a young-adult peak around 20 and an older peak over 55) and is one of the most curable human cancers.[1]

Hodgkin lymphoma — classical and the odd one out

[1]

NHL by behaviour — indolent, aggressive, highly aggressive

Clinical behaviour is the most useful way to hold NHL in your head. Each bucket carries its own translocation, its own tempo and its own first-line plan.[1]

[7] [8]

Cell of origin in DLBCL matters: the germinal-centre B-cell (GCB) subtype does better with R-CHOP than the activated B-cell (ABC) subtype, which relapses more often. The T-cell NHLs (peripheral T-cell NOS, anaplastic large cell, angioimmunoblastic) are rarer and generally worse.[2]

Who gets it, and the bugs that cause it

The infection-to-subtype pairings are pure viva gold. The examiner wants the bug and the lymphoma it drives.[1]

[1]

Other risk factors: immunosuppression — HIV (driving aggressive B-cell NHL and Burkitt), post-transplant (PTLD, often EBV-related), congenital immunodeficiency; autoimmune and chronic inflammatory disease — Sjögren and Hashimoto (MALT), coeliac disease (enteropathy-associated T-cell lymphoma); prior chemo or radiotherapy; chemical exposures (pesticides, Agent Orange, solvents, hair dyes); and family history.[1]

The mechanism — why Hodgkin spreads contiguously and NHL disseminates

The malignant cell of classical Hodgkin lymphoma is the Reed-Sternberg cell — a large (20 to 50 micrometre) binucleate giant cell with owl-eye nucleoli, derived from a germinal-centre B-cell that crippled its immunoglobulin rearrangement and would normally die, but is rescued by constitutive NF-κB, JAK/STAT3 and PI3K/AKT signalling. EBV-encoded LMP1 often drives it (mimicking CD40 signalling), and amplification of 9p24.1 (the PD-L1/PD-L2 locus) is the basis for PD-1 inhibitor activity. The Reed-Sternberg cell is rare within its own tumour — it secretes IL-5, IL-13, eotaxin and TGF-beta, recruiting the reactive background (T-cell rosettes, eosinophils, fibrosis) that dominates the histology.[1][12]

Pattern of spread is the teaching point that earns marks. Hodgkin lymphoma spreads contiguously and orderly — cervical to supraclavicular to mediastinal — which is why staging drives therapy and radiotherapy stays relevant. NHL spreads non-contiguously and haematogenously, skipping node groups and seeding extranodal sites (GI, marrow, CNS, skin, testis, Waldeyer ring), so it is systemic from early on and chemotherapy-centred.[1]

The defining molecular lesions of NHL each fuse a proto-oncogene to the immunoglobulin heavy-chain locus on chromosome 14:[1]

[7] [8]

How rituximab works is itself examinable. It is a chimeric anti-CD20 monoclonal antibody that triggers complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity and direct apoptosis of CD20+ B cells. Adding it to CHOP transformed DLBCL from a 40 percent cure to a roughly 60 to 70 percent cure disease; plasma cells survive (so immunoglobulin is partly preserved) and stem cells are spared (so counts recover).[6][11]

Tumour lysis syndrome stalks the highly proliferative tumours — especially Burkitt (doubling time about 24 to 48 hours, Ki67 about 100 percent) and high-burden aggressive NHL. Cells lysed on therapy release potassium (hyperkalaemia), phosphate (hyperphosphataemia and secondary hypocalcaemia) and nucleic acids (metabolised to uric acid, causing acute urate nephropathy and AKI). The risk peaks in the first 24 to 72 hours of treatment, which is why Burkitt is a haemato-oncology emergency within hours, with prophylaxis already running.[8]

How it walks in — the painless node and the B symptoms

The classic presentation is painless, rubbery lymphadenopathy, most often cervical (then supraclavicular, axillary, inguinal), that persists beyond 4 to 6 weeks and enlarges progressively. Nodes are non-tender, firm and rubbery, and may become matted. Up to a third of patients have B symptoms, which must be elicited and recorded verbatim because they alter stage and prognosis.[1]

Hodgkin patterns: cervical or supraclavicular nodes with a mediastinal mass (nodular sclerosis in young women) producing cough, dyspnoea or SVC syndrome; alcohol-induced pain in involved nodes (rare but classical); and generalised pruritus. Spread is contiguous.[1]

NHL patterns are extranodal-focussed: the GI tract (the commonest extranodal site — abdominal mass, pain, bleeding, obstruction or intussusception in ileocaecal Burkitt); bone marrow (cytopenias); CNS (primary CNS lymphoma, periventricular and EBV-related in HIV); skin (mycosis fungoides and its leukaemic variant Sézary syndrome, with Pautrier microabscesses); testis (relapses in CNS and the contralateral testis); Waldeyer ring; and bone (a lytic lesion with pain).[1]

Burkitt has two faces: endemic (African) — a jaw or orbital mass in a child, strongly EBV-associated; and sporadic — an abdominal or ileocaecal mass in a child or young adult, presenting with obstruction, intussusception and florid tumour lysis.[8]

The differential — and why FNA is not enough

A painless node has a wide differential. The task is to distinguish lymphoma from its benign and malignant mimics by tempo, character, distribution and — definitively — histology.[1]

[1]

Generalised lymphadenopathy (cervical, axillary and inguinal together) should trigger thought of HIV, EBV, sarcoidosis, autoimmune disease (SLE, rheumatoid) and drug reaction — all excluded before committing to a lymphoma diagnosis.[1]

The bedside round — examine every node group

A systematic node examination covers all peripheral groups in a fixed order — submental, submandibular, cervical (anterior and posterior chain), supraclavicular, occipital, pre- and post-auricular, axillary, epitrochlear, inguinal and popliteal. Describe each node by site, size, consistency (rubbery in lymphoma, hard in carcinoma, soft in reactive), tenderness, mobility and matting. Palpate the supraclavicular fossa carefully — a node here is always abnormal (it drains the thoracic duct and the abdomen).[1]

Beyond the nodes, assess for hepatosplenomegaly, Waldeyer ring enlargement, skin lesions (mycosis fungoides), and signs of marrow failure — pallor, purpura, infection. Examine for SVC syndrome (facial plethora, jugular distension, arm swelling), mediastinal-mass airway compromise (stridor, orthopnoea) and spinal cord compression (back pain, a sensory level, sphincter dysfunction).[1]

Document two things at the bedside that drive staging and prognosis: performance status (ECOG) and the presence of B symptoms.[2]

[1]

Investigations — EXCISIONAL biopsy, never FNA

The diagnostic standard is an EXCISIONAL lymph-node biopsy — removing an entire representative node intact so that architecture, immunohistochemistry, flow cytometry, cytogenetics and molecular studies can all be done. Fine-needle aspiration is inadequate for a primary diagnosis: it destroys architecture, cannot subtype reliably and yields too little material. Core biopsy is acceptable when a node is surgically inaccessible, but excisional biopsy remains the gold standard.[1][2]

The histological workup of the excised node:[1]

• Morphology (H&E) — architecture (nodular versus diffuse), cell size, Reed-Sternberg cells, the Ki67 rate.
• Immunohistochemistry — the decisive discriminator: classical HL is CD15+ CD30+, CD20 weak or negative; NLPHL is CD20+ CD45+, CD15-negative CD30-negative (popcorn cells); B-cell NHL is CD20+, CD19+, CD79a+; Burkitt is CD20+, CD10+, BCL6+, BCL2-negative, Ki67 about 100 percent.
• Flow cytometry on a fresh fragment — defines clonality (light-chain restriction) and immunophenotype.
• Cytogenetics or FISH — the translocations: t(8;14) Burkitt, t(14;18) follicular, t(11;14) mantle cell, t(11;18) MALT.
• Molecular — clonal immunoglobulin or T-cell receptor gene rearrangement, MYD88 mutation (lymphoplasmacytic).[1]

Staging — Ann Arbor/Cotswolds plus PET-CT and Deauville

PET-CT (FDG) is the modern staging and response-assessment standard for FDG-avid lymphomas (HL, DLBCL, follicular, Burkitt, mantle cell). The Lugano response criteria integrate PET with the Deauville 5-point scale:[2]

[2]

Baseline bloods and supportive tests: FBC and film (cytopenias from marrow involvement), ESR/CRP, U&E and creatinine, LFTs, LDH (tumour burden and an IPI component), beta-2 microglobulin, hepatitis B (surface antigen and core antibody — rituximab can reactivate HBV), hepatitis C and HIV serology, bone-marrow aspirate and trephine (increasingly omitted for early-stage PET-negative disease), ECG and echocardiogram before anthracyclines, and pulmonary function tests before bleomycin. Offer sperm or egg cryopreservation before gonadotoxic chemo.[1]

The International Prognostic Index (IPI) — NHL

One point each for: age 60 or older; performance status (ECOG) 2 or higher; stage III or IV; extranodal involvement in 2 or more sites; and serum LDH elevated.[4]

Risk groups: low (0 to 1) — 5-year survival about 73 percent; low-intermediate (2) about 51 percent; high-intermediate (3) about 43 percent; high (4 to 5) about 26 percent. The revised IPI (R-IPI) for the R-CHOP era collapses these into very good (0, 4-year PFS 94 percent), good (1 to 2, 80 percent) and poor (3 to 5, 53 percent).[4][5]

The Hasenclever International Prognostic Score (IPS) — Hodgkin lymphoma

One point each for: serum albumin below 40 g/L; haemoglobin below 105 g/L; male sex; age 45 or older; stage IV; leucocytosis (WCC at least 15×10⁹/L); and lymphocytopenia (lymphocytes below 0.6×10⁹/L, or below 8 percent of WCC).[3]

A score of 0 carries the best prognosis (freedom from progression at 5 years about 84 percent); the rate falls steadily to about 42 percent for a score of 5 or more.[3]

The emergencies — MASS: mediastinal, SVC, cord, tumour lysis

Treat the presenting oncological emergencies first, then start systemic therapy. Four recur:[1]

[1]

Tumour-lysis prophylaxis starts before the first chemotherapy dose in any high-risk patient (Burkitt, high-burden aggressive NHL, a markedly raised LDH, bulky disease): aggressive IV hydration (isotonic saline 2 to 3 L/m²/day, urine output at least 100 mL/m²/h); rasburicase 0.15 to 0.2 mg/kg IV daily for high-risk (contraindicated in G6PD deficiency) or allopurinol 300 mg orally daily for moderate risk; and monitoring of potassium, phosphate, calcium, urate and creatinine every 4 to 6 hours for 24 to 72 hours.[8]

Febrile neutropenia from chemotherapy gets blood cultures and an empirical broad-spectrum IV antibiotic within one hour — typically an antipseudomonal beta-lactam such as piperacillin-tazobactam 4.5 g IV every 6 to 8 hours or ceftazidime.[1]

Hodgkin lymphoma — ABVD and PET-adapted therapy

[1]

ABVD is given every 28 days for 2 to 6 cycles by stage and PET response. PET-adapted therapy is the modern standard — a positive interim PET drives escalation to escalated BEACOPP; a negative interim PET allows de-escalation (omit bleomycin to spare the lungs). Limited (early) stage disease typically gets 2 cycles of ABVD plus involved-site radiotherapy (ISRT); advanced disease gets 6 cycles of ABVD, or escalated BEACOPP for unfavourable advanced disease. Brentuximab vedotin (anti-CD30 antibody-drug conjugate, 1.8 mg/kg IV every 3 weeks) with doxorubicin, vinblastine and dacarbazine is a frontline alternative.[12][11]

DLBCL — R-CHOP

[1]

R-CHOP is given every 21 days for 6 cycles; limited-stage non-bulky DLBCL may get 3 cycles plus involved-site radiotherapy. Adding rituximab to CHOP (established by the GELA LNH-98.5 and MInT trials) improved complete response and overall survival in all age groups and is non-negotiable first-line. Six cycles of intrathecal methotrexate CNS prophylaxis is added for high-CNS-risk DLBCL (testicular, renal or adrenal, paranasal sinus, bone marrow, high IPI, double-hit). DA-EPOCH-R is an alternative, especially for double-hit or MYC-rearranged DLBCL.[5][6]

Follicular lymphoma — watch-and-wait or rituximab

Follicular lymphoma is indolent and, in advanced stage, incurable but with a long natural history (median survival well over 10 to 15 years). Asymptomatic advanced-stage disease can be managed with watch-and-wait without a survival disadvantage — therapy starts at symptoms, cytopenias, organ compromise, bulky disease or transformation. When treatment is needed: rituximab alone (375 mg/m² weekly for 4) for low-burden disease, or rituximab plus chemotherapy (R-CHOP, R-CVP or BR) followed by rituximab maintenance every 2 months for 2 years. Watch for histological transformation to DLBCL (a rising LDH, rapid nodal growth) — treat as DLBCL.[7]

Burkitt lymphoma — the fastest human tumour, treated within hours

Burkitt is the fastest-growing human tumour (doubling time about 24 to 48 hours) and is treated as an emergency with intensive, short-course chemotherapy including CNS prophylaxis (intrathecal methotrexate or cytarabine) and tumour-lysis prophylaxis from the first cycle. Regimens include CODOX-M/IVAC and DA-EPOCH-R. With modern intensive therapy, cure rates exceed 80 to 90 percent in children and adults.[8]

Mantle cell, MALT and primary CNS lymphoma

Mantle cell lymphoma carries t(11;14) with cyclin D1 overexpression, is CD5+ CD20+ and has an aggressive course. Fit younger patients get intensive induction (R-CHOP or Nordic alternating regimens) followed by consolidation with autologous stem-cell transplant and rituximab maintenance; older or frail patients get BR with rituximab maintenance. Targeted agents — bortezomib, ibrutinib or acalabrutinib (BTK inhibitors) and lenalidomide — work in relapse.[11]

Gastric MALT lymphoma is the clearest example of an infection-driven malignancy reversed by treating the infection. For early-stage, H. pylori-positive disease, eradication therapy (a proton-pump inhibitor plus amoxicillin plus clarithromycin for 14 days, with metronidazole replacing amoxicillin if penicillin-allergic) can achieve complete durable remission. The t(11;18) API2-MALT1 translocation predicts a poor response to eradication and the need for radiotherapy or chemotherapy.[9]

Primary CNS lymphoma is typically diffuse large B-cell, periventricular and strongly EBV-associated in HIV. Treat with high-dose methotrexate-based chemotherapy (avoid radiotherapy first-line in older patients because of neurotoxicity).[10]

Relapsed and refractory disease

[11]

The subtypes that bite

• Nodular sclerosis classical HL — the commonest HL subtype, young women, mediastinal mass, lacunar cells and fibrous bands; ABVD with excellent cure rates.[1]
• DLBCL — the commonest aggressive NHL and commonest NHL overall; R-CHOP; the GCB subtype does better than ABC; double-hit (MYC plus BCL2 or BCL6) and double-expressor fare worse and need DA-EPOCH-R.[5]
• Burkitt — t(8;14) MYC, Ki67 about 100 percent, the fastest-growing human tumour; endemic African jaw mass versus sporadic abdominal mass; intensive chemo plus CNS prophylaxis.[8]
• Gastric MALT — H. pylori; eradication for early-stage H. pylori-positive disease.[9]
• Primary CNS lymphoma — diffuse large B-cell, periventricular, EBV-related in HIV; high-dose methotrexate.[10]
• Mycosis fungoides and Sézary syndrome — cutaneous T-cell lymphoma; Pautrier microabscesses, epidermotropism; skin-directed then systemic therapy.[2]

When it goes wrong — complications and the traps that cost marks

Treatment complications are themselves heavily examined:[1][11]

• Bleomycin lung toxicity — pneumonitis and pulmonary fibrosis; the reason for PET-adapted de-escalation and pre-treatment lung function tests.
• Anthracycline (doxorubicin) cardiotoxicity — dose-dependent heart failure; baseline echo and ECG.
• Febrile neutropenia — empirical IV antibiotic within one hour.
• Infertility — offer sperm or egg cryopreservation before ABVD or R-CHOP.
• Second malignancies in HL survivors — breast cancer (chest radiotherapy), lung cancer, acute leukaemia or MDS (alkylators and radiotherapy), non-melanoma skin cancer.
• Cardiovascular disease — accelerated atherosclerosis and valve disease from mediastinal radiotherapy, a leading cause of late death in HL survivors.
• Rituximab — hepatitis B reactivation (screen HBsAg and anti-HBc; antiviral prophylaxis if positive), infusion reactions, late neutropenia.
• CAR-T — cytokine release syndrome and immune-effector-cell neurotoxicity syndrome (ICANS).[1]

The classic diagnostic pitfalls: relying on FNA instead of excisional biopsy; missing HIV; omitting PET-CT for staging or response; under-treating Burkitt or failing to prophylax tumour lysis; not screening for hepatitis B before rituximab; forgetting CNS prophylaxis in high-risk DLBCL; and failing to plan fertility preservation.[1]

Disease complications: superior vena cava syndrome, airway compromise from a mediastinal mass, spinal cord compression from epidural lymphoma, bone-marrow failure, and bowel obstruction from an abdominal mass.[1]

Prognosis and disposition

Hodgkin lymphoma is one of the most curable human cancers — overall survival exceeds 80 to 85 percent, and early-stage disease approaches 95 percent. The challenge in HL is now minimising late toxicity (second cancers, cardiovascular disease, infertility) through PET-adapted de-escalation.[1][3]

DLBCL is cured in roughly 60 to 70 percent with R-CHOP, with the IPI/R-IPI predicting outcome. Follicular lymphoma is incurable but indolent (median survival over 10 to 15 years). Burkitt is curable in over 80 to 90 percent with modern intensive therapy but rapidly fatal untreated.[5][7][8]

[1]

Disposition is to a haemato-oncology unit; the safety-net for the discharging clinician is patient education on febrile neutropenia (temperature over 38°C is an emergency) and tumour-lysis symptoms.[1]

Special populations

• Pregnancy — staging is adapted (avoid CT abdomen or pelvis; use MRI and a shielded X-ray; defer PET-CT if possible in the first trimester). ABVD is acceptable in pregnancy; avoid radiotherapy to the fetus; time multidisciplinary care to defer treatment to the second trimester where possible.[1]
• HIV — aggressive B-cell NHL (DLBCL, Burkitt, primary effusion lymphoma, primary CNS lymphoma) is AIDS-defining. Treat with an appropriate regimen plus antiretroviral therapy, watching for IRIS and drug interactions.[1]
• Elderly — comorbidity-adapted, lower-intensity regimens (R-mini-CHOP, BR); R-CHOP remains tolerable in fit older adults; CAR-T increasingly used for relapse.
• Children — Burkitt and lymphoblastic lymphoma predominate; paediatric-inspired protocols (less radiotherapy) have excellent survival; fertility preservation is essential.[8]
• Post-transplant (PTLD) — often EBV-driven B-cell proliferation; the first step is reduction of immunosuppression plus rituximab.[11]

The evidence and regional differences

The Lugano classification (Cheson 2014) standardised staging and PET response assessment, with the Deauville scale standardising PET scoring. NCCN (US) and ESMO (Europe) provide the contemporary treatment framework; BSH/BHOPA guidance applies in the UK.[2]

Landmark trials and what they changed:[1][2]

• Hasenclever and Diehl (NEJM 1998) — the IPS for advanced HL, seven factors predicting freedom from progression.[3]
• International NHL Prognostic Factors Project (NEJM 1993) — the original IPI.[4]
• Sehn (Blood 2007) — the R-IPI, recalibrated for the rituximab era.[5]
• GELA LNH-98.5 and MInT — R-CHOP superior to CHOP in elderly and young good-prognosis DLBCL.[6]
• ECHELON-1 (brentuximab plus AVD frontline HL) and CHECKMATE 205 (nivolumab in relapsed HL).[11]
• ZUMA-1, JULIET, TRANSCEND — CAR-T (axicabtagene, tisagenlecleucel, lisocabtagene) in relapsed DLBCL.[11]

Regional deltas. PET-CT, CAR-T, brentuximab and PD-1 inhibitors are routine in high-income settings but access-limited in India and other low- and middle-income countries, where cost drives treatment toward generic CHOP, ABVD, thalidomide-based and palliative regimens and transplant capacity is constrained. H. pylori-driven gastric MALT is over-represented where H. pylori prevalence is high.[1]

The mantra, and the mnemonics

[1]

The mantra: Reed-Sternberg splits the family; excisional biopsy makes the diagnosis; B symptoms are verbatim; Burkitt is treated within hours — and the first node you biopsy is the largest, most abnormal, and never FNA.[1][8]

Ward-round test — three stems, thirty seconds each

Stem 1 — the young man with the supraclavicular node (answer)

A 24-year-old with a painless left supraclavicular node for 8 weeks, drenching night sweats, 6 kg weight loss, and a mediastinal mass on chest X-ray. The registrar proposes a fine-needle aspirate of the node. What do you say, and what is the staging approach? Model: This is classical Hodgkin lymphoma until proven otherwise. Do not do an FNA — it destroys architecture and cannot subtype. The diagnostic standard is an excisional lymph-node biopsy with immunohistochemistry (classical HL is CD15+ CD30+), flow cytometry and FISH. Stage with PET-CT and a bone-marrow biopsy if advanced, using Ann Arbor/Cotswolds (this is at least stage II, likely IIB with B symptoms). The IPS (albumin, Hb, male, age, stage IV, leucocytosis, lymphocytopenia) stratifies prognosis. First-line is ABVD with PET-adapted therapy.[1][2]

Stem 2 — the child with the abdominal mass and tumour lysis (answer)

A 6-year-old presents with an ileocaecal abdominal mass, obstruction and a markedly raised LDH. The biopsy shows a high-grade B-cell lymphoma, Ki67 about 100 percent, t(8;14). What is this, and what must be running before the first dose of chemotherapy? Model: This is Burkitt lymphoma — the fastest-growing human tumour (t(8;14) c-MYC, Ki67 about 100 percent). Before the first chemotherapy dose, tumour-lysis prophylaxis must be running: aggressive IV hydration (isotonic saline 2 to 3 L/m²/day), rasburicase 0.15 to 0.2 mg/kg IV daily for this high-risk patient (check G6PD first), and monitoring of potassium, phosphate, calcium, urate and creatinine every 4 to 6 hours. Treat with intensive short-course chemotherapy (CODOX-M/IVAC or DA-EPOCH-R) with CNS prophylaxis. Burkitt is a haemato-oncology emergency treated within hours.[8]

Stem 3 — the elderly man with an SVC syndrome (answer)

A 68-year-old arrives with facial and arm swelling, jugular distension and orthopnoea over a large mediastinal mass. What is the immediate management, and what must you NOT do? Model: This is superior vena cava syndrome from a mediastinal mass — an oncological emergency. Elevate the head of the bed, give oxygen, start IV dexamethasone, and call urgent haemato-oncology; the syndrome often resolves rapidly once chemotherapy starts. Do NOT lay the patient flat (worsens airway compromise), avoid sedation, and defer a general-anaesthetic biopsy to a controlled setting — the mediastinal mass makes airway collapse under anaesthesia a real and lethal risk. Biopsy under local or after the airway is secured. The same caution applies to any mediastinal mass with orthopnoea or stridor.[1]

References

1. [1]Connors JM, Cozen W, Steidl C, et al. Hodgkin lymphoma Nat Rev Dis Primers, 2020.PMID 32703953
2. [2]Cheson BD, Fisher RI, Barrington SF, et al. Recommendations for initial evaluation, staging, and response assessment of Hodgkin and non-Hodgkin lymphoma: the Lugano classification J Clin Oncol, 2014.PMID 25113753
3. [3]Hasenclever D, Diehl V. A prognostic score for advanced Hodgkin's disease. International Prognostic Factors Project on Advanced Hodgkin's Disease N Engl J Med, 1998.PMID 9819449
4. [4]The International Non-Hodgkin's Lymphoma Prognostic Factors Project. A predictive model for aggressive non-Hodgkin's lymphoma N Engl J Med, 1993.PMID 8141877
5. [5]Sehn LH, Berry B, Chhanabhai M, et al. The revised International Prognostic Index (R-IPI) is a better predictor of outcome than the standard IPI for patients with diffuse large B-cell lymphoma treated with R-CHOP Blood, 2007.PMID 17105812
6. [6]Pfreundschuh M, Trümper L, Osterborg A, et al. CHOP-like chemotherapy plus rituximab versus CHOP-like chemotherapy alone in young patients with good-prognosis diffuse large-B-cell lymphoma: a randomised controlled trial by the MabThera International Trial (MInT) Group Lancet Oncol, 2006.PMID 16648042
7. [7]Carbone A, Roulland S, Gloghini A, et al. Follicular lymphoma Nat Rev Dis Primers, 2019.PMID 31831752
8. [8]López C, Burkhardt B, Chan JKC, et al. Burkitt lymphoma Nat Rev Dis Primers, 2022.PMID 36522349
9. [9]Zucca E, Bertoni F. Marginal zone lymphomas Hematol Oncol, 2023.PMID 37294969
10. [10]Ferreri AJM, Calimeri T, Cwynarski K, et al. Primary central nervous system lymphoma Nat Rev Dis Primers, 2023.PMID 37322012
11. [11]Batlevi CL, Matsuki E, Brentjens RJ, Younes A. Novel immunotherapies in lymphoid malignancies Nat Rev Clin Oncol, 2016.PMID 26525683
12. [12]Ansell SM Hodgkin lymphoma: 2025 update on diagnosis, risk-stratification, and management Am J Hematol, 2024.PMID 39239794