Hodgkin Lymphoma

Overview
Epidemiology and Risk Factors
Pathology and Reed-Sternberg Cells
Histologic Subtypes
Clinical Presentation
Staging: Ann Arbor and PET-CT
Treatment: Chemotherapy and Targeted Therapy
Relapsed and Refractory Disease
Late Effects and Long-Term Survivorship
Key Research Papers
Connections
Featured Videos

1. Overview

Hodgkin lymphoma (HL) is a cancer of the lymphatic system. The National Cancer Institute's PDQ summary states that up to 90% of all newly diagnosed patients with HL can be cured with combination chemotherapy and/or radiation therapy (NCI PDQ, adult Hodgkin lymphoma treatment). The SEER program estimates 8,920 new cases and 1,100 deaths in the United States in 2026 (0.4% of all new cancer cases) and reports a 5-year relative survival of 89.3% for 2016–2022. By stage at diagnosis, SEER's 5-year relative survival is 92.7% for stage I, 95.4% for stage II, 87.7% for stage III and 82.8% for stage IV (SEER Cancer Stat Facts: Hodgkin lymphoma). Because many patients are young adults, the long-term effects of treatment matter a great deal: NCI PDQ reports that HL is the main cause of death for the first 15 years after treatment, and that by 15 to 20 years after therapy the cumulative mortality from a second cancer, cardiovascular disease or pulmonary fibrosis exceeds the cumulative mortality from HL.

The defining feature of classical HL is the Hodgkin and Reed-Sternberg (HRS) cell. A 2021 review describes these tumor cells as rare among an extensive and complex microenvironment; they derive from B cells, apparently from pre-apoptotic germinal center B cells, but have largely lost the typical B-cell gene expression program. Bi- or multinucleated Reed-Sternberg cells arise from mononuclear Hodgkin cells through incomplete cytokinesis and refusion, and HRS cells attract many kinds of immune cells into the affected tissue to support their own survival and create an immunosuppressive environment PubMed PMID: 33686198. Preclinical studies suggest that Reed-Sternberg cells use the programmed death 1 (PD-1) pathway to evade immune detection, the rationale for testing PD-1-blocking antibodies in HL PubMed PMID: 25482239.

2. Epidemiology and Risk Factors

SEER reports a rate of new cases of 2.5 per 100,000 men and women per year (2019–2023, age-adjusted). HL is more common among young adults and among men than women; it is most frequently diagnosed at ages 20–34 (31.7% of new cases), and the median age at diagnosis is 38. An estimated 240,775 people were living with HL in the United States in 2023 (SEER). NCI PDQ lists early adulthood (ages 20–39, most often) or late adulthood (65 and older, less often), male sex, previous Epstein-Barr virus infection in the teenage years or early childhood, and a first-degree relative with HL as risk factors.

Findings on specific risk factors include:

Epstein-Barr virus (EBV) — a 2026 meta-analysis of 307 studies found a pooled EBV prevalence of 53.0% in HL tumors from HIV-negative people (measured by EBV-encoded RNA in situ hybridisation) PubMed PMID: 41947331. In Danish and Swedish cohorts of 38,555 people with infectious mononucleosis, serologically confirmed mononucleosis was linked to a higher risk of EBV-positive HL (relative risk 4.0), with no increase in EBV-negative HL; the estimated median time from mononucleosis to EBV-positive HL was 4.1 years PubMed PMID: 14523140.
HIV infection and transplant immunosuppression — a 2007 meta-analysis found HL incidence raised in people with HIV/AIDS (standardized incidence ratio 11.03) and in transplant recipients (3.89), a pattern the authors attribute to immune deficiency PubMed PMID: 17617273.
Family history — in Swedish and Danish registry data, relatives of people with HL had a pooled relative risk of 3.11, with stronger familial risk in families of patients diagnosed before age 40, in males and in siblings; the authors note that the cumulative lifetime risks remain very small PubMed PMID: 15112271. Among 432 twin sets, 10 of 179 identical-twin pairs became concordant for HL and none of 187 fraternal pairs did, which the authors read as genetic susceptibility to the young-adult form PubMed PMID: 7824015.

3. Pathology and Reed-Sternberg Cells

NCI PDQ gives the typical immunophenotype of classical HL as CD15+, CD20−, CD30+, CD45−, and that of nodular lymphocyte-predominant disease as CD15−, CD20+, CD30−, CD45+. CD30 is the target of brentuximab vedotin, an antibody-drug conjugate; PDQ notes that CD30 is expressed on malignant Reed-Sternberg cells but has limited expression on normal cells.

On the molecular side, the 2021 review reports that sequencing has not revealed any highly recurrent HRS-cell-specific lesion, but that genetic lesions in members of the NF-κB and JAK/STAT pathways and in immune-evasion factors play major roles, and that HRS cells show constitutive activation of numerous signaling pathways. In EBV-positive cases, EBV is described as a main player in rescuing “crippled” germinal center B cells from apoptosis PubMed PMID: 33686198. Alterations in chromosome 9p24.1 increase the abundance of the PD-1 ligands PD-L1 and PD-L2 PubMed PMID: 25482239; the CheckMate 205 investigators describe genetic alterations causing overexpression of these ligands as near universal in classical HL PubMed PMID: 29584546.

4. Histologic Subtypes

NCI PDQ lists the WHO/REAL classification of HL as classical HL — nodular sclerosis, mixed cellularity, lymphocyte-depleted and lymphocyte-rich — and the distinct nodular lymphocyte-predominant HL (NLPHL), an entity of B-cell origin.

Nodular sclerosis — in a SEER analysis of 21,734 cases diagnosed 1988–2005, nodular sclerosis made up 61% of adult cases and 76% of cases in children and adolescents PubMed PMID: 21054151.
Mixed cellularity — in the same SEER analysis it made up 22% of cases in children under 10 and 8.5% in older children and adolescents.
Lymphocyte-depleted — among 10,019 patients whose pathology was centrally reviewed for the German Hodgkin Study Group, 84 (<1%) had this subtype; they presented more often with advanced-stage disease and B symptoms (NCI PDQ).
Lymphocyte-rich — a classical subtype; NCI PDQ reports that a retrospective series of 426 lymphocyte-predominant cases (NLPHL and lymphocyte-rich classical HL) found no significant difference in response or outcome between the two when they present at stage I or II.
NLPHL — NCI PDQ reports earlier-stage disease and longer survival than classical HL; it is usually diagnosed in asymptomatic younger patients with cervical or inguinal nodes, usually without mediastinal involvement, and bulky disease and B symptoms are uncommon. Options described in PDQ include watchful waiting, limited-field radiation for early stage, chemotherapy for advanced stage, and rituximab. Unlike HRS cells, NLPHL tumor cells have largely kept their germinal center B-cell expression program PubMed PMID: 33686198.

5. Clinical Presentation

NCI PDQ lists painless, swollen lymph nodes in the neck, axilla or groin; fever of 38°C or higher; drenching, recurrent night sweats; weight loss of 10% or more of baseline weight in the previous 6 months; pruritus, especially after bathing or after drinking alcohol; and fatigue. HL most often presents in lymph node groups above the diaphragm and/or in the mediastinal nodes; involvement of Waldeyer's ring or the tonsils is rarely seen.

B symptoms, as NCI PDQ defines them for staging:

Unexplained fever with temperatures above 38°C.
Drenching and recurrent night sweats.
Unexplained weight loss of more than 10% of body weight in the 6 months before diagnosis.

Any of these adds the letter “B” to the stage (for example, IIIB rather than IIIA). PDQ states that fevers and weight loss are the most significant B symptoms and that night sweats alone do not confer an adverse prognosis. In the SEER analysis, systemic symptoms were recorded in 48% of adults and 39% of children and adolescents PubMed PMID: 21054151.

6. Staging: Ann Arbor and PET-CT

NCI PDQ reports that the American Joint Committee on Cancer has adopted the Lugano classification, which replaces the 1971 Ann Arbor system and its later Cotswolds modifications:

Stage I: involvement of a single lymphatic site (nodal region, Waldeyer's ring, thymus or spleen).
Stage II: two or more lymph node regions on the same side of the diaphragm; stage II with bulk may be counted as early or advanced disease depending on histology and prognostic factors.
Stage III: lymph node regions on both sides of the diaphragm, or nodes above the diaphragm with spleen involvement.
Stage IV: diffuse or disseminated involvement of one or more extralymphatic organs, including any involvement of the bone marrow, liver, cerebrospinal fluid or multiple lung lesions.

HL keeps the A or B designation; in the Lugano classification, bulk in HL is a mass greater than one-third of the thoracic diameter on chest CT, or a mass larger than 10 cm (NCI PDQ). The 2014 Lugano recommendations formally incorporated FDG PET-CT into standard staging of FDG-avid lymphomas, stated that bone marrow biopsy is no longer indicated for routine staging of HL, and set the 5-point scale for PET-CT response assessment PubMed PMID: 25113753.

In a Danish study of 99 patients, FDG-PET/CT would have upstaged 17% and downstaged 5% of patients compared with conventional staging, changing treatment in 7%; the authors caution against giving patients with an excellent prognosis more intensive treatment because of these methods PubMed PMID: 16585015. In an Italian-Danish study of 260 patients with advanced HL treated with ABVD, 2-year progression-free survival was 12.8% after a positive PET scan following two cycles (PET-2) and 95.0% after a negative one; in multivariate analysis only PET-2 remained significant PubMed PMID: 17646666. NCI PDQ describes the PET-CT scan after two cycles as the best predictor of treatment failure, with frequent false positives in limited-stage disease.

7. Treatment: Chemotherapy and Targeted Therapy

Early-stage favorable HL

NCI PDQ defines early favorable classical HL as clinical stage I or II without B symptoms, extranodal disease, bulky disease, three or more nodal sites, or a sedimentation rate of 50 mm/h or higher. The options it lists are ABVD (doxorubicin, bleomycin, vinblastine, dacarbazine) for three to six cycles; ABVD for two to four cycles plus involved-field radiation therapy (20 Gy or 30 Gy); or, in certain circumstances such as older adults who cannot receive chemotherapy, radiation alone. In the German HD10 trial of 1,190 patients, two or four cycles of ABVD with 20 or 30 Gy gave the same 10-year progression-free survival (87%) and overall survival (94%) in all four groups. In three PET-guided trials (H10, RAPID and HD16; 2,889 patients), radiation could be omitted after a negative PET-CT with no significant loss of overall survival, but two of the trials showed a higher relapse risk without radiation; in HD16, 5-year progression-free survival was 93.4% with combined-modality therapy and 86.1% with ABVD alone (NCI PDQ).

Advanced-stage HL (IIB with bulky disease, III–IV)

NCI PDQ states that six cycles of N-AVD (nivolumab with doxorubicin, vinblastine and dacarbazine) or BV-AVD (brentuximab vedotin with the same three drugs) have replaced ABVD, the previous standard for three decades, and that ABVD remains a viable option in cost-conscious settings.

The ECHELON-1 trial randomized 1,334 patients with previously untreated stage III or IV classical HL to BV-AVD or ABVD. At a median 24.6 months, 2-year modified progression-free survival was 82.1% vs. 77.2% (hazard ratio 0.77). Neutropenia (58% vs. 45%) and peripheral neuropathy (67% vs. 43%) were more common with BV-AVD, while grade 3 or higher pulmonary toxicity was reported in less than 1% vs. 3%; 11 of 13 on-treatment deaths in the ABVD group were associated with pulmonary toxicity PubMed PMID: 29224502. At a median 73 months, 39 vs. 64 patients had died (hazard ratio 0.59), 6-year overall survival was 93.9% vs. 89.4%, and fewer second cancers were reported with BV-AVD (23 vs. 32 patients) PubMed PMID: 35830649.

The SWOG S1826 trial randomized 994 patients aged 12 or older with stage III or IV HL to N-AVD or BV-AVD. At a median 2.1 years, 2-year progression-free survival was 92% with N-AVD vs. 83% with BV-AVD (hazard ratio 0.45); immune-related adverse events were infrequent with nivolumab, and brentuximab vedotin was associated with more treatment discontinuation PubMed PMID: 39413375. NCI PDQ reports discontinuation for side effects in 22% vs. 11%, mainly from peripheral sensory neuropathy, and states that N-AVD has become the treatment of choice for stage III and IV HL.

Response-adapted therapy with interim PET changes treatment according to the scan after two cycles. In the RATHL trial (1,214 patients registered), 937 of 1,119 scanned patients (83.7%) were PET-negative after two cycles of ABVD and were randomized to continue ABVD or omit bleomycin (AVD). Three-year progression-free survival was 85.7% vs. 84.4%; the authors report that the result fell just short of the prespecified non-inferiority margin, and that omitting bleomycin lowered pulmonary toxicity without significantly lower efficacy. The 172 PET-positive patients received BEACOPP, with a 3-year progression-free survival of 67.5% PubMed PMID: 27332902. NCI PDQ reports that at a median 7.3 years, 7-year overall survival was 93.2% with ABVD and 93.5% with AVD.

Escalated BEACOPP (bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, procarbazine and prednisone in escalated doses) is described by the HD18 investigators as very active, at the expense of severe toxicities. In HD18, patients who were PET-negative after two cycles had a 5-year progression-free survival of 92.2% with four cycles vs. 90.8% with six or eight, with fewer severe infections (8% vs. 15%) and organ toxicities (8% vs. 18%); adding rituximab did not improve outcomes in PET-2-positive patients PubMed PMID: 29061295. A 2013 network meta-analysis of 14 trials (9,993 patients) found the highest overall survival with six cycles of escalated BEACOPP (hazard ratio 0.38 vs. ABVD; 5-year survival 95% vs. 88%) PubMed PMID: 23948348, while NCI PDQ summarizes multiple trials and a meta-analysis as showing equivalent overall survival for ABVD and the other regimens. In the HD21 trial of 1,500 adults aged 60 or younger, PET-guided BrECADD (brentuximab vedotin, etoposide, cyclophosphamide, doxorubicin, dacarbazine and dexamethasone) had less treatment-related morbidity than escalated BEACOPP (42% vs. 59%) and a 4-year progression-free survival of 94.3% vs. 90.9% (hazard ratio 0.66); 4-year overall survival was 98.6% vs. 98.2% PubMed PMID: 38971175.

8. Relapsed and Refractory Disease

NCI PDQ reports that more than half of patients with recurrent HL can achieve long-term disease-free survival, or cure, with reinduction therapy followed by stem cell transplant, describing a “75% rule”: about 75% reach a clinical complete remission with salvage reinduction, and about 75% of those who undergo autologous stem cell transplant (ASCT) are free of disease at 4 years. The poor prognostic factors it lists include primary refractory disease, relapse less than 12 months after initial therapy, failure to reach a complete remission after reinduction (a PET-CT Deauville score of 4 or 5 followed by progression), B symptoms or extranodal disease at relapse, and more than two previous salvage regimens.

Brentuximab vedotin consolidation after ASCT — in the placebo-controlled AETHERA trial of 329 patients at risk of relapse or progression, progression-free survival was significantly longer with brentuximab vedotin (hazard ratio 0.57; median 42.9 vs. 24.1 months); peripheral sensory neuropathy occurred in 56% vs. 16% PubMed PMID: 25796459. NCI PDQ reports 5-year progression-free survival of 59% vs. 41%.

PD-1 checkpoint inhibitors have been studied in heavily pretreated disease. In a phase 1 study of 23 patients, nivolumab produced an objective response in 20 (87%), including 17% complete responses PubMed PMID: 25482239. In the phase 2 CheckMate 205 trial, the objective response rate was 66.3% in 80 patients whose disease had progressed after both ASCT and brentuximab vedotin PubMed PMID: 27451390 and 69% across all 243 patients, with a median progression-free survival of 14.7 months PubMed PMID: 29584546; at about 5 years, overall survival was 71.4% PubMed PMID: 37530622. In the phase 2 KEYNOTE-087 trial of pembrolizumab in 210 patients, the overall response rate was 69.0% and the complete response rate 22.4% PubMed PMID: 28441111; at a median 27.6 months these were 71.9% and 27.6%, with a median duration of response of 16.5 months PubMed PMID: 31409671. NCI PDQ also reports a randomized trial of 304 patients in which median progression-free survival was 13.2 months with pembrolizumab vs. 8.3 months with brentuximab vedotin (hazard ratio 0.65).

The FDA-approved labels (DailyMed) list these classical HL indications: nivolumab with AVD for previously untreated stage III or IV disease in patients 12 and older, and as a single agent after relapse or progression following autologous HSCT and brentuximab vedotin, or after 3 or more lines of therapy that include autologous HSCT (nivolumab label); pembrolizumab for adults with relapsed or refractory classical HL (pembrolizumab label); and brentuximab vedotin with AVD for adults with previously untreated stage III or IV disease, as consolidation after autologous HSCT in patients at high risk of relapse or progression, and after failure of autologous HSCT or of at least two prior multi-agent chemotherapy regimens in patients who are not transplant candidates (brentuximab vedotin label).

NCI PDQ reports that allogeneic transplant from an HLA-matched sibling gives lower relapse rates, but that the benefit may be offset by increased toxic effects; reduced-intensity conditioning for allogeneic transplant is still under clinical evaluation.

9. Late Effects and Long-Term Survivorship

A 2016 review reports that second cancers and cardiovascular disease are the leading causes of death in long-term HL survivors, who have two- to fourfold higher risks of both than the general population; other late effects include pulmonary dysfunction, thyroid dysfunction, infertility, neck muscle atrophy and persistent fatigue PubMed PMID: 27913498.

Second cancers — the review reports that radiotherapy is associated with a 1.5- to 15-fold increased risk of solid cancers, rising with follow-up time and with younger age at treatment and remaining elevated for at least 40 years; alkylating chemotherapy, especially procarbazine, raises the risk of leukemia and of lung and gastrointestinal cancers; gonadotoxic chemotherapy lowers radiation-associated breast cancer risk by inducing premature menopause; and smoking multiplies the treatment-associated lung cancer risk PubMed PMID: 27913498. NCI PDQ gives the cumulative risk of a second solid tumor as about 13% at 15 years, 17% at 20 years, 22% at 25 years and 48% at 40 years, notes that breast cancer risk appears greatest in females treated with radiation before age 30, and lists mesothelioma among the observed second tumors. PDQ puts the 10-year risk of acute myeloid leukemia at about 3% after MOPP-containing regimens and below 1% after ABVD.
Cardiovascular disease — radiotherapy increases the risk of coronary heart disease, valvular heart disease, heart failure and pericarditis, while anthracycline-containing chemotherapy increases the risks of heart failure and valvular disease; radiation-related cardiovascular toxicity is usually seen from 5 to at least 35 years after therapy PubMed PMID: 27913498.
Pulmonary toxicity — NCI PDQ reports that bleomycin lung toxicity in ABVD is seen in patients older than 40, and that mantle-field radiation can impair pulmonary function, usually without clinical signs, with recovery on testing often after 2 to 3 years.
Endocrine effects — NCI PDQ describes hypothyroidism as a late complication primarily related to radiation and states that survivors who had neck radiation are followed with annual thyroid-stimulating hormone testing. Infertility follows mainly MOPP or BEACOPP: after six to eight cycles of BEACOPP, 82% of women younger than 30 recovered menses but only 45% of women older than 30, while ABVD appears to spare long-term testicular and ovarian function.

Several treatment changes have been aimed partly at these effects: NCI PDQ reports that since 2010 radiation techniques have used smaller target volumes, lower-dose involved-field radiation (20 Gy), deep-inspiration breath holding, intensity-modulated radiation and proton therapy, and that their effect on cardiovascular risk still needs evaluation; PET-guided trials have tested omitting radiation or bleomycin, and the BV-AVD and N-AVD regimens leave out bleomycin.

Key Research Papers

Connors JM, Jurczak W, Straus DJ, et al. (2018). Brentuximab Vedotin with Chemotherapy for Stage III or IV Hodgkin's Lymphoma. N Engl J Med 378:331-344 — PubMed PMID: 29224502
Johnson P, Federico M, Kirkwood A, et al. (2016). Adapted Treatment Guided by Interim PET-CT Scan in Advanced Hodgkin's Lymphoma. N Engl J Med 374:2419-29 — PubMed PMID: 27332902
Ansell SM, Lesokhin AM, Borrello I, et al. (2015). PD-1 blockade with nivolumab in relapsed or refractory Hodgkin's lymphoma. N Engl J Med 372:311-9 — PubMed PMID: 25482239
Moskowitz CH, Nademanee A, Masszi T, et al. (2015). Brentuximab vedotin as consolidation therapy after autologous stem-cell transplantation in patients with Hodgkin's lymphoma at risk of relapse or progression (AETHERA): a randomised, double-blind, placebo-controlled, phase 3 trial. Lancet 385:1853-62 — PubMed PMID: 25796459
Skoetz N, Trelle S, Rancea M, et al. (2013). Effect of initial treatment strategy on survival of patients with advanced-stage Hodgkin's lymphoma: a systematic review and network meta-analysis. Lancet Oncol 14:943-52 — PubMed PMID: 23948348
Gallamini A, Hutchings M, Rigacci L, et al. (2007). Early interim 2-[18F]fluoro-2-deoxy-D-glucose positron emission tomography is prognostically superior to international prognostic score in advanced-stage Hodgkin's lymphoma: a report from a joint Italian-Danish study. J Clin Oncol 25:3746-52 — PubMed PMID: 17646666
Ansell SM, Bröckelmann PJ, von Keudell G, et al. (2023). Nivolumab for relapsed/refractory classical Hodgkin lymphoma: 5-year survival from the pivotal phase 2 CheckMate 205 study. Blood Adv 7:6266-6274 — PubMed PMID: 37530622
Borchmann P, Goergen H, Kobe C, et al. (2017). PET-guided treatment in patients with advanced-stage Hodgkin's lymphoma (HD18): final results of an open-label, international, randomised phase 3 trial by the German Hodgkin Study Group. Lancet 390:2790-2802 — PubMed PMID: 29061295
Hutchings M, Loft A, Hansen M, et al. (2006). Position emission tomography with or without computed tomography in the primary staging of Hodgkin's lymphoma. Haematologica 91:482-9 — PubMed PMID: 16585015
van Leeuwen FE, Ng AK (2016). Long-term risk of second malignancy and cardiovascular disease after Hodgkin lymphoma treatment. Hematology Am Soc Hematol Educ Program 2016:323-330 — PubMed PMID: 27913498
Chen R, Zinzani PL, Fanale MA, et al. (2017). Phase II Study of the Efficacy and Safety of Pembrolizumab for Relapsed/Refractory Classic Hodgkin Lymphoma. J Clin Oncol 35:2125-2132 — PubMed PMID: 28441111
Swerdlow SH, Campo E, Pileri SA, et al. (2016). The 2016 revision of the World Health Organization classification of lymphoid neoplasms. Blood 127:2375-90 — PubMed PMID: 26980727
Ansell SM, Radford J, Connors JM, et al. (2022). Overall Survival with Brentuximab Vedotin in Stage III or IV Hodgkin's Lymphoma. N Engl J Med 387:310-320 — PubMed PMID: 35830649
Herrera AF, LeBlanc M, Castellino SM, et al. (2024). Nivolumab+AVD in Advanced-Stage Classic Hodgkin's Lymphoma. N Engl J Med 391:1379-1389 — PubMed PMID: 39413375
Borchmann P, Ferdinandus J, Schneider G, et al. (2024). Assessing the efficacy and tolerability of PET-guided BrECADD versus eBEACOPP in advanced-stage, classical Hodgkin lymphoma (HD21): a randomised, multicentre, parallel, open-label, phase 3 trial. Lancet 404:341-352 — PubMed PMID: 38971175
Younes A, Santoro A, Shipp M, et al. (2016). Nivolumab for classical Hodgkin's lymphoma after failure of both autologous stem-cell transplantation and brentuximab vedotin: a multicentre, multicohort, single-arm phase 2 trial. Lancet Oncol 17:1283-94 — PubMed PMID: 27451390
Armand P, Engert A, Younes A, et al. (2018). Nivolumab for Relapsed/Refractory Classic Hodgkin Lymphoma After Failure of Autologous Hematopoietic Cell Transplantation: Extended Follow-Up of the Multicohort Single-Arm Phase II CheckMate 205 Trial. J Clin Oncol 36:1428-1439 — PubMed PMID: 29584546
Chen R, Zinzani PL, Lee HJ, et al. (2019). Pembrolizumab in relapsed or refractory Hodgkin lymphoma: 2-year follow-up of KEYNOTE-087. Blood 134:1144-1153 — PubMed PMID: 31409671
Hjalgrim H, Askling J, Rostgaard K, et al. (2003). Characteristics of Hodgkin's lymphoma after infectious mononucleosis. N Engl J Med 349:1324-32 — PubMed PMID: 14523140
Mack TM, Cozen W, Shibata DK, et al. (1995). Concordance for Hodgkin's disease in identical twins suggesting genetic susceptibility to the young-adult form of the disease. N Engl J Med 332:413-8 — PubMed PMID: 7824015
Goldin LR, Pfeiffer RM, Gridley G, et al. (2004). Familial aggregation of Hodgkin lymphoma and related tumors. Cancer 100:1902-8 — PubMed PMID: 15112271
Grulich AE, van Leeuwen MT, Falster MO, et al. (2007). Incidence of cancers in people with HIV/AIDS compared with immunosuppressed transplant recipients: a meta-analysis. Lancet 370:59-67 — PubMed PMID: 17617273
Hirabayashi M, Georges D, Combes JD, et al. (2026). Attributable Fraction of Epstein-Barr Virus in Subtypes of Lymphoma: A Systematic Review and Global Meta-Analysis. Int J Cancer 159:896-903 — PubMed PMID: 41947331
Bazzeh F, Rihani R, Howard S, et al. (2010). Comparing adult and pediatric Hodgkin lymphoma in the Surveillance, Epidemiology and End Results Program, 1988-2005: an analysis of 21 734 cases. Leuk Lymphoma 51:2198-207 — PubMed PMID: 21054151
Weniger MA, Küppers R (2021). Molecular biology of Hodgkin lymphoma. Leukemia 35:968-981 — PubMed PMID: 33686198
Cheson BD, Fisher RI, Barrington SF, et al. (2014). Recommendations for initial evaluation, staging, and response assessment of Hodgkin and non-Hodgkin lymphoma: the Lugano classification. J Clin Oncol 32:3059-68 — PubMed PMID: 25113753

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Connections

Hematology
Non-Hodgkin Lymphoma — the larger, more heterogeneous family of lymphomas; shares many staging, imaging, and treatment concepts with HL.
Leukemia — related hematologic malignancy; lymphocyte biology and bone marrow involvement bridge the two disease families.
Oncology — full cancer index on this site.
Autoimmune Disease — the inflammatory tumor microenvironment of HL mimics autoimmune tissue reactions; immune-related adverse events are among the reported side effects of the PD-1 inhibitors used in HL.
Mononucleosis — serologically confirmed infectious mononucleosis was linked to a higher risk of EBV-positive Hodgkin lymphoma in Danish and Swedish cohorts.
Complete Blood Count — a complete blood count is part of the diagnostic evaluation NCI PDQ lists for HL; a low lymphocyte count and a white-cell count of 15 × 10⁹/L or higher are factors in the International Prognostic Score.
All Conditions — complete disease index.
Lymphoma — overview of the lymphoma family as a whole, where HL sits alongside the non-Hodgkin subtypes.