Introduction

Non-Hodgkin lymphoma is one of the most common cancers worldwide. The disease starts in lymphocytes, the white blood cells that normally protect the body from infection. When a lymphocyte's DNA is damaged in the wrong place, the cell can multiply unchecked and crowd out healthy tissue.

These abnormal cells collect in lymph nodes and make them swell. The medical term for swollen lymph nodes is lymphadenopathy. The cancer can also spread to the bone marrow, spleen, gut, skin, and even the brain. Each location produces a different set of symptoms, which is one reason non-Hodgkin lymphoma can be tricky to recognize.

This article walks through the classification, signs, workup, and treatment of non-Hodgkin lymphoma. We will also flag the modern updates: the 2022 WHO classification, CAR-T therapy, and the newest bispecific antibodies [1,2].

The Lymphatic System: A Quick Refresher

The lymphatic system is the highway and staging ground of the immune system. It has two parts.

Primary lymphoid organs are where lymphocytes are made and mature. Bone marrow produces all blood cells, and B lymphocytes finish maturing there. T lymphocytes leave the bone marrow as immature cells and mature in the thymus.

Secondary lymphoid organs are where mature lymphocytes meet antigens and launch immune responses. These include lymph nodes (in the neck, armpits, groin, and elsewhere), the spleen, the tonsils, and the adenoids. Lymph fluid travels between these stations through a network of lymphatic vessels.

Because lymphocytes circulate everywhere, non-Hodgkin lymphoma can appear almost anywhere in the body.ody.

Types of Lymphoma

Lymphoma splits into two main families: Hodgkin lymphoma and non-Hodgkin lymphoma. Non-Hodgkin lymphoma is more common and accounts for roughly 85% of all lymphoma cases [3]. The distinction matters because they look different under the microscope and respond to different treatments.

Hodgkin vs. Non-Hodgkin Lymphomas (NHL)

Epidemiology

Non-Hodgkin lymphoma accounts for about 4% of new cancer diagnoses in the United States [3]. Globally, it represents close to 3% of cancer cases. Incidence increased substantially in the second half of the 20th century but has been roughly stable to slightly declining over the past decade.

Three demographic patterns that matter:

• Age. The median age at diagnosis is 67, and more than half of patients are over 65. Some subtypes, like Burkitt lymphoma and lymphoblastic lymphoma, are more common in children.
• Sex. Men have a slightly higher incidence than women across most subtypes.
• Race and geography. In the US, white populations have the highest rates. The T-cell subtype mycosis fungoides is more common in Black populations, and adult T-cell leukemia/lymphoma clusters in regions where HTLV-1 infection is endemic, such as parts of Japan, the Caribbean, and West Africa.

Classifications of Non-Hodgkin Lymphoma (NHL)

The current standards are the WHO classification of haematolymphoid tumours, 5th edition (WHO-HAEM5, 2022) and the International Consensus Classification (ICC, 2022) [1,2]. Both recognize more than 50 mature B-cell entities and more than 30 mature T-cell and NK-cell entities.

Cell of origin

• B-cell non-Hodgkin lymphoma makes up 85–90% of cases [3]. B-cells normally produce antibodies.
• T-cell and NK-cell non-Hodgkin lymphoma makes up the remaining 10–15%. T-cells normally kill infected cells directly.

Clinical pace

• Indolent (slow-growing) lymphomas, like follicular lymphoma and marginal zone lymphoma, can be present for years before causing problems. They are usually not curable but are very manageable.
• Aggressive (fast-growing) lymphomas, like DLBCL and Burkitt lymphoma, cause symptoms quickly and need urgent treatment. They are often curable.

Mantle cell lymphoma sits awkwardly between the two and is generally treated as aggressive disease.

Pathogenesis of Non-Hodgkin Lymphoma

Non-Hodgkin lymphoma is driven by a combination of genetic accidents, viral infections, and environmental exposures. No single cause is found in most patients.

Genetic Changes

Two kinds of genetic damage matter most.

Mutations in tumor suppressor genes like TP53 and PTEN remove the brakes on cell division. Chromosomal translocations swap pieces between chromosomes and can switch oncogenes on. Classic examples in non-Hodgkin lymphoma include:

• t(14;18)(q32;q21) — fuses BCL2 to the immunoglobulin heavy chain locus; the genetic hallmark of follicular lymphoma.
• t(11;14)(q13;q32) — drives overexpression of cyclin D1; the defining lesion of mantle cell lymphoma.
• t(8;14)(q24;q32) — places MYC under immunoglobulin gene control; characteristic of Burkitt lymphoma.

Viral Infections

Several viruses are linked to specific subtypes:

• Epstein-Barr virus (EBV) is associated with Burkitt lymphoma, extranodal NK/T-cell lymphoma, and post-transplant lymphoproliferative disorders.
• Human T-cell lymphotropic virus type 1 (HTLV-1) causes adult T-cell leukemia/lymphoma.
• Human herpesvirus 8 (HHV-8) is linked to primary effusion lymphoma.
• Helicobacter pylori (a bacterium, but worth knowing) drives gastric MALT lymphoma, which can sometimes be cured by antibiotics alone.

Environmental and Other Risk Factors

Long-term exposure to certain pesticides and industrial solvents has been linked to a higher risk, although the absolute increase is small. High-dose radiation raises risk. Immune suppression (whether from HIV, transplant medication, or autoimmune disease) strongly increases risk. A family history of lymphoma slightly raises risk, but most non-Hodgkin lymphoma is not inherited.

Non-Hodgkin Lymphoma Symptoms

Symptoms depend on subtype, location, and pace. Some patients feel completely well at diagnosis; others arrive critically ill.

Common Symptoms

• Painless swollen lymph nodes, usually in the neck, armpit, or groin. This is the most common presenting sign.
• B symptoms, a constellation that has prognostic weight in staging:
  • Fever above 38°C with no clear cause, lasting several days
  • Drenching night sweats that soak through clothing or bedding
  • Unexplained weight loss greater than 10% of body weight over 6 months
• Persistent fatigue, often disproportionate to activity.
• Itchy skin, sometimes severe.

Symptoms by Location

Swollen nodes in different regions cause different problems. Chest nodes can press on airways and cause a dry cough, breathlessness, or chest pressure. Abdominal nodes can produce a vague ache, nausea, or early fullness after meals. Pelvic nodes sometimes cause leg swelling.

When non-Hodgkin lymphoma spreads beyond lymph nodes (extranodal disease), symptoms reflect the organ involved. Bone marrow involvement causes anemia (low red cells), infections from low white cells, or bleeding from low platelets. Spleen involvement causes left upper abdominal discomfort. Skin involvement causes rash or plaques.

Indolent lymphomas can stay quiet for years. Aggressive lymphomas can go from "I noticed a lump last month" to a hospital admission in weeks. Pace itself is a clinical clue.

Laboratory Investigations

No single test confirms non-Hodgkin lymphoma. The workup combines tissue, blood, imaging, and genetics.

The Cornerstone: Lymph Node Biopsy

A lymph node biopsy is essential [3]. A pathologist examines the tissue under the microscope and uses immunophenotyping (staining for surface markers like CD20 (B-cells), CD3 (T-cells), CD10, BCL2, and BCL6) to confirm the subtype. Without this step, you cannot stage or treat correctly. Fine-needle aspiration alone is usually not enough; excisional or core biopsy is preferred.

Blood Tests

A complete blood count screens for anemia, low platelets, or circulating lymphoma cells. Liver and kidney function tests assess organ status and guide chemotherapy choices. Lactate dehydrogenase (LDH) is often elevated in fast-growing lymphomas and is part of the IPI score. Uric acid is checked because rapidly dying tumor cells can cause tumor lysis syndrome. Viral serology for HIV, hepatitis B, hepatitis C, EBV, and HTLV-1 may be added based on subtype.

Cytogenetic and Molecular Tests

Karyotyping and fluorescence in situ hybridization (FISH) detect translocations that define specific subtypes:

• t(14;18) in follicular lymphoma
• t(11;14) in mantle cell lymphoma
• MYC rearrangements in Burkitt lymphoma (and "double-hit" lymphomas)
• ALK rearrangements in a subset of anaplastic large cell lymphoma

In DLBCL, the cell-of-origin (germinal center B-cell type, or GCB, versus activated B-cell type, or ABC / non-GCB) is determined by the Hans algorithm or gene expression profiling. It carries prognostic and treatment implications.

Imaging

PET-CT is the imaging standard for staging and response assessment in most lymphomas [7]. Response is graded using the Deauville 5-point score, which compares tumor uptake to liver and blood-pool background. A Deauville score of 1–3 generally indicates a good response; 4–5 indicates residual or progressing disease.

Bone Marrow Biopsy

A bone marrow aspirate and trephine are performed when bone marrow involvement is suspected or when the subtype commonly involves it. PET-CT has reduced the need for bone marrow biopsy in DLBCL, but it remains important in many indolent and T-cell lymphomas.

Staging of Non-Hodgkin Lymphoma

The Lugano classification is the current standard for staging non-Hodgkin lymphoma [7]. It uses Roman numerals I to IV.

• Stage I — one lymph node region or one extranodal site
• Stage II — two or more lymph node regions on the same side of the diaphragm
• Stage III — lymph node regions on both sides of the diaphragm
• Stage IV — widespread involvement of one or more extranodal organs, such as bone marrow or liver

Modifiers add useful detail. "E" marks extranodal involvement. "B" marks the presence of B symptoms. Bulky disease — a single mass larger than about 7.5–10 cm depending on subtype — is noted because it influences treatment.

Prognostic Scoring

Stage alone does not predict outcome well. Two scoring systems are used alongside stage:

• The International Prognostic Index (IPI) for aggressive lymphomas like DLBCL [11]. Points are added for age over 60, elevated LDH, poor performance status, advanced stage, and more than one extranodal site.
• The Follicular Lymphoma International Prognostic Index (FLIPI) for follicular lymphoma [10], which uses age, hemoglobin, LDH, stage, and number of nodal sites.

Treatment of Non-Hodgkin Lymphoma

Treatment depends on subtype, stage, the patient's overall health, and goals of care. There is no single "lymphoma protocol." The big picture is that aggressive subtypes are treated hard and fast with curative intent, while indolent subtypes are managed more like chronic illness.

Watchful Waiting

For asymptomatic patients with low-tumor-burden indolent disease, watchful waiting (active surveillance) is appropriate. Treatment begins only when symptoms develop or disease progresses. This is well established for low-tumor-burden follicular lymphoma based on GELF criteria, and it is also used in some marginal zone lymphomas and CLL/SLL.

Chemoimmunotherapy

R-CHOP remains the backbone first-line regimen for DLBCL and many other aggressive B-cell lymphomas. It combines rituximab (anti-CD20 antibody) with cyclophosphamide, doxorubicin, vincristine, and prednisone. Six cycles cure roughly 60–70% of fit patients with DLBCL.

Pola-R-CHP — polatuzumab vedotin, an antibody-drug conjugate, combined with rituximab, cyclophosphamide, doxorubicin, and prednisone has improved progression-free survival in patients with higher-risk DLBCL (IPI ≥ 2) in the POLARIX trial [4]. It is now a preferred first-line option for many such patients.

DA-EPOCH-R (dose-adjusted etoposide, prednisone, vincristine, cyclophosphamide, doxorubicin, plus rituximab) is used for primary mediastinal B-cell lymphoma and selected high-grade B-cell lymphomas.

Intrathecal chemotherapy (drugs given directly into the cerebrospinal fluid) is added for patients at high risk of central nervous system spread, such as some patients with DLBCL with high CNS-IPI scores or with Burkitt lymphoma.

Targeted Therapy

These drugs aim at specific molecular weak points in lymphoma cells:

• BTK inhibitors (ibrutinib, acalabrutinib, zanubrutinib) for mantle cell lymphoma, marginal zone lymphoma, and Waldenström macroglobulinemia. For patients with mantle cell lymphoma who develop resistance to these initial covalent BTK inhibitors, pirtobrutinib (a non-covalent BTK inhibitor) is now an approved standard option [12]. Furthermore, in May 2026, the FDA granted accelerated approval to the next-generation BCL-2 inhibitor sonrotoclax for patients with relapsed or refractory mantle cell lymphoma who have previously received a BTK inhibitor [13].
• BCL-2 inhibitors (venetoclax) for selected B-cell lymphomas.
• PI3K inhibitors and EZH2 inhibitors for refractory follicular lymphoma.
• Tafasitamab + lenalidomide and loncastuximab tesirine for relapsed DLBCL.

CAR-T Cell Therapy

Chimeric antigen receptor (CAR) T-cell therapy takes a patient's own T-cells, genetically engineers them to recognize CD19 on B-cells, and infuses them back to attack the lymphoma [8]. Approved products for non-Hodgkin lymphoma include axicabtagene ciloleucel, tisagenlecleucel, lisocabtagene maraleucel, and brexucabtagene autoleucel. CAR-T can produce durable remissions in relapsed or refractory large B-cell lymphoma, mantle cell lymphoma, and follicular lymphoma.

The two main toxicities to know are:

• Cytokine release syndrome (CRS) — a systemic inflammatory response with fever, low blood pressure, and hypoxia. Managed with tocilizumab and supportive care.
• Immune effector cell-associated neurotoxicity syndrome (ICANS) — confusion, tremor, or seizures, usually reversible with steroids.

Bispecific Antibodies

This is the newest major class of drug in non-Hodgkin lymphoma. Bispecific antibodies have two binding arms: one grabs CD20 on the lymphoma B-cell, the other grabs CD3 on a T-cell, forcing them together so the T-cell kills the cancer.

• Glofitamab and epcoritamab are approved as single agents for relapsed/refractory DLBCL after at least two prior treatment lines [5, 6].
• Mosunetuzumab is approved for relapsed/refractory follicular lymphoma.
• Odronextamab has European approval for relapsed DLBCL and follicular lymphoma.
• In November 2025, epcoritamab in combination with rituximab and lenalidomide received US FDA approval for relapsed/refractory follicular lymphoma after one prior line — the first bispecific combination therapy in lymphoma.

Like CAR-T, bispecific antibodies can cause CRS and ICANS, but generally at lower severity. Because bispecific antibodies are "off-the-shelf" treatments, they bypass the weeks-long laboratory manufacturing delays associated with CAR-T cell therapy. This rapid availability is shifting clinical practice, making bispecifics an increasingly preferred option in community oncology settings, especially for patients with rapidly progressing disease who cannot afford to wait for CAR-T cell manufacturing.

Radiation Therapy

Radiation is highly effective for localized disease. It is curative for stage I/II low-grade follicular lymphoma, used as consolidation after chemotherapy in bulky DLBCL, and used in palliation for symptom control.

Stem Cell Transplant

Autologous stem cell transplant (using the patient's own stem cells) consolidates remission in relapsed aggressive B-cell lymphomas after salvage chemotherapy. Allogeneic transplant (donor stem cells) is reserved for selected high-risk or relapsed cases. CAR-T therapy has reduced but not eliminated the role of transplant.

Differential Diagnosis

Several conditions can mimic non-Hodgkin lymphoma and must be ruled out.

Hodgkin lymphoma shares the symptoms but contains Reed-Sternberg cells under the microscope. Biopsy distinguishes the two. (Of note, the frontline treatment paradigm for advanced classical Hodgkin lymphoma shifted significantly in March 2026, when the FDA approved the immunotherapy drug nivolumab in combination with AVD chemotherapy for previously untreated patients aged 12 and older, demonstrating superior progression-free survival compared to older standard regimens [14].)

Acute lymphoblastic leukemia (ALL) primarily fills the bone marrow with lymphoblasts, while lymphoma fills lymph nodes. Lymphoblastic lymphoma blurs this line and is treated like ALL.

Infectious mononucleosis from EBV causes swollen, tender lymph nodes and fatigue. The tenderness, sore throat, and atypical lymphocytes on a blood film usually clarify the picture.

Other infections (tuberculosis, cytomegalovirus, HIV seroconversion) and autoimmune disease (lupus, rheumatoid arthritis, Sjögren's syndrome) can all cause persistent lymphadenopathy.

When in doubt, biopsy. Persistent, painless, firm lymph nodes, especially with B symptoms, should not be watched indefinitely.

Major Subtypes 

The list is not exhaustive; the WHO-HAEM5 classification recognizes more than 80 entities [1].

Indolent B-cell Lymphomas

Chronic lymphocytic leukemia / small lymphocytic lymphoma (CLL/SLL) — These are the same disease at different sites. CLL involves blood and bone marrow; SLL primarily involves lymph nodes. Both are slow-growing, common in older adults, and managed with BTK inhibitors, BCL-2 inhibitors, and anti-CD20 antibodies.

Follicular lymphoma — The most common indolent B-cell lymphoma. Defined by t(14;18) and BCL2 overexpression. Treatment ranges from watchful waiting to rituximab-based regimens and, for relapse, CAR-T or bispecific antibodies.

Marginal zone lymphomas (MZL) — Three subtypes: extranodal (MALT, often gastric and H. pylori–driven), splenic, and nodal. Often respond to local therapy, antibiotics (for MALT), or rituximab.

Waldenström macroglobulinemia / lymphoplasmacytic lymphoma — Produces an IgM paraprotein and can cause hyperviscosity. BTK inhibitors are the mainstay.

Aggressive B-cell Lymphomas

Diffuse large B-cell lymphoma (DLBCL) — The most common non-Hodgkin lymphoma overall, accounting for around 30% of cases. Subdivided into GCB and non-GCB by cell of origin. R-CHOP cures most localized cases; Pola-R-CHP is preferred for higher-risk disease [4]. For relapse, options include CAR-T, bispecific antibodies, and antibody-drug conjugates.

Mantle cell lymphoma — Defined by t(11;14) and cyclin D1 overexpression. Usually aggressive despite slow microscopic appearance. Treated with intensive chemoimmunotherapy, BTK inhibitors, and CAR-T for relapse.

Burkitt lymphoma — Highly aggressive. Defined by MYC rearrangement. Associated with EBV (endemic African form) and HIV. Curable with intensive regimens; tumor lysis syndrome is a major early risk.

Primary CNS lymphoma — Aggressive DLBCL arising in the brain or spinal cord. Often EBV-associated in immunocompromised patients. Treated with high-dose methotrexate-based regimens.

Primary mediastinal B-cell lymphoma — Affects young adults, particularly women. Often treated with DA-EPOCH-R.

High-grade B-cell lymphoma with MYC and BCL2 rearrangements ("double-hit" lymphoma) — A distinct aggressive entity that needs intensified therapy [1].

T-cell and NK-cell Lymphoma

These are rarer and generally carry a worse prognosis than B-cell lymphomas.

Peripheral T-cell lymphoma, not otherwise specified (PTCL-NOS) — The most common T-cell NHL.

Angioimmunoblastic T-cell lymphoma (AITL) — Often associated with EBV and immune dysregulation.

Anaplastic large cell lymphoma (ALCL) — Comes in ALK-positive (better prognosis) and ALK-negative forms. Brentuximab vedotin is highly active.

Mycosis fungoides and Sézary syndrome — Cutaneous T-cell lymphomas; mycosis fungoides starts in the skin, Sézary syndrome adds blood involvement.

Adult T-cell leukemia/lymphoma (ATLL) — Caused by HTLV-1 infection.

Extranodal NK/T-cell lymphoma, nasal type — EBV-driven, often affects the nasal cavity and palate.

Enteropathy-associated T-cell lymphoma (EATL) — Linked to celiac disease.

Prognosis and Survival Rate

Outcomes vary widely. Subtype, stage, IPI/FLIPI score, age, performance status, and response to first treatment all matter.

Better outcomes are linked to younger age, normal LDH, limited stage, no B symptoms, good performance status, and disease confined to lymph nodes.

Frequently Asked Questions (FAQs)

What is non-Hodgkin lymphoma in simple terms?

Non-Hodgkin lymphoma is a cancer of lymphocytes, a type of white blood cell that fights infection. The cancerous cells build up in lymph nodes, causing them to swell, and can spread to the bone marrow, spleen, or other organs. It is the most common blood cancer worldwide and includes more than 60 subtypes that behave very differently from one another.

How is non-Hodgkin lymphoma different from Hodgkin lymphoma?

The two diseases look different under the microscope. Hodgkin lymphoma contains a specific abnormal cell called the Reed-Sternberg cell, while non-Hodgkin lymphoma does not. Hodgkin lymphoma tends to spread in a predictable pattern from one lymph node group to the next, while NHL can appear in scattered locations. NHL is far more common and includes a wider range of subtypes.

What are the warning signs of non-Hodgkin lymphoma?

The most common sign is a painless lump caused by a swollen lymph node, usually in the neck, armpit, or groin. Other signs include drenching night sweats, unexplained fever above 38°C, weight loss greater than 10% of body weight over six months, persistent fatigue, and itchy skin. These three constitutional symptoms — fever, night sweats, and weight loss — are called B symptoms.

How is non-Hodgkin lymphoma diagnosed?

A confirmed diagnosis requires a lymph node biopsy. A pathologist examines the tissue under a microscope and uses immunophenotyping (testing surface markers like CD20, CD3, and CD10) to identify the subtype. Blood tests, a PET-CT scan, and sometimes a bone marrow biopsy or cerebrospinal fluid analysis complete the workup and determine the stage.

Can non-Hodgkin lymphoma be cured?

It depends on the subtype. Aggressive lymphomas like diffuse large B-cell lymphoma are often cured with chemoimmunotherapy such as R-CHOP. Indolent lymphomas like follicular lymphoma grow slowly and can be controlled for many years, but they are usually not curable with standard treatment. New therapies including CAR-T cells and bispecific antibodies are now offering durable remissions for patients whose disease has come back.

What is CAR-T cell therapy for non-Hodgkin lymphoma?

CAR-T (chimeric antigen receptor T-cell) therapy uses a patient's own T-cells, genetically reprogrammed in the laboratory to recognize a marker called CD19 on lymphoma cells. The modified T-cells are infused back into the patient, where they multiply and kill the cancer. It is approved for relapsed or refractory large B-cell lymphoma, mantle cell lymphoma, and follicular lymphoma, and can produce long-lasting remissions when other treatments fail.

Glossary of Related Medical Terms

• Lymphocyte — a white blood cell of the immune system; the cell type that becomes cancerous in lymphoma.
• B-cell — a lymphocyte that makes antibodies. Most NHL cases arise from B-cells.
• T-cell — a lymphocyte that directly kills infected cells. T-cell NHL is less common but often more aggressive.
• Lymphadenopathy — enlargement of lymph nodes; the most common sign of NHL.
• Extranodal — outside the lymph nodes (for example, bone marrow, stomach, brain).
• Indolent lymphoma — slow-growing lymphoma, often manageable but rarely curable.
• Aggressive lymphoma — fast-growing lymphoma; often curable with prompt treatment.
• B symptoms — fever, drenching night sweats, and unexplained weight loss greater than 10% in six months.
• Biopsy — removal of a tissue sample so a pathologist can examine it under a microscope.
• Immunophenotyping — laboratory test that identifies cell surface markers to confirm the lymphoma subtype.
• Translocation — a chromosomal rearrangement where pieces of two chromosomes swap places; many translocations drive specific NHL subtypes.
• R-CHOP — a chemoimmunotherapy regimen of Rituximab, Cyclophosphamide, Hydroxydaunorubicin (doxorubicin), Oncovin (vincristine), and Prednisone.
• Rituximab — a monoclonal antibody that targets CD20 on B-cells.
• CAR-T therapy — chimeric antigen receptor T-cell therapy; a patient's T-cells are genetically engineered to attack lymphoma cells.
• Bispecific antibody — an engineered antibody that binds a cancer cell on one arm and a T-cell on the other, bringing them together so the T-cell can kill the cancer.
• Cytokine release syndrome (CRS) — a sometimes severe inflammatory reaction that can follow CAR-T or bispecific antibody therapy.
• Lugano classification — the standard staging system for lymphoma (Stages I–IV).
• Deauville score — a 5-point scale used to interpret PET-CT scans during and after lymphoma treatment.
• IPI — International Prognostic Index, a scoring tool that predicts outcomes in aggressive NHL.
• FLIPI — Follicular Lymphoma International Prognostic Index, the equivalent tool for follicular lymphoma.

Disclaimer: This article is intended for educational and informational purposes only. It is not intended to be a substitute for informed professional medical advice, diagnosis, or treatment. While the information presented here is derived from credible medical sources and is believed to be accurate and up-to-date, it is not guaranteed to be complete or error-free. See additional information.

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14. U.S. Food and Drug Administration. (2026, March 20). FDA approves nivolumab with chemotherapy for previously untreated Hodgkin lymphoma. https://www.fda.gov/drugs/resources-information-approved-drugs/fda-approves-nivolumab-chemotherapy-previously-untreated-hodgkin-lymphoma