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A slow-growing MALT lymphoma that grows in the lining of the stomach, usually caused by a long-standing infection with the bacterium Helicobacter pylori. It is the one lymphoma that is often cured by a fortnight of antibiotics, and a single chromosome change predicts the minority in whom antibiotics will not work.
What it is. The stomach has no lymphoid tissue of its own. Chronic infection with Helicobacter pylori creates some, as part of the immune response to the bacterium, and over years a clone of B cells in that tissue can become a lymphoma. The lymphoma depends on the signals the infection provides, which is the reason for the treatment that follows.
How it differs from its parent. Extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue arises at many sites and the sites differ genetically: WHO-HAEM5 sets out that ocular adnexal disease commonly carries mutation or deletion of TNFAIP3, salivary gland disease carries recurrent GPR34 mutation, and thyroid disease carries deleterious mutations of CD274, TNFRSF14 or TET2. What the stomach has, and only the stomach and the lung among the common sites, is the translocation t(11;18)(q21;q21), which fuses BIRC3 to MALT1. WHO-HAEM5 states its clinical application in one sentence: that fusion identifies the cases of gastric extranodal marginal zone lymphoma that will not respond to eradication of Helicobacter pylori.
How it presents and how it is found. Indigestion, pain, nausea, anaemia from slow bleeding, or nothing at all, found when an endoscopy is done for something else. The appearance at endoscopy is often unimpressive: thickened folds, redness, erosions, rather than an obvious tumour. Multiple biopsies are taken from the abnormal area and from each part of the normal-looking stomach, because the lymphoma is patchy. The depth of the lymphoma in the stomach wall is measured by endoscopic ultrasound, and the depth is part of the decision about antibiotics.
The treatment, and the numbers behind it. Eradicating Helicobacter pylori is the first treatment, and in early disease it is often the only one. In a prospective multicentre trial that followed 120 patients with stage I disease for a median of 75 months, 80 per cent (96 of 120) achieved a complete histological remission, 80 per cent of those remained in continuous remission, 3 per cent relapsed and were referred for other treatment, and five-year survival was 90 per cent. Seventeen per cent of those in remission showed residual lymphoma histologically at some point during follow-up; they were watched rather than treated and all entered a second remission, which is the evidence for not reacting to a single abnormal biopsy. Fifteen per cent of the lymphomas carried t(11;18), and both that translocation and a persisting monoclonal band were associated with a higher risk of not responding or of relapsing, although both were also found in patients who stayed in remission.
What follows if antibiotics do not work. Radiotherapy to the stomach at a low dose, or an anti-CD20 antibody, or both, depending on the stage and on whether the translocation is present. Surgery has essentially no role, which is the main thing that separates this disease from gastric adenocarcinoma. Follow-up is by repeated endoscopy and biopsy, and a small number of people develop a gastric carcinoma later, so the endoscopies serve two purposes. The regimens sit in the treatment layer of this family and on the MALT lymphoma page.
The stomach is the commonest of those sites. The corpus does not quote a gastric-only incidence figure because it could not verify one.
Averages across everyone diagnosed, often years ago. A median is the middle of a group: half the people counted lived longer than the figure shown, and some lived far longer. Your stage, subtype, age, fitness and the treatment you receive matter more than the average, and the numbers are improving quickly.
Leukaemias, myeloma and MDS live in the marrow and blood; lymphomas grow in lymph nodes and spleen. The node stations are the disease map, not a route of spread, and staging counts them.
In lymphoma the node stations are the disease itself; staging (Ann Arbor / Lugano) counts how many regions and sides of the diaphragm are involved.
Same organ: High-grade B-cell lymphoma with MYC and BCL2 rearrangements (double-hit lymphoma), Mediastinal grey zone lymphoma, Primary effusion lymphoma, Plasmablastic lymphoma, T-cell/histiocyte-rich large B-cell lymphoma, EBV-positive diffuse large B-cell lymphoma, Primary large B-cell lymphoma of the testis, Ocular adnexal MALT lymphoma, Extranodal NK/T-cell lymphoma, Adult T-cell leukaemia/lymphoma, ALK-positive anaplastic large cell lymphoma, ALK-negative anaplastic large cell lymphoma, Breast implant-associated anaplastic large cell lymphoma, Primary cutaneous anaplastic large cell lymphoma, Lymphomatoid papulosis, Mycosis fungoides, Enteropathy-associated T-cell lymphoma, Monomorphic epitheliotropic intestinal T-cell lymphoma, Extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma), Splenic marginal zone lymphoma, Nodal marginal zone lymphoma, Primary cutaneous marginal zone lymphoma, Primary cutaneous follicle centre lymphoma, Sezary syndrome, Nodal T-follicular helper cell lymphoma, angioimmunoblastic type (angioimmunoblastic T-cell lymphoma), Hepatosplenic T-cell lymphoma, Intravascular large B-cell lymphoma, Lymphomatoid granulomatosis, T-cell prolymphocytic leukaemia, Splenic B-cell lymphoma/leukaemia with prominent nucleoli (formerly B-cell prolymphocytic leukaemia and hairy cell leukaemia variant), T-cell large granular lymphocytic leukaemia, Mixed-phenotype acute leukaemia, Myeloid leukaemia of Down syndrome, Burkitt leukaemia, Marginal zone lymphoma, Cutaneous T-cell lymphoma (mycosis fungoides and Sezary syndrome), Primary mediastinal (thymic) large B-cell lymphoma, Leukaemia (all types), Acute myeloid leukaemia, Acute lymphoblastic leukaemia, Chronic lymphocytic leukaemia, Chronic myeloid leukaemia (CML), Diffuse large B-cell lymphoma, Follicular lymphoma, Hodgkin lymphoma, Mantle cell lymphoma, Multiple myeloma, Non-Hodgkin lymphoma (all types), Myelodysplastic syndromes / neoplasms (MDS), Myeloproliferative neoplasms (PV, ET, myelofibrosis), Polycythaemia vera (PV), Essential thrombocythaemia (ET), Waldenström macroglobulinaemia, Hairy cell leukaemia, Peripheral T-cell lymphomas (including cutaneous T-cell lymphoma), Blastic plasmacytoid dendritic cell neoplasm (BPDCN), Burkitt lymphoma, HIV-associated (AIDS-related) lymphomas, Chronic myelomonocytic leukaemia and MDS/MPN overlap neoplasms, Systemic mastocytosis, Erdheim-Chester disease, Rosai-Dorfman disease and other histiocytic neoplasms, Langerhans cell histiocytosis (LCH), Post-transplant lymphoproliferative disorder (PTLD), FLT3-mutated acute myeloid leukaemia, IDH1- and IDH2-mutated acute myeloid leukaemia, NPM1-mutated and KMT2A-rearranged acute myeloid leukaemia, Secondary and therapy-related acute myeloid leukaemia, Acute promyelocytic leukaemia, Acute myeloid leukaemia in older or unfit patients, Smouldering multiple myeloma, Newly diagnosed multiple myeloma, transplant-eligible, Newly diagnosed multiple myeloma, transplant-ineligible, Relapsed or refractory multiple myeloma, Plasma cell leukaemia, Lower-risk myelodysplastic syndromes, Higher-risk myelodysplastic syndromes, Chronic lymphocytic leukaemia, first treatment, Relapsed or refractory chronic lymphocytic leukaemia, Richter transformation of chronic lymphocytic leukaemia, Chronic myeloid leukaemia, chronic phase, Chronic myeloid leukaemia, accelerated and blast phase, Primary myelofibrosis, Standard-risk B-cell acute lymphoblastic leukaemia in children, High-risk acute lymphoblastic leukaemia in children (high-risk B-ALL and T-ALL), Philadelphia chromosome-positive acute lymphoblastic leukaemia in children (Ph-positive ALL), Philadelphia chromosome-like acute lymphoblastic leukaemia (Ph-like or BCR::ABL1-like ALL), Infant acute lymphoblastic leukaemia (KMT2A-rearranged, under one year), Relapsed and refractory acute lymphoblastic leukaemia in children, Acute myeloid leukaemia in children, Erdheim-Chester disease, Rosai-Dorfman-Destombes disease, Single-system Langerhans cell histiocytosis (bone, skin or one other organ), Multisystem Langerhans cell histiocytosis (with or without risk-organ involvement), Indolent and smouldering systemic mastocytosis, Advanced systemic mastocytosis (aggressive SM, SM with an associated haematological neoplasm, mast cell leukaemia), Early-stage classical Hodgkin lymphoma (stage I to II), Advanced-stage classical Hodgkin lymphoma (stage III to IV), Nodular lymphocyte-predominant Hodgkin lymphoma (nodular lymphocyte-predominant B-cell lymphoma), Relapsed and refractory classical Hodgkin lymphoma
Endoscopy with multiple biopsies from the abnormal area and from every region of the stomach, because the lymphoma is patchy and a single biopsy can miss it. Helicobacter pylori is sought by more than one method. Endoscopic ultrasound measures how deep the lymphoma goes, which predicts whether antibiotics alone will work; in a prospective comparison against the resected stomach it judged the depth correctly in 91.5 per cent of cases. Fluorescence in situ hybridisation for t(11;18) is done where it will change the plan. Staging uses the gastrointestinal system that counts depth and node involvement rather than the ordinary node-region count.
A standard eradication regimen of a proton pump inhibitor with two antibiotics, chosen by local resistance patterns, is the first treatment for Helicobacter pylori-positive disease and is also offered in negative disease, where a minority still respond. Success is confirmed by a breath or stool test after treatment, and the lymphoma is then followed by repeated endoscopy and biopsy over months, because regression is slow. In the prospective series of 120 patients with stage I disease, 80 per cent achieved complete histological remission and 80 per cent of those remained in continuous remission at a median follow-up of 75 months.
Residual lymphoma on a biopsy after successful eradication is common and usually does not need treatment. In the same series, 17 per cent of those who had reached complete remission later showed histological residual disease; they were watched rather than treated, and all of them entered a second remission. A persisting monoclonal band in the immunoglobulin genes is also common and is not by itself a reason to treat. What does need action is growth, new symptoms, or large cells appearing on the biopsy.
Radiotherapy to the stomach at a low dose is the usual next step for disease that stays localised, and anti-CD20 antibody treatment, alone or with chemotherapy, for disease that has spread or that carries t(11;18) and is therefore unlikely to respond to eradication. Surgery has essentially no role at any stage, which is the main difference from gastric cancer. The regimens, the doses and the evidence are on the MALT lymphoma page and in the treatment layer of this family.
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The site-specific and stage-specific approach on the marginal zone lymphoma page follows this guideline.
Antibiotic eradication is the first-line treatment for Helicobacter pylori-positive gastric MALT lymphoma, curing most patients without chemotherapy or radiotherapy.
Query for this cancer: (TITLE:"Gastric MALT lymphoma" OR ABSTRACT:"Gastric MALT lymphoma" OR TITLE:"Gastric mucosa-associated lymphoid tissue lymphoma" OR ABSTRACT:"Gastric mucosa-associated lymphoid tissue lymphoma" OR TITLE:"Gastric marginal zone lymphoma" OR ABSTRACT:"Gastric marginal zone lymphoma" OR TITLE:"Gastric MALToma" OR ABSTRACT:"Gastric MALToma" OR TITLE:"Extranodal marginal zone lymphoma of the stomach" OR ABSTRACT:"Extranodal marginal zone lymphoma of the stomach" OR TITLE:"Helicobacter pylori-associated gastric lymphoma" OR ABSTRACT:"Helicobacter pylori-associated gastric lymphoma") AND (treatment OR therapy OR trial OR survival OR diagnosis). Results are unfiltered search hits about Gastric MALT lymphoma, not a curated reading list.
Wotherspoon and colleagues showed in the Lancet that eradicating Helicobacter pylori made gastric MALT lymphoma regress, the first time an antibiotic had been shown to treat a cancer.
In 120 patients with stage I disease followed for a median of 75 months, 80 per cent reached complete histological remission, 80 per cent of those stayed in it, five-year survival was 90 per cent, and 15 per cent of lymphomas carried t(11;18), which predicted failure to respond.
WHO-HAEM5 sets out that BIRC3::MALT1 from t(11;18) is recurrent in gastric and pulmonary disease and rare at other sites, and that it identifies the gastric cases that will not respond to eradication.
The targets of this cancer's medicines and the ones linked to it directly.
Cases by country, the UK and NHS pathway and other country lenses, the expert centres with trials on record, and the centres named on this cancer's subtypes.
One section per setting: the options named, what each is for, the trials behind them, the recorded trade-offs and the questions to ask.
Bleeding that does not stop by itself, bleeding from more than one site, or new bruising in several places or one large area.
Anyone who has ever had hepatitis B can have the virus wake up when rituximab strips out their B cells, sometimes months later and sometimes fatally. A blood test before the first dose, and a tablet for those who need it, prevents almost all of it.
A shortage of antibodies because treatment has wiped out the B cells or plasma cells that make them, as CD19 CAR-T, CD20 antibodies and BCMA therapies deliberately do. It leaves patients prone to infections, sometimes for years, and is managed with immunoglobulin infusions.
Treatments that remove B cells also remove the antibodies B cells make, and some people never make them again. When repeated chest and sinus infections follow, donated antibody given monthly by drip or weekly under the skin prevents them.
Several lymphoma treatments knock out the part of the immune system that keeps a particular lung infection, Pneumocystis, at bay. A low-dose antibiotic three times a week prevents it, and a separate tablet prevents shingles.
Reactions around the moment a drug is given: chills, fever or breathlessness from antibodies (infusion reactions), true allergy (hypersensitivity, rarely anaphylaxis), and leakage of a damaging drug into tissue around the vein (extravasation).
See all on the product pages:BendamustineRituximab·Printable cards in the navigator
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