MALT lymphoma

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Sujit Routray, M.D. [2], Ahmed Younes M.B.B.CH [3]

MALT lymphoma is a common form of non-Hodgkin lymphoma (NHL) involving the mucosa-associated lymphoid tissue (MALT), frequently of the stomach, but virtually any mucosal site can be affected. It is a cancer originating from the B-cells in the marginal zone of the MALT. The evolution of gastric MALT lymphoma is a multistage process starting with the infection of H. pylori resulting in the recruitment of B- and T-cells and other inflammatory cells to the gastric mucosa. Genes involved in the pathogenesis of MALT lymphoma include FOXP1 and BCL6. A characteristic feature of MALT lymphoma is the presence of neoplastic cells within epithelial structures with associated destruction of the glandular architecture to form lymphoepithelial lesions. Most MALT lymphomas occur among individuals of 60 years of age. Males are more commonly affected with gastric MALT lymphoma than females. MALT lymphoma is usually slow growing (indolent), but some can be high grade. If left untreated, MALT lymphoma may progress to develop fever, anemia, weight loss, and large cell lymphoma. Complications of MALT lymphoma include anemia, cachexia, obstruction, and perforation of small intestine. The prognosis is good, and the 10-year survival rate for gastric MALT lymphoma is approximately 90% with a disease-free survival of approximately 70%. However, in rare instances, MALT lymphoma can progress and transform into aggressive high-grade tumors, such as extranodal diffuse large B cell lymphoma (eDLBCL), whereby the 10-year survival rate drops to approximately 42%. The staging of MALT lymphoma is based on two staging systems: Ann Arbor staging system and the TNM staging system. If the disease is limited to the stomach (which is assessed with computed tomography), then 70-80% of patients will have a complete regression on treatment with antibiotic eradication of H. pylori. The optimal therapy for MALT lymphoma depends on the stage at diagnosis. The treatment options for early stage (localized) gastric MALT lymphoma include antibiotic therapy, radiotherapy, chemotherapy, surgery, and monoclonal antibodies. The treatment options for advanced stage gastric MALT lymphoma include observation, radiotherapy, chemotherapy, and monoclonal antibodies. Secondary prevention strategies following MALT lymphoma include urease breath test, performed 4-6 weeks after completion of the course of antibiotic therapy, and endoscopy with concurrent biopsy, performed 3-6 months after the treatment is finished.

MALT lymphoma was first described by Isaacson and Wright in 1983.

There is no classification system established for MALT lymphoma.

MALT lymphoma is a form of lymphoma involving the mucosa-associated lymphoid tissue (MALT), frequently of the stomach, but virtually any mucosal site can be afflicted. It is a cancer originating from B cells in the marginal zone of the MALT. The evolution of gastric MALT lymphoma is a multistage process starting with the infection of H. pylori resulting in the recruitment of B- and T-cells and other inflammatory cells to the gastric mucosa. Genes involved in the pathogenesis of MALT lymphoma include FOXP1 and BCL6. Chromosomal translocations are also involved in the pathogenesis of MALT lymphoma, which include t(1;14)(p22;q32), t(11;18)(q21;q21), t(14;18)(q32;q21), and t(3;14)(p14.1;q32). Gastric MALT lymphoma is frequently associated with chronic inflammation as a result of the presence of Helicobacter pylori (72-98%). On microscopic histopathological analysis, MALT lymphoma is characterized by the presence of dense diffuse lymphoid infiltrate of marginal‐zone cells in lamina propria with prominent lymphoepithelial lesions and consisting of small atypical cells with monocytoid features. A characteristic feature of MALT lymphoma is the presence of neoplastic cells within epithelial structures with associated destruction of the glandular architecture to form lymphoepithelial lesions. The neoplastic cells of MALT lymphoma may be positive for B-cell associated antigens (CD19, CD20, CD22, CD79a) that co-express BCL-2, and are negative for CD5, CD10, CD43, and cyclin D1.

Common causes of gastric MALT lymphoma include H.pyroli infection, long-term immunosuppressant drug therapy, and HIV infection. Common causes of non gastric MALT lymphoma include autoimmune disorders, such as Hashimoto’s thyroiditis and Sjogren’s syndrome.

MALT lymphoma must be differentiated from gastric carcinoma, gastritis, diffuse large B cell lymphoma, follicular lymphoma, small cell lymphocytic lymphoma, and mantle cell lymphoma.

MALT lymphoma is the third most common type and accounts for approximately 8% of all cases of non-Hodgkin lymphoma. MALT lymphoma is a disease that tends to affect the elderly population. Most MALT lymphomas occur in people in their 60’s. Males are more commonly affected with gastric MALT lymphoma than females. The male to female ratio is approximately 2.43 to 1. There is no racial predilection to MALT lymphoma.

The most potent risk factor in the development of gastric MALT lymphoma is H.pylori infection. Approximately 5–10% of people with gastric MALT lymphoma, however, do not have an H. pylori infection (H. pylori negative). Other risk factors for gastric MALT lymphoma include long-term immunosuppressant drug therapy and HIV infection. Common risk factors in the development of MALT lymphoma, in areas of the body other than the stomach, are autoimmune disorders such as Hashimoto’s thyroiditis, Sjogren’s syndrome, and Celiac disease.

There is insufficient evidence to recommend routine screening for MALT lymphoma.

MALT lymphoma is usually slow growing (indolent), but some can be high grade. If left untreated, MALT lymphoma may progress to develop fever, anemia, weight loss, and large cell lymphoma. Complications of MALT lymphoma include anemia, cachexia, obstruction, and perforation of small intestine. The prognosis is good, and the 10-year survival rate for gastric MALT lymphoma is approximately 90% with a disease-free survival of approximately 70%. However, in rare instances, MALT lymphoma can progress and transform into aggressive high-grade tumors, such as extranodal diffuse large B cell lymphoma (eDLBCL), whereby the 10-year survival rate drops to approximately 42%.

The staging of MALT lymphoma is based on two staging systems: Ann Arbor staging system and the TNM staging system.

When evaluating a patient for MALT lymphoma, detailed history of the presenting symptom (onset, duration, and progression), other associated symptoms, and a thorough family and past medical history should be reviewed. Other specific areas of focus when obtaining the history include the review of common associated conditions such as H. pylori associated gastritis and autoimmune disorders, such as Hashimoto’s thyroiditis, Sjogren’s syndrome, and Celiac disease. Symptoms of MALT lymphoma depend on the location of the tumor: gastric and non gastric. Symptoms of MALT lymphoma include epigastric pain, fatigue, heartburn, fever, cough with blood in sputum, shortness of breath, and/or lump in the superior lateral quadrant of the orbit, breast, neck, or salivary gland.

Physical examination findings of MALT lymphoma depend on the location of the tumor: Gastric and non gastric. The majority of patients with MALT lymphoma often have no physical findings and lymphadenopathy is uncommon.

Complete blood count is performed to check the blood counts. Liver function tests and renal function tests are performed to assess the liver and kidneys, respectively.

The gastric lesion of MALT lymphoma on upper GI endoscopy may look inflamed or ulcerated. Occasionally, a nodular mass, similar to a reactive lymph node, may be visualized.

Chest, abdominal, and/or pelvic CT scan is generally performed to evaluate the extent and spread of MALT lymphoma. If the disease is limited to the stomach (which is assessed with computed tomography), then 70-80% of patients will have a complete regression on treatment with antibiotic eradication of H. pylori.

Chest, abdominal, and/or pelvic CT scan is generally performed to evaluate the extent and spread of MALT lymphoma.

Endoscopic ultrasound may be performed to detect the extent of spread of MALT lymphoma through the stomach wall. The endoscopic ultrasound scan may demonstrate the deeper tissues that lie to the stomach lining and also involvement of any adjacent lymph nodes.

Organ specific endoscopic tissue biopsy is diagnostic of MALT lymphoma. To view findings on biopsy characteristic of MALT lymphoma, click here.

Other imaging studies for MALT lymphoma include barium studies and PET scan. Barium contrast studies of the esophagus, stomach, small intestine, or the colon may be performed to demonstrate any filling defect in the barium flow which denotes to the presence of any infiltrative mass due to MALT lymphoma. FDG-PET scan may be helpful in diagnosis, staging, and follow-up of MALT lymphoma.

There are no other diagnostic studies associated with MALT lymphoma.

The optimal therapy for MALT lymphoma depends on the stage at diagnosis. The treatment options for early stage (localized) gastric MALT lymphoma include antibiotic therapy, radiotherapy, chemotherapy, surgery, and monoclonal antibodies. The treatment options for advanced stage gastric MALT lymphoma include observation, radiotherapy, chemotherapy, and monoclonal antibodies.

Surgery is not the first-line treatment option for patients with gastric MALT lymphoma. Partial or total gastrectomy is usually reserved for patients with early stage gastric MALT lymphoma, if the lymphoma remains after antibiotic therapy or if the gastric lymphoma progresses.

There are no primary preventive measures available for MALT lymphoma.

Secondary prevention strategies following MALT lymphoma include urease breath test, performed 4-6 weeks after completion of the course of antibiotic therapy, and endoscopy with concurrent biopsy, performed 3-6 months after the treatment is finished.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Sujit Routray, M.D. [2], Ahmed Younes M.B.B.CH [3]

MALT lymphoma was first described by Isaacson and Wright in 1983.^[1]

• MALT lymphoma was first described by Isaacson and Wright in 1983.^[1]
• Isaacson and Wright discovered that primary low-grade gastric B cell lymphomas that had more histological features in common with those of mucosa associated lymphoid tissue than with peripheral lymph nodes.
• Extranodal low-grade lymphomas arising at other mucosal organs, including the salivary gland, lung, and thyroid, showed similar histological and clinical features establishing the term “MALT lymphoma”.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Sujit Routray, M.D. [2], Ahmed Younes M.B.B.CH [3]

There is no classification system established for MALT lymphoma.

There is no classification system established for MALT lymphoma.

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For more information about H.pylori infection click here.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sujit Routray, M.D. [2], Ahmed Younes M.B.B.CH [3], Ahmed Elsaiey, MBBCH [4]

MALT lymphoma is a form of lymphoma involving the mucosa-associated lymphoid tissue (MALT), frequently of the stomach, but virtually any mucosal site can be afflicted. It is a cancer originating from B cells in the marginal zone of the MALT. The evolution of gastric MALT lymphoma is a multistage process starting with the infection of H. pylori resulting in the recruitment of B- and T-cells and other inflammatory cells to the gastric mucosa. Genes involved in the pathogenesis of MALT lymphoma include FOXP1 and BCL6. Chromosomal translocations are also involved in the pathogenesis of MALT lymphoma, which include t(1;14)(p22;q32), t(11;18)(q21;q21), t(14;18)(q32;q21), and t(3;14)(p14.1;q32). Gastric MALT lymphoma is frequently associated with chronic inflammation as a result of the presence of Helicobacter pylori (72-98%). Chronic immune stimulation is also suspected in the pathogenesis of non-gastric MALT lymphoma, and hence often have a history of autoimmune disorders, such as Hashimoto’s thyroiditis, Sjögren’s syndrome, Celiac disease, and relapsing polychondritis. On microscopic histopathological analysis, MALT lymphoma is characterized by the presence of dense diffuse lymphoid infiltrate of marginal‐zone cells in the lamina propria with prominent lymphoepithelial lesions consisting of small atypical cells with monocytoid features. A characteristic feature of MALT lymphoma is the presence of neoplastic cells within epithelial structures with associated destruction of the glandular architecture to form lymphoepithelial lesions. The neoplastic cells of MALT lymphoma may be positive for B-cell associated antigens (CD19, CD20, CD22, CD79a) that co-express BCL-2, and are negative for CD5, CD10, CD43, and cyclin D1.

• Mucosa Associated Lymphoid Tissue lymphoma (MALT lymphoma) resembles an extranodal subtype of Non-Hodgkin lymphoma. MALT lymphoma can occur in many sites extranodal but the most common site is the stomach.^{[1][2][3][4][5][6]}

• MALT lymphoma can take place in other tissues as lung, thyroid, small intestine, and ocular adnexa.

• The beginning of MALT lymphoma can be from H. pylori infection which results in recruiting a large amount of lymphocytes to the site of infection in the stomach.
• T-cell lymphocytes recruited to the site of infection they stimulate B-cells and with underlying genetic abnormalities, B-cells undergo malignant transformation.
• Lymphocytes activation take place as the following:^[5]
  • Epithelial cells are activated with the chronic infection. They express class HLA-DR and CD80 costimulatory molecules. They present the antigens to T-cells.
  • CD80 can react with CD28 on CD4 T-cells activating T-cells.
  • CD40 ligand expressed on activated T-cells interact with CD40 on B-cells. Along side the cytokines and chemokines released from T-cells, this interaction leads to B-cell activation.
  • Activating B and T cells will result in lymphoepithelial proliferation.

• MALT lymphoma is strongly associated with chromosomal translocations as well as genetic mutations.
• Chromosomal translocations:
  • MALT lymphoma can arise as a result of many chromosomal translocation. The primary translocations associated with MALToma are the following:^[7][8]
    • t(1;14) (p22;q32)
    • t(11;18) (q21;q21)
    • t(14;18) (q32;q21)
    • t(3;14) (p14.1;q32)
  • Translocation t(1;14):^[9]
    • It is associated more with MALToma of stomach, lung, and skin. Translocation between BCL10 gene on chromosome 1 and immunoglobulin heavy chain on chromosome 14.
    • BCL10 gene is responsible for preventing apoptosis. This translocation leads to unhindered BCL10 expression and no apoptosis takes place ending up with uncontrolled proliferation of B cells.
    • Patients with t(1;14) are refractory to Helicobacter pylori (H. pylori) eradication therapy.
  • Translocation t(11;18):^[10][11]
    • This translocation was mainly reported in MALToma of lung and stomach. It is considered the most common translocation occurs in MALT lymphoma as overall.
    • It has been found associated with lymphoma at other sites as intestine, orbit and salivary glands.
    • This translocation shows fusion of BIRC2 gene on chromosome 11 and MALT1 gene on chromosome 18.
    • BIRC2 is antiapoptotic factor and overexpression can lead to unlimited cell proliferation.
    • Moreover, deletions of both genes have been reported. Deletions lead to DNA breaks which are repaired through a mechanism called non-homologous end joining (NHEJ) repair. The NHEJ repair mechanism has a high rate of error that may result in the genetic mutation responsible for the lymphoma.
  • Translocation t(14;18):
    • The translocation occurs between the heavy chain gene of immunoglobulin on chromosome 14 and MALT1 gene on chromosome 18.
    • This occurs mainly in MALT lymphomas outside the gastrointestinal tract.
  • Translocation t(3:14):
    • This translocation has shown a closer position of FOXP1 to the heavy chain gene of immunoglobulins.
    • FOXP1 is a transcription factor which plays a role in suppression of the apoptosis especially the genes suppressing the caspases.
• General role of the translocation in pathogenesis of MALT lymphoma:^[5][12]
  • The previous translocations are responsible for activating Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-kB) pathway as well as the uncontrolled expression of BCL10 and MALT1 which are antiapoptic mechanisms.
  • The BCL10 and MALT1 can bind together forming BCL2-MALT1 complex which has an important role in activating NF-kB via activation IkB kinase.
  • When the NF-kB be activate, it translocates into the nucleus to stimulate genes transcriptions especially those which encode growth factors important for cell growth and proliferation.
• TNFAIP3 gene deletion is another gene mutation associated with adnexal MALToma. It is believed that TNFAIP3 also has an important role in NF-kB pathway activation. TNFAIP3 is normaly a tumor suppressor gene.

• Other somatic mutations:
  • Missense mutations of PIM1 and cMyc are reported with some of the MALT lymphomas.^[13]
  • Framshift mutations of p53 has also been linked with pathogenesis of MALT lymphomas both gastric and extra-gastric.^[14]
  • Card11, CD79B, and Myd88 somatic mutations are also important in NF-kB activation. However, they may be associated with other subtypes of Non-Hodgkin lymphomas as splenic marginal zone lymphoma and noda marginal zone lymphoma.^[15]

• Gastric MALT lymphoma is frequently associated with chronic inflammation as a result of the presence of Helicobacter pylori (72-98%).^[1]
• Chronic immune stimulation is also suspected in the pathogenesis of non-gastric MALT lymphoma, and hence often have a history of autoimmune disorders, such as:^[6]

• Hashimoto’s thyroiditis
• Sjögren’s syndrome
• Celiac disease
• Relapsing polychondritis

• MALT lymphoma may be associated with infectious agents, which include:^[3]
  • Ocular adnexal MALT lymphoma and Chlamydia psittaci
  • Salivary gland MALT lymphoma and hepatitis C virus
  • Small intestinal MALT lymphoma and Campylobacter jejuni
  • Cutaneous MALT lymphoma and Borrelia afzelii infection
• MALT lymphoma can be associated with the following genetic conidtions:^[16]
  • Trisomies 3, 12, and 18: it is believed that increased the gene copies is related to lymphoma pathogenesis.

MALT lymphoma starts in the tissues or organs outside of the lymph nodes (extranodal). MALT lymphoma develops in mucosa-associated lymphoid tissue, in the mucosa, or tissue that lines body organs or body cavities including:^[6]

• Gastrointestinal tract (30-40%)
  • The stomach is the most common location for MALT lymphoma, but they can also occur in the small bowel and colon.
• Lungs
• Eyes, including the orbit
• Skin
• Salivary glands
• Thyroid gland
• Breasts

• On microscopic histopathological analysis, MALT lymphoma is characterized by the presence of dense diffuse lymphoid infiltrate of marginal‐zone cells in lamina propria with prominent lymphoepithelial lesions and consisting of small atypical cells with monocytoid features.^[17][3]
• A characteristic feature of MALT lymphoma is the presence of neoplastic cells within epithelial structures with associated destruction of the glandular architecture to form lymphoepithelial lesions.^[18]
• The morphology of the neoplastic cells is variable with small mature lymphocytes, cells resembling centrocytes (centrocyte-like cells), or marginal zone/monocytoid B cells.
• Plasmacytoid or plasmacytic differentiation is frequent.
• Lymphoid follicles are ubiquitous to MALT lymphoma but may be indistinct as they are often overrun or colonized by the neoplastic cells. Large transformed B cells are present scattered among the small cell population. If these large cells are present in clusters or sheets, a diagnosis of associated large B-cell lymphoma should be considered.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Sujit Routray, M.D. [2], Ahmed Younes M.B.B.CH [3]

Common causes of gastric MALT lymphoma include H.pyroli infection, long-term immunosuppressant drug therapy, and HIV infection. Common causes of nongastric MALT lymphoma include autoimmune disorders, such as Hashimoto’s thyroiditis and Sjogren’s syndrome.

• Most common causes of gastric MALT lymphoma include H.pyroli infection. Other causes of gastric MALT lymphoma include:^[1]

• Long-term immunosuppressant drug therapy
• HIV infection
• autoimmune disorders
  • Hashimoto’s thyroiditis
  • Sjogren’s syndrome
  • Celiac disease

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sowminya Arikapudi, M.B,B.S. [2], Sujit Routray, M.D. [3], Ahmed Younes M.B.B.CH [4]

MALT lymphoma must be differentiated from gastric carcinoma, gastritis, diffuse large B cell lymphoma, follicular lymphoma, small cell lymphocytic lymphoma, and mantle cell lymphoma.^[1][2][3]

• Gastric MALT lymphoma must be differentiated from:^[1]

• Gastric carcinoma
• Gastrointestinal stromal tumor (GIST)
• Gastritis
• Peptic ulcer disease
• Menetrier’s disease

• In general, MALT lymphoma must be differentiated from:^[4][3]

• B-cell lymphoma
• Non Hodgkins lymphoma
• Diffuse large B-cell lymphoma
• Follicular lymphoma
• Reactive follicular hyperplasia
• Small cell lymphocytic lymphoma
• Mantle cell lymphoma

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Sujit Routray, M.D. [2], Ahmed Younes M.B.B.CH [3]

MALT lymphoma is the third most common type and accounts for approximately 8% of all cases of non-Hodgkin lymphoma. MALT lymphoma is a disease that tends to affect the elderly population. Most MALT lymphomas occur among individuals aged 60 years. Males are more commonly affected with gastric MALT lymphoma than females. The male to female ratio is approximately 2.43 to 1. There is no racial predilection to MALT lymphoma.

• MALT lymphoma is the third most prevalent type of lymphoma and accounts for approximately 8% of all cases of non-Hodgkin lymphoma.^[1]

• MALT lymphoma is a disease that tends to affect the elderly population.
• Most MALT lymphomas occur among individuals aged 60 years.

• Males are more commonly affected with gastric MALT lymphoma than females.
• The male to female ratio is approximately 2.43 to 1.^[2]

• There is no racial predilection to MALT lymphoma.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Sujit Routray, M.D. [2], Ahmed Younes M.B.B.CH [3]

The most potent risk factor in the development of gastric MALT lymphoma is H.pyroli infection. About 5–10% of people with gastric MALT lymphoma do not have an H. pylori infection (H. pylori negative). Other risk factors for gastric MALT lymphoma include long-term immunosuppressant drug therapy and HIV infection. Common risk factors in the development of MALT lymphoma, in areas of the body other than the stomach, are autoimmune disorders such as Hashimoto’s thyroiditis, Sjogren’s syndrome, and Celiac disease.

• The most potent risk factor in the development of gastric MALT lymphoma is H.pyroli infection.
• About 5–10% of people with gastric MALT lymphoma do not have an H. pylori infection (H. pylori negative). Other risk factors for gastric MALT lymphoma include:
  • Long-term immunosuppressant drug therapy
  • HIV infection

• Common risk factors in the development of MALT lymphoma, in areas of the body other than the stomach, are autoimmune disorders such as:
  • Hashimoto’s thyroiditis
  • Sjogren’s syndrome
  • Celiac disease

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Sujit Routray, M.D. [2], Ahmed Younes M.B.B.CH [3]

There is insufficient evidence to recommend routine screening for MALT lymphoma.

There is insufficient evidence to recommend routine screening for MALT lymphoma.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Sujit Routray, M.D. [2], Ahmed Younes M.B.B.CH [3]

MALT lymphoma is usually slow growing (indolent), but some can be high grade. If left untreated, MALT lymphoma may progress to develop fever, anemia, weight loss, and large cell lymphoma. Complications of MALT lymphoma include anemia, cachexia, obstruction, and perforation of small intestine. The prognosis is good, and the 10-year survival rate for gastric MALT lymphoma is approximately 90% with a disease-free survival of approximately 70%. However, in rare instances, MALT lymphoma can progress and transform into aggressive high-grade tumors, such as extranodal diffuse large B cell lymphoma (eDLBCL), whereby the 10-year survival rate drops to approximately 42%.

• Many people are diagnosed with localized or early stage disease that has not spread elsewhere in the body. MALT lymphoma is usually slow growing (indolent), but some can be high grade. They often remain in the area in which they started for a long period of time.
• If left untreated, MALT lymphoma may progress to develop fever, anemia, weight loss, and large cell lymphoma.

Complications of MALT lymphoma include:

• Anemia
• Cachexia
• Obstruction of small intestine
• Perforation of small intestine

• The prognosis is good, and the 10-year survival rate for gastric MALT lymphoma is approximately 90% with a disease-free survival of approximately 70%.^[1]
• However, in rare instances, MALT lymphoma can progress and transform into aggressive high-grade tumors, such as extranodal diffuse large B cell lymphoma (eDLBCL), whereby the 10-year survival rate drops to approximately 42%.
• A t(11;18)(q21;q21) chromosomal translocation, giving rise to a AP12-MLT fusion gene, is predictive of poor response to eradication therapy.^[2]

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