Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0079731 (B-cell lymphoma)
 16,671 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lymphoma of gastric-mucosa-associated lymphatic tissue (MALT) type has been linked to infection with Helicobacter pylori. We investigated the effect on MALT lymphoma of eradicating H pylori infection. 33 patients with primary gastric low-grade MALT lymphoma associated with H pylori gastritis were treated with omeprazole (120 mg daily) and amoxycillin (2.25 g daily) for 14 days to eradicate H pylori. In addition to histology, PCR was used to examine proliferation of monoclonal B cells before treatment and during follow-up. All patients had at least two post-treatment examinations, and all became negative for H pylori, 2 after a second treatment course. On histology, 23 (70%) patients showed complete regression and 4 (12%) partial regression of lymphoma. 6 (18%) patients had no change after cure of H pylori infection. 1 was treated with chemotherapy. Of 5 treated surgically, 4 were found to have high-grade B-cell lymphoma on histology of the resected stomach and 1 a high-grade T-cell lymphoma. PCR showed complete disappearance of monoclonal B cells after cure of H pylori infection in 13 of 16 patients investigated. During median follow-up of 1 year no relapse of MALT lymphoma occurred. Low-grade primary gastric MALT lymphoma can completely regress after eradication of H pylori infection. However, longer follow-up is needed to clarify whether the remission is lasting.
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PMID:Regression of primary gastric lymphoma of mucosa-associated lymphoid tissue type after cure of Helicobacter pylori infection. MALT Lymphoma Study Group. 862 73

There is an increasing body of evidence implicating a causal association between Helicobacter pylori and the development of mucosa-associated lymphoid tissue (MALT) associated B-cell gastric lymphoma. Investigators have noted that almost all patients with H pylori-associated chronic gastritis develop lymphoid follicles. Some of these patients demonstrate infiltration of B cells and lymphoepithelial lesions typical of MALT lymphoma. When gastric tissue from patients with gastric B-cell lymphoma is analyzed for H pylori infection, the overwhelming majority of patients demonstrate this condition. Epidemiologic nested case-control studies have shown that patients with gastric non-Hodgkin's lymphoma are substantially more likely that matched controls to have H pylori infection. This situation may be analogous to the linkage between chronic Epstein-Barr virus and lymphoma. The mechanisms inducing the development of lymphoma are not clear, but it has been suggested that chronic infection with H pylori results in the stimulation of H pylori-responsive T cells which in turn activate B cells with the subsequent development of a mutation to a monoclonal B-cell population. Recent evidence indicates that cure of H pylori infection produces regression of MALT lymphoma within 3 to 12 months in approximately 75% of antibiotic-treated patients. Individual responsiveness remains unpredictable, however, and careful and prolonged endoscopic and histologic follow-up is needed. Large, well-controlled studies are necessary, however, to determine the duration of 'cure' and the appropriate setting for treatment.
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PMID:Eradication of Helicobacter pylori and regression of B-cell lymphoma. 920 82

Helicobacter pylori infection of the stomach is one of the commonest chronic infections worldwide and in the Caribbean, over 50% of the population are affected. H pylori is probably transmitted from person to person by oro-faecal and oro-oral means. H pylori is directly associated with peptic ulcer disease, chronic antral gastritis, gastric carcinoma and B-cell lymphoma of the stomach. In patients with peptic ulcers and H pylori infection, eradication of infection with antibiotics significantly decreases recurrence of ulcers. All patients with H pylori related disease should be tested and treated if positive. The treatment of H pylori infection has evolved over the years but at present triple therapy which includes two antibiotics is recommended.
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PMID:Helicobacter pylori infection in the Caribbean: update in management. 1139 98

Long term follow up data are not available for cases of diffuse large B cell gastric lymphoma treated by eradicating Helicobacter pylori alone. We present the case of an 82 year old man with diffuse large B cell lymphoma localised to the stomach which responded to H pylori eradication and which has not recurred after more than five years of close follow up. Our patient was not a candidate for other modalities of treatment. This case demonstrates that the option of treating H pylori infection as the initial trial of treatment for localised diffuse large B cell lymphoma is appropriate for consideration. If medical therapy using eradication of H pylori is used, it is essential that the patient undergoes close observation and repeated surveillance endoscopies.
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PMID:Five years of complete remission of gastric diffuse large B cell lymphoma after eradication of Helicobacter pylori infection. 1291 79

Gastric mucosa associated lymphoid tissue (MALT) lymphoma has recently been incorporated into the World Health Organization (WHO) lymphoma classification, termed as extranodal marginal zone B-cell lymphoma of MALT-type. In about 90% of cases this lymphoma is associated with H pylori infection which has been clearly shown to play a causative role in lymphomagenesis. Although much knowledge has been gained in defining the clinical features, natural history, pathology, and molecular genetics of the disease in the last decade, the optimal treatment approach for gastric MALT lymphomas, especially locally advanced cases, is still evolving. In this review we focus on data for the therapeutic, stage dependent management of gastric MALT lymphoma. Hence, the role of eradication therapy, surgery, chemotherapy and radiotherapy is critically analyzed. Based on these data, we suggest a therapeutic algorithm that might help to better stratify patients for optimal treatment success.
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PMID:Therapy of gastric mucosa associated lymphoid tissue lymphoma. 1765 5

Low-grade mucosa-associated lymphoid tissue (MALT) lymphoma of the stomach, gastric MALT lymphoma, is associated with Helicobacter pylori infection. The eradication of H pylori using antibiotics is successful in 60% to 80% of affected patients. In contrast to the previous paradigm, we and other investigators have shown that a certain proportion of patients with H pylori-positive early-stage diffuse large B-cell lymphoma (DLBCL) of the stomach with histological evidence of MALT lymphoma, including high-grade transformed gastric MALT lymphoma and gastric DLBCL(MALT), achieved long-term complete pathological remission (pCR) after first-line H pylori eradication therapy, indicating that the loss of H pylori dependence and high-grade transformation are separate events in the progression of gastric lymphoma. In addition, patients with H pylori-positive gastric DLBCL without histological evidence of MALT (gastric pure DLBCL) may also respond to H pylori eradication therapy. A long-term follow-up study showed that patients who achieved pCR remained lymphoma free. Gastric MALT lymphoma is indirectly influenced by H pylori infection through T-cell stimulation, and recent studies have shown that H pylori-triggering chemokines and their receptors, H pylori-associated epigenetic changes, H pylori-regulated miRNA expression, and tumor infiltration by CD4+CD25+ regulatory T cells contribute to lymphomagenesis of gastric MALT lymphoma. Recent studies have also demonstrated that the translocation of CagA into B lymphocytes inhibits apoptosis through p53 accumulation, BAD phosphorylation, and the up-regulation of Bcl-2 and Bcl-XL expression. In gastric MALT lymphoma, CagA may stimulate lymphomagenesis directly, through the regulation of signal transduction, and intracellular CagA is associated with H pylori dependence. These findings represent a substantial paradigm shift compared with the classical theory of H pylori-reactive T cells contributing indirectly to the development of MALT lymphoma. In conclusion, a wide range of H pylori-related gastric lymphomas have been identified. The use of antibiotics as the sole first-line therapy for early-stage gastric pure DLBCL requires validation in a prospective study. The clinical and biological significance of the CagA oncoprotein in the lymphomagenesis of gastric MALT lymphoma warrants further study.
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PMID:Helicobacter pylori and mucosa-associated lymphoid tissue: what's new. 2431 71

Gastrointestinal diffuse large B-cell lymphoma (GI DLBCL) is the most common gastrointestinal lymphoma. Enhancer of zeste homolog 2 (EZH2) has been implicated in the pathogenesis of several cancers. However, EZH2 has not been studied in GI DLBCL. Thus, we investigated EZH2 expression and EZH2 Y641 mutation in 100 GI DLBCL specimens by immunohistochemistry and sequencing. In addition, trimethylated H3K27 (H3K27me3), BCL2, c-MYC, and Ki-67 expression and Helicobacter pylori infection were detected, and BCL2 and c-MYC gene translocation was assessed. EZH2 was overexpressed in 50% of cases. EZH2 overexpression was significantly associated with higher stage (P = .014), higher International Prognostic Index score (P = .003), reduced overall survival rate (P = .030), and H3K27me3 (P = .001) and c-MYC expression (P = .008). We detected EZH2 mutations in 1 of 33 (3.0%) DLBCLs with a germinal center immunophenotype. The frequency of EZH2 Y641 mutation in GI DLBCL was significantly lower than that in patients with DLBCL without gastrointestinal features (P = .022). BCL2 and c-MYC translocation was detected in 6.5% and 5.1% of cases, respectively. BCL2 translocation was detected exclusively in the germinal center B-cell-like subtype. Chronic gastroenteritis was present in all cases, and 36.4% of gastric DLBCL cases had H pylori infection. The data indicate that primary GI DLBCL is closely related with chronic inflammation and has a low frequency of molecular abnormality, and EZH2 overexpression is significantly associated with inferior outcome in patients with primary GI DLBCL; evaluating EZH2 expression has therapeutic implications.
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PMID:EZH2 overexpression in primary gastrointestinal diffuse large B-cell lymphoma and its association with the clinicopathological features. 2843 23