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)

Extranodal marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue (MALT) is rarely found in the large intestine. Because of its rarity, the underlying epigenetic and genetic changes in the pathogenesis and prognostic factors have yet to be well established. For this purpose, methylation profiles and API2/MALT1 fusion in marginal zone B-cell lymphoma of MALT in the colorectum were studied and compared with treatment outcomes. For methylation analyses, 7 independent CpG islands (p15, p16, DAP kinase, hMLH1, MINT1, MINT2, and MINT31) were examined and RT-PCR for detection of API2/MALT1 fusion transcripts were performed in 15 colorectal marginal zone B-cell lymphoma of MALT in a single institution. Marginal zone B-cell lymphomas of MALT from both gastric and colorectal locations were also examined. In methylation analyses (n=13), 8 of 13 (62%) cases were classified as CIMP (CpG island methylator phenotype)-positive. Methylation was more frequently observed in cases with advanced disease stages than with earlier stages; an average of two methylated loci for earlier stages (IE or IIE) versus four loci in advanced ones (IVE; P=0.02). The estimated 5-year progression-free survival was 42% for CIMP-positive and 100% for CIMP-negative cases (P=0.03). API2/MALT1 fusion transcripts were found in two of nine cases (22%). In two cases with concurrent gastric and colorectal involvement of marginal zone B-cell lymphoma of MALT, methylation patterns and API2/MALT1 fusion results were different by location. Our results suggest that methylation profiles define a clinically more aggressive subgroup and multiclonal origin for marginal zone B-cell lymphoma of MALT with multiorgan involvement.
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PMID:Methylation and API2/MALT1 fusion in colorectal extranodal marginal zone lymphoma. 1906 Aug 47

Aberrant DNA hypermethylation is an important mechanism for the inactivation of tumor-related genes in human tumors. Gastric mucosa-associated lymphoid tissue (MALT) lymphomas arise from Helicobacter pylori-associated chronic gastritis; most patients are H. pylori-positive and eradication therapy is highly effective. In the present study, we used methylation-specific PCR to analyze the DNA methylation status of 11 tumor-related genes (Kip2, p16, hMLH-1, p15, p73, MGMT, DAPK, MINT1, MINT2, MINT31 and HCAD) in 21 specimens of MALT lymphoma, 5 specimens of MALT lymphoma with large cell component (high-grade MALT lymphoma), 15 specimens of diffuse large B-cell lymphoma (DLBCL), 8 specimens of complete remission of MALT lymphoma after eradication therapy, 5 specimens with no evidence of malignancy and PBMCs from 10 healthy donors. The average number of methylated genes was significantly greater in gastric lymphomas as compared to normal controls (P<0.001). The CpG island methylator phenotype (CIMP) was observed in 93.3% (14/15) of DLBCLs, 100% (5/5) of high-grade MALT lymphomas and 61.9% (13/21) of MALT lymphomas; in contrast, CIMP was not found in the control group (0%). The average number of methylated genes and the CIMP incidence significantly increased with H. pylori infection. Furthermore, aberrant CpG methylation of specific genes, such as p16, MGMT and MINT31, was consistently associated with H. pylori infection. These findings strongly suggest that H. pylori infection causes the aberrant DNA hypermethylation of specific genes and induces CIMP, which is an important epigenetic mechanism for the development and progression of gastric MALT lymphoma; additionally, our findings provide new epigenetic markers.
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PMID:Accumulation of aberrant CpG hypermethylation by Helicobacter pylori infection promotes development and progression of gastric MALT lymphoma. 1963 75