Mucosa-associated lymphoid tissue (MALT) lymphoma is characterized by t(11;18)(q21;q21)/API2-MALT1, t(1;14)(p22;q32)/ BCL10-IGH and t(14;18)(q32;q21)/IGH-MALT1, which commonly activate the nuclear factor (NF)-jB pathway. Gastric MALT lymphomas harboring such translocations usually do not respond to Helicobacter pylori eradication, while most of those without translocation can be cured by antibiotics. To understand the molecular mechanism of these different MALT lymphoma subgroups, we performed gene expression profiling analysis of 21 MALT lymphomas (13 translocation-positive, 8 translocation-negative). Gene set enrichment analysis (GSEA) of the NF-jB target genes and 4394 additional gene sets covering various cellular pathways, biological processes and molecular functions have shown that translocation-positive MALT lymphomas are characterized by an enhanced expression of NF-jB target genes, particularly toll like receptor (TLR)6, chemokine, CC motif, receptor (CCR)2, cluster of differentiation (CD)69 and B-cell CLL/lymphoma (BCL)2, while translocationnegative cases were featured by active inflammatory and immune responses, such as interleukin-8, CD86, CD28 and inducible T-cell costimulator (ICOS). Separate analyses of the genes differentially expressed between translocation-positive and -negative cases and measurement of gene ontology term in these differentially expressed genes by hypergeometric test reinforced the above findings by GSEA. Finally, expression of TLR6, in the presence of TLR2, enhanced both API2-MALT1 and BCL10-mediated NF-jB activation in vitro. Our findings provide novel insights into the molecular mechanism of MALT lymphomas with and without translocation, potentially explaining their different clinical behaviors.

We found a higher rate of perforation and lower frequency of GCB phenotype in PI-DLBL in Taiwan compared with other geographical areas; perforation is a poor prognostic indicator.

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992-996. 7. Lucendo AJ, Navarro M, Comas C et al. Immunophenotype characterization and quantitation of the epithelial inflammatory infiltrate in eosinophilic esophagitis through stereology. Am. J. Surg. Pathol. 2007; 31; 598-606. 8. Aceves SS, Newbury RO, Dohil R et al. Distinguishing eosinophilic esophagitis in pediatric patients. Clinical, endoscopic and histological features of an emerging disorder. J. Clin. Gastroenterol. 2007; 41; 252-256. 9. Kagalwalla AF, Shah A, Ritz DS, Melin-Aldana H, Li B. Cow's milk protein-induced eosinophilic esophagitis in a child with gluten-sensitive enteropathy. J. Pediatr. Gastroenterol. Nutr. 2007; 44; 386-388. 10. Ronkainen J, Talley NJ, Aro P et al. Prevalence of oesophageal eosinophils and eosinophilic oesophagitis in adults: the population-based Kalixanda study. Gut 2007; 56; 615-620. 11. Rothenberg ME. Pathogenesis and clinical features of eosinophilic esophagitis. J. Allergy Clin. Immunol. 2001; 108; 891-894. 12. Spechler SJ, Genta RM, Souza RF. Thoughts on the complex relationship between gastroesophageal reflux disease and eosinophilic esophagitis.Sir: The cell cycle regulatory protein cyclin D1 is aberrantly expressed in mantle cell lymphomas (MCL) as a result of the t(11;14)(q13;q32) ⁄ CCND1-IGH. 1,2 Consequently, immunohistochemistry for cyclin D1 is a valuable tool in the distinction of MCL from other small B-cell lymphomas. 2 Cyclin D1 immunohistochemistry is also central to the discrimination between the pleomorphic blastoid variant of MCL, an aggressive form of MCL with large cell morphology, high proliferative activity and complex karyotypes, and diffuse large B-cell lymphoma (DLBCL), a biologically and genetically heterogeneous group of aggressive lymphomas not associated with t(11;14)(q13;q32). 2 However, in this report we present a case of DLBCL expressing cyclin D1 in the absence of t(11;14)(q13;q32), suggesting that aberrant expression of cyclin D1 may play a role in the pathogenesis of some DLBCLs and demonstrating that cyclin D1 immunopositivity alone is not sufficient for distinction between pleomorphic blastoid MCL and DLBCL in all cases. The patient, a 77-year-old woman, had widespread lymphadenopathy, pulmonary and splenic nodules and erythematous cutaneous papules on the thigh, but no bone marrow involvement (Ann Arbor stage 4A disease). Laboratory investigation showed a normal white cell count (5.7 · 10 9 ⁄ l) and a markedly raised lactate dehydrogenase level (1572 units ⁄ l). The patient began immunochemotherapy with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisolone (R-CHOP), but died before completion of therapy.Examination of an inguinal lymph node biopsy specimen ( Figure 1) showed a diffuse infiltrate of large atypical lymphoid cells with round, oval or elongated nuclei, one or more prominent nucleoli and moderately abundant cytoplasm. There were numerous mitoses and scattered tingible body macrophages and apoptotic cells. Immunohistochemistry showed the neoplastic cells to be CD20+ B cells which expressed Bcl-6, MUM1 and ...