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 ...