AIM:To assess NY-ESO-1 expression in a cohort of esophageal adenocarcinomas.METHODS:A retrospective search of our tissue archive for esophageal resection specimens containing esophageal adenocarcinoma was performed,for cases which had previously been reported for diagnostic purposes,using the systematised nomenclature of human and veterinary medicine coding system.Original haematoxylin and eosin stained sections were reviewed,using light microscopy,to confirm classification and tumour differentiation.A total of 27 adenocarcinoma resection specimens were then assessed using immunohistochemistry for NY-ESO-1 expression:4 well differentiated,14 moderately differentiated,4 moderatepoorly differentiated,and 5 poorly differentiated.RESULTS:Four out of a total of 27 cases of esophageal adenocarcinoma examined(15%)displayed diffuse cytoplasmic and nuclear expression for NY-ESO-1.They displayed a heterogeneous and mosaic-type pattern of diffuse staining.Diffuse cytoplasmic staining was not identified in any of these structures:stroma,normal squamous epithelium,normal submucosal gland and duct,Barrett’s esophagus(goblet cell),Barrett’s esophagus(non-goblet cell)and high grade glandular dysplasia.All adenocarcinomas showed an unexpected dot-type pattern of staining at nuclear,paranuclear and cytoplasmic locations.Similar dot-type staining,with varying frequency and size of dots,was observed on examination of Barrett’s metaplasia,esophageal submucosal gland acini and the large bowel negative control,predominantly at the crypt base.Furthermore,a prominent pattern of apical(luminal)cytoplasmic dot-type staining was observed in some cases of Barrett’s metaplasia and also adenocarcinoma.A further morphological finding of interest was noted on examination of haematoxylin and eosin stained sections,as aggregates of lymphocytes were consistently noted to surround submucosal glands.CONCLUSION:We have demonstrated for the first time NY-ESO-1 expression by esophageal adenocarcinomas,Barrett’s metaplasia and normal tissues other than germ cells. AIM: To assess NY-ESO-1 expression in a cohort of esophageal adenocarcinomas. METHODS: A retrospective research of our tissue archive for esophageal resection specimens containing esophageal adenocarcinoma was performed, for cases which previously previously reported for diagnostic purposes, using the systematised nomenclature of human and veterinary medicine coding system. Native haematoxylin and eosin stained sections were reviewed, using light microscopy, to confirm the classification and differentiation differentiation. A total of 27 adenocarcinoma resection specimens were then assessed using immunohistochemistry for NY-ESO-1 expression: 4 well differentiated, 14 moderately differentially differentiated, 4 moderately differentially differentiated, and 5 poorly differentiated .RESULTS: Four out of a total of 27 cases of esophageal adenocarcinoma examined (15%) displayed diffuse cytoplasmic and nuclear expression for NY-ESO-1.They displayed a heterogeneous and mosaic-type pattern of diffuse staining. Diffuse cytoplasmic staining was not iden tified in any of these structures: stroma, normal squamous epithelium, normal submucosal gland and duct, Barrett’s esophagus (goblet cell), Barrett’s esophagus (non-goblet cell) and high grade glandular dysplasia. All adenocarcinomas showed an unexpected dot-type pattern of staining at nuclear, paranuclear and cytoplasmic locations. Similar dot-type staining, with varying frequency and size of dots, was observed on examination of Barrett’s metaplasia, esophageal submucosal gland acini and the large bowel negative control, predominantly at the crypt base. Stillmore, a prominent pattern of apical (luminal) cytoplasmic dot-type staining was observed in some cases of Barrett’s metaplasia and also adenocarcinoma. A further morphological finding of interest was noted on examination of haematoxylin and eosin stained sections, as aggregates of lymphocytes were consistently noted surround submucosal glands.CONCLUSION: We have demonstrated for the first time NY-ESO-1 expression by esophageal adenocarcino mas, Barrett’s metaplasia and normal tissues other than germ cells.