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We applied immunohistochemical procedures to detect hEGF in salivary glands and pleomorphic adenomas of salivary-gland origin using a polyclonal hEGF antiserum and a monoclonal antibody against hEGF synthesized by applying the synthetic gene technique using Escherichia coli. In normal salivary glands, hEGF was mainly localized in the ductal system (i.e., intercalated, striated, and excretory ducts). The staining intensity and intracellular localization exhibited some variation depending on the fixative used. When a polyclonal hEGF antiserum was used for immunostaining, slight background staining was observed in sections prepared using the fixatives tested. Therefore, precise localization of hEGF was obtainable only in formalin-fixed sections using the monoclonal antibody against hEGF. In pleomorphic adenomas, positive hEGF staining was seen on the luminal side of tumors and in cells of ductal origin; no reactivity was present on the outer side of tumors or in cells of myoepithelial origin. Occasionally, long, spindle-shaped tumor cells and chondroidally changed tumor cells also exhibited positive staining for hEGF.

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Lectin‐binding profiles and keratin distribution in obstructive adenitis of human submandibular glands (SMGs) are reported and compared those of normal SMGs. Histologically, obstructive changes in the SMGs included acinar atrophy, duct‐like structure formation in the early stage, and disappearance of acinar cells and dilation of ductal segments in the later, chronic stage. The following lectins were used: Con A (Glc. Man), PNA(Gal, GalNAc). RCA1I(Gal), DBA(GalNAc). SBA(Gal, Gal‐NAc). UEA‐1(α‐L‐Fuc) and WGA((GlcNAC, NeuNAc). Lectin staining in atrophie acinar cells was usually reduced except for SUA binding and was irregularly distributed in altered acinar and ductal epithelia. Binding of DBA and UEA‐1 lectins were particularly intense along the luminar borders of ductal segments in the lesions. Immunohistochemically detectable keratins were characterized by intense staining in atrophie acinar cells and in all the ductal segments, whereas normal acinar cells, either serous or mucous, were negative.