Histochemical detection of lectin binding was carried out using the HRP-conjugated lectin method in hyperkeratinized lesions including leukoplakia, carcinoma in situ, Paget's disease, keratoacanthoma, and condyloma acuminatum. The lectins used for demonstrating sugar residues were: Con A (hexose), PNA and RCA-1 (Gal), DBA and SBA (GalNAc), UEA -1 (Fuc), and WGA (GlcNAc). Lectin binding in normal squamous epithelium showed regional distribution patterns of keratinized, spinous and basal layer types. Histochemical localization of lectin binding was generally at the cellular surface and in the intercellular substance and sometimes in the cytoplasm of normal epithelial cells. Dysplastic cells or carcinoma cell, in contrast, displayed a loss of cellular surface and intercellular staining. Paget's cells were devoid of lectin staining. In keratoacanthoma and condyloma specimens, spinous cells, which were PAS-positive, showed an intense PA/Con A-HRP staining and moderate binding by other lectins, which was somewhat decreased when compared with that in the surrounding intact epithelium. The cytochemical distribution of epithelial lectin binding might be indicative of the expression of normal stratification and keratinocytic differentiation , and the disappearance of this typical epithelial pattern may suggest severe dysplasia and malignancy.

An immunohistochemical survey of the distribution of keratin was studied in chemically induced carcinomas of the submandibular glands of mice. Initial signs of premalignant changes were degranulation of granular convoluted tubule cells and deposition of keratin protein in small limited areas of the degranulated cells. There was a gradual increase in the area showing keratin staining in altered tubule cells. Duct‐like and cystic structures stained intensely for keratin, as did squamous metaplastic epithelial cells. Induced carcinomas were variably keratinized. Basal layers of cells of squamous‐cell carcinomas displayed weak keratin staining, and spinous tumor cells and parakeratotic tumor cells showed somewhat increased levels of keratin staining. Some desquamated keratotic tumor cells stained intensely for keratin. Just as the localization of epidermal and nerve growth factors and lectin‐binding histochemistry have been used in studying tumorigenesis in the mouse submandibular gland, immunohistochemically detected keratin proved to be a useful marker of tumor cells of ductal segment origin.

No abstract