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Histopathologie observations of 9,10-dimethyl-l ,2-benzanthraeene (DMBA)-indueed tumors in the motise submandibular glands are reported using eryoprobe treatment. The experimental animals were divided into 2 groups; one received a eaieinogen iitjection into the normal submanditiular gland, and the other was injeeted with DMBA on the 14th day following cryosurgety of the gland using a -60°C eryoprobe. Pathologie findings were elassified as premalignant lesions or squamous-cell eareinomas with varying degrees of keratiiiizalion, fibrosarcoma and mixed carcinoma. There was also one case eaeh of malignant pleomorphie adenoma and eystie adenoma. Tumor incidenee was nearly the same in the 2 groups. Most of the catcinomas and sareottias in the submandibular gland were induced during the 12th and 17th weeks. DMBA application during the proliferating stage which followed the etyosutgety did not enhance epithelial-tumor itiduction. During submandibular gland eareinogenesis, alterations in the granular convoluted tubule eells suggests they were the initial target eells undergoing malignant ttansfonnation. St|uamous-eell careinottias with varying degrees of keratinization were indueed following squamous metaplasia in duet4ike struetures or multieystic lesions.

Immunohistochemical identification of factor VIII related antigen (F VIII RAG) filament proteins (actin, myosin, filamin, vimentin and desmin) and lectin binding patterns of Con A, PNA, SBA, WGA, RCA-1, UEA-1 and DBA in the endothelial cells and the muscular layers of haemangiomas and normal blood vessels are reported, using paraffin sections with the HRP method. The endothelial cells of haemangiomas were usually strongly positive to F VIII RAG as were those from capillary vessels and other small vessels. Some of the endothelium from haemangiomas and angiokeratomas was negative for factor VIII. The vessel walls of hemangiomas showed staining slightly positive for microfilaments (actin, myosin, filamin). The smooth muscle layer in small vessels showed a more marked staining with actin. Vimentin and desmin reactions in the vessel walls of haemangioma and in normal vessels were slight or moderate. UEA-1 lectin binding was constantly positive in endothelial cells from hemangiomas and in blood vessels. SBA and WGA binding appeared in the border layer of endothelium in haemangiomas and normal vessels.

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.

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