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This unusual case is that of a middle-aged man exhibiting a tumor diathesis including a basal cell adenocarcinoma with features of adenoid cystic carcinoma arising in minor salivary gland of lip in association with multiple primary malignant cylindromas of skin. The labial lesion showed invasive tubules, solid epithelial sheets and cribriform structures. It did not exhibit PAS positive juxta-tubular basement membrane material. The skin lesions all showed features of a highly infiltrative cylindromatous carcinoma with two cell types, peripheral palisading and prominent PAS positive juxta-tubular basement membrane material. Immunocytochemical studies of the lip lesion and one of the skin lesions showed similarities, including positive staining for high and low molecular weight keratins and S-100 with negative staining for CEA. The precious descriptions of tumor diatheses involving dermal cylindromas and dermal analogue tumors of salivary glands and the distinctions with the present study are noted. If benign and even malignant cylindromas were described in the literature to be associated with basal cell adenocarcinoma of the major salivary glands, our case is unique by its association with this rare malignant tumor in a minor salivary gland.

Activation of c-Ki-ras by point mutation within exon 1 was studied in 33 specimens of dysplastic gastrointestinal lesions or of cancers presumed to arise from dysplasia. Samples were obtained from patients with underlying ulcerative colitis or Barrett's esophagus, two diseases associated with dysplasia and increased rates of colonic or esophageal adenocarcinoma, respectively. Genomic DNA was amplified using primers bounding this exon in the polymerase chain reaction. Polymerase chain reaction products were analyzed by direct dideoxy sequencing. Three point mutations in codon 13 of c-Ki-ras were found, all in colonic specimens (two high-grade dysplasias and one adenocarcinoma arising in ulcerative colitis). No point mutations were observed in the second exon of c-Ki-ras or in and around codons 12, 13, and 61 of c-N-ras and C-Ha-ras in a partial sampling of the specimens. These data indicate that ras family protooncogene activation is an uncommon event at this level of malignant progression in these disease states. Carcinogenesis in ulcerative colitis and Barrett's esophagus may proceed via different pathways than in sporadic colon cancer, perhaps involving loss or inactivation of suppressor genes.

Eleven endometrial adenoacenthomas were studied ultrastructurally. Special emphasis was placed on patterns of squamous metaplasia and the appearance of the basal laminae. Tonofibrils, irregular keratohyaline, abundant desmosomes, and foci of frank keratinization were observed. However, the granule population was small, with relatively scanty keratohyaline and no definite membrane coating granules. These features resemble squamous metaplasia observed in various epithelia; experimental models utilizing estrogens also resulted in similar changes. This observation appears pertinent in view of the possible etiologic role played by high estrogen levels in the development of human endometrial carcinoma. Most tumor cell clusters were surrounded by a well-defined basal lamina; focal basal lamina reduplication was also observed. These observations suggest a high level of differentiation in respect to synthetic capabilities and cell surface recognition. They correlate well with the relatively favorable prognosis generally observed in endometrial adenoacanthomas. However, these conclusions are tempered by the finding of occasionally absent or defective basal lamine, indicative of partial dedifferentiation of some neoplastic cells.